Lec 1 Reading

MVS 110 EXERCISE PHYSIOLOGY PAGE 1
READING #1
INTRODUCTION TO SCIENCE
The Scientific Method and Exercise Physiology

As the academic discipline of exercise physiology emerged, so also developed research strategies for
objective measurement and problem solving, and the need to report discoveries of new knowledge. For the
beginning exercise physiology student, familiarization with the methods of science helps to separate fact from
“hype” - most often encountered in advertising about an endless variety of products sold in the health,
fitness, and nutrition marketplace. How does one really know for sure whether a product really works as
advertised? Does warming up really “warm” the muscles to prevent injury or enhance subsequent
performance? Will breathing oxygen on the sidelines during a football game really help the athlete recover?
Do vitamins “supercharge” energy metabolism during exercise? Will creatine, chromium, or vanadium
supplements add muscle mass during resistance training? Understanding the role of science in problem
solving can help to make informed decisions about these and many other questions. The following section
examines the goals of science, including different aspects of the scientific method of problem solving.
General Goals of Science

The two distinct goals of science often seem at odds. One goal aims to serve mankind, to provide solutions
to important problems, and improve life’s overall quality. This view of science, most prevalent among
nonscientists, maintains that all scientific endeavors should exhibit practicality and immediate application.
The opposing view, predominant among scientists, maintains that science should describe and understand all
occurrences without necessity for practical application - understanding phenomena becomes a worthy goal in
itself. The desire for full knowledge implies being able to:
 Account for (explain) behaviors or events
 Predict (and ultimately control) future occurrences and outcomes.
Regardless of one’s position concerning the goal of science, its ultimate aims include:
 Explanation
 Understanding
 Prediction
 Control
Hierarchy in Science
Full appreciation of science requires
understanding its structure and three levels of
conceptualization (see figure 1):
 Finding facts
 Developing laws
 Establishing theories
Figure 4. Foundations of science: facts, laws and theories.
Fact Finding
The most fundamental level of scientific inquiry requires the systematic observation of measurable
(empirical) phenomena. Often referred to as fact-finding, this process requires standardized procedures and
levels of agreement about what constitutes acceptable observation, measurement, and data recording
procedures. In essence, fact-finding involves recording information (data) about the behavior of objects.
While facts provide the “building blocks” of science, the uncovering of facts represents only the first level in
the hierarchy of scientific inquiry.
Fact gathering occurs in many ways. We usually observe phenomena through visual, auditory, and tactile
sensory input. Regardless of the observation method, to establish something as fact demands that different
researchers reproduce observations under identical conditions on different occasions. For example, the
healthy human heart’s four chambers and the average sea level barometric pressure of 760 mm Hg represent
indisputable, easily verifiable “facts.” Facts usually take the form of objective statements about the
observation such as: “Jesse’s body mass measured on a balance scale equals 70 kg (154 lb.), or “Jesse’s heart
rate upon rising following eight hours of sleep averages 63 beats per minute.”
FOR YOUR INFORMATION

FACTS ARE FACTS…
Facts exhibit no moral quality; once established, any question about facts arises only from
interpretation. While some may disagree with the meaning and implications of an established fact
(e.g., the average woman possesses 50% of absolute upper body strength of a male counterpart),
no question exists about the “correctness” of the observation (that women have less upper body
strength than males). In essence, a fact is a fact....
Interpreting Facts
Fact-finding evaluates the observed object, occurrence, or phenomenon along a continuum, either
imagined or real that represents its underlying measurable “dimension.” The term variable identifies this
measurable characteristic. Frequently, quantification of the variable results from assigning numbers to objects
or events to describe their properties. For example, consider the variable percent body fat with numerical
values ranging from 3 to 60% of total body mass. Other examples include the weight of an object along a
“heaviness” continuum, order of team finish in the NFL's American Conference, or heart rate from rest to
maximal exercise.
Some variables like 50-m swim time or blood cholesterol level distribute in a continuous nature; they can
take on any numerical value, depending on the precision of the measuring instrument. Continuous variables
can further categorize into ordinal, interval, and ratio numerical data. Ordinal variables have rank-ordered
values (e.g., small, medium, large bone frame size; first through tenth place finish in a race; standings in
league competition) according to some property about each person, group, object, or event compared to
others studied. In ordered ranking, no inference exists of equal differences between specific ranks (e.g., race
time difference between first and second place finish equals difference between ninth and tenth place).
Interval variables exhibit similar properties as ordinal variables, except the distance between successive
values on an unbroken scale from low to high represents the same amount of change. For example, in
marathon running, the temporal 20-minute difference between a finish time of 2 hr: 10 min and 2 hr: 30 min
equals that of 3 hr: 50 min and 4 hr: 10 min. The ratio scale possesses properties of interval and ordinal
scoring, but also contains an absolute zero point. Thus, a variable scored on a ratio basis with a value of 4
represents twice as much characteristic as a value of 2; this does not occur with interval-scored variables like
temperature where 30°F is not twice as “hot” as 15°F.
In addition to continuous variables, some variables possess discrete properties. Scores for discrete
variables fall only at certain points along a scale, like scores in most sporting events - “almost in” does not
count in golf, soccer, basketball, or lacrosse. Discrete variables occur when the score’s value simply reflects
some characteristic of the object (e.g., male or female, hit or miss, win or lose, or true or false).
Casual and Causal Relationships

A fundamental scientific process involves observing and objectively measuring the quantity of a variable.
However, it sometimes becomes more important to consider how data from one variable relate to data from
another variable. Understanding how variables change in relation to each other represents a higher level of
science than merely describing and quantifying diverse isolated variables. For example, quantifying the
degree of association between maximal oxygen uptake capacity (abbreviated VO 2max) and chronological age
reflects a higher level of understanding than describing the “facts” concerning each variable separately.
An extreme example to illustrate that association between variables does not necessarily infer causality
considers the strong direct association in western culture between the length of one’s trousers and stature
(i.e., taller individuals wear longer-length pants than shorter counterparts). It seems highly unlikely that
increasing trouser length would increase stature! In reality, this association is casual, not causal, being driven
more by cultural mores that “require” trousers to descend to ankle level - and leg length relates closely with
overall body stature.
The well established positive relationship between increasing age and increasing systolic blood pressure
among adults does not necessarily mean that one should expect to inevitably become hypertensive with
advancing years. Rather, the relationship exists between aging and blood pressure because other factors -
sedentary lifestyle, obesity, arteriosclerosis, increased stress, and poor diet - often increase with age. Each of
these variables independently can elevate blood pressure. From a scientific perspective, a change in one
variable (X) does not necessarily cause changes in the other variable(Y), simply because X and Y relate in a
manner that seems to “makes sense.”

CAUSALITY AND SCIENCE
To infer causality, science requires that a change in the X-variable (independent manipulated
variable) precedes a change in the Y-variable (dependent variable expected to change), with
consideration, accounting for, or control of other variables that might actually cause the
relationship. Understanding causal factors in relationships among variables enhances one’s
understanding about observed facts.
INDEPENDENT AND DEPENDENT VARIABLES

Two categories of variables, independent and dependent, take on added importance when defining the
nature of relationships among occurrences. This categorization relates to the manner of the variable’s use, not
the nature of the variable itself. For causal relationships, manipulation of the value of the independent
variable (X-variable) changes the value of the dependent variable (Y-variable). For example, increases in
dietary intake of saturated fatty acids (independent X-variable) increase levels of serum cholesterol
(dependent Y-variable), while decreases in saturated fatty acid intake reduce serum cholesterol levels. In
other words, the value of the dependent variable literally “depends upon” the value of the independent
variable.
For noncausal relationships, the distinction between dependent and independent variables becomes less
clear. In such cases, the independent variable (e.g., the sum of five skinfolds or recovery heart rate on a step
test) usually becomes the predictor variable, while the dependent variable (percent body fat or maximal
oxygen uptake) represents the quality predicted. In some cases, an independent variable becomes the
dependent variable, and vice versa. For example, body temperature represents the independent variable
when used to predict change in regional blood flow or sweating response; body temperature assumes a
dependent variable role when evaluating effectiveness of thermoregulation during heat stress.
ESTABLISHING CAUSALITY BETWEEN VARIABLES
Scientists attempt to establish cause and effect relationships between independent and dependent
variables by one of two methods:
 Experimental studies
 Field studies
NATURE OF EXPERIMENTAL STUDIES
An experiment represents a set of operations to determine the underlying nature of the causal relationship
between independent and dependent variables. Systematically changing the value of the independent
variable and measuring the effect on the dependent variable characterizes experimentation. In some cases,
the experiment evaluates the effect of combinations of independent variables (e.g., anabolic steroid
administration plus resistance training; pre-exercise warm-up plus creatine supplementation) relative to one
or more dependent variables. Regardless of the number of variables studied, an experiment’s ultimate goal
attempts to systematically isolate the effect of at least one independent variable in relation to at least one
dependent variable. Only when this occurs can one decide which variable(s) really explains the phenomenon.
NATURE OF FIELD STUDIES
Field studies mostly investigate events as they occur in normal living. Under such “natural” conditions, it
becomes impossible to experimentally vary the independent variable, or exert full control over potential
interacting factors that might affect the relationships. In medical areas, field studies (termed epidemiological
research) investigate the characteristics of a group as they relate to the risks, prevalence, and severity of
specific diseases. To a large extent, “risk profiles” for coronary artery disease, various cancers, and AIDS have
emerged from associations generated from field studies. In exercise physiology, a field study might involve
collecting data during a “real world” test of a new piece of exercise equipment, as shown in Figure 2.
In this field experiment the subject wears a wristwatch that receives signals
from a chest strap transmitter that sends the heart's electrical signals to the
watch. The subject then pedals the “Surfbike” at different speeds to estimate
heart rate during different exercise durations. Prior to the aquatic experiments,
the subject’s heart rate and oxygen uptake were determined in the laboratory
while pedaling a bicycle ergometer at different speeds. A linear relationship
between laboratory determined heart rate and oxygen uptake allowed the
researcher to “predict” the subject's oxygen uptake from heart rate measured
during Surfbike exercise. An estimate of oxygen uptake permits calculation of
caloric expenditure. In this particular experiment, Surfbike exercise at a heart
rate of 178 beats per minute translated to 10.4 calories expended per minute.
While field studies provide objective insight about possible causes for
observed phenomena, the lack of full control inherent in such research limits
their ability to infer causality. Because neither active manipulation of the
independent variable by the experimenter nor control over potential
intervening factors occurs, no certainty exists that any observed variation in the
dependent variable will result from variations in the independent variable.
Figure 2. Field study in exercise to
estimate energy expenditure
individuals pedaling a “surfbike”.
Establishing Laws
Fact gathering generally does not generate much controversy; after all, facts are facts! Interpretation of
facts, however, raises science to a level rife for debate. Interpreting facts leads to the second level of the
scientific process - creating statements that describe, integrate, or summarize facts and observations. Such
statements are known as laws. More precisely, a law represents a statement describing the relationships
among independent and dependent variables. Laws generate from inductive reasoning (moving from
specific facts to general principles). Many examples of laws exist in physiology. For example, blood flows
through the vascular circuit in general accord with the physical laws of hydrodynamics applied to rigid,
cylindrical vessels. Although true only in a qualitative sense when applied to the body, one law of
hydrodynamics, termed Poiseuille's law, describes the interacting relationships among a pressure gradient,
vessel radius, vessel length, and fluid viscosity on the force impeding blood flow.
Laws are purposely not very specific; thus, they remain powerful because they generalize to many
different situations. One variation of Hooke’s law of springs, made in 1678 by Robert Hooke (1635-1703), a
contemporary of sir Issac Newton, states that elongation of a spring relates in direct proportion to the force
needed to produce the elongation. Engineers apply this law to design springs for different kinds of
instruments via simple calculations in accordance with Hooke’s law.
A good (useful) law accounts for all of the facts among variables. Many laws have limits because they
apply to only certain situations. A limited law proves less useful in predicting new facts. A fundamental
aspect of science tests predictions generated from a particular law. If the prediction holds up, the law expands
to additional situations; if not, the law becomes restated in more restrictive terms. Developing new
technologies often permits testing laws in situations heretofore thought impossible; this allows for
development of a more comprehensive law.
Laws do not provide an explanation why variables behave the way they do; laws only provide a general
summary of the relationship among variables. Theories explain the how and whys about a laws.
Developing Theories
Theories attempt to explain the fundamental nature of laws. Theories offer abstract explanations of laws
and facts. They try to explain the “why” of laws. Theories involve a more complex understanding (and
explanation) of variables than do laws. Examples of theories include Darwin's theory of natural selection and
evolution, Einstein's theory of relativity, Canon's theory of emotions, Freud's theory of personality formation
and development, and Helmholtz's theories of color vision and hearing.
Theories consist of three aspects:
1. Hypothetical construct
Hypothetical constructs represent non-observable abstract entities, consciously invented and
generalized for use in theories. For example, the construct of “intelligence” emerged from
observations of presumably intelligent and non-intelligent behaviors. “Physical fitness”
represents another common construct in areas related to exercise physiology.
2. Associations among constructs
Scientific inquiry often requires defining relationships among constructs. For example, the
construct “physical ability” becomes clarified by its association to the construct “physical
fitness,” which itself becomes operationally defined (see below) by numerous specific “fitness”
tests. In essence, the meaning of one construct becomes understood through its relationship to
other more clearly defined constructs.
3. Operational definitions
The scientific process requires refinement of constructs into observable characteristics for
objective quantification and recording. Operational definitions assign meaning to a construct by
clearly outlining the set of operations (like an instruction manual) to measure the quantity of
that construct or to manipulate it. For example, the construct intelligence only becomes
understood when operationally defined (score on a specific IQ test).
The Surety of Science

Experimentation represents the scientific mechanism for testing hypothesis; scientists either reject or fail to
reject an hypothesis. Rejecting a hypothesis represents a powerful outcome because it may nullify a theory
and specific predictions generated from the theory. Failure to reject an hypothesis indicates that the
observable results appear to support the theory. The terms reject and fail to reject (in contrast to prove and
disprove) deserve special attention. Failure to reject does not indicate confirmation or proof, only inability to
reject an hypothesis. However, if other experiments (particularly from independent laboratories) also fail to
reject a given hypothesis, a strong likelihood exists (high probability) of a correct hypothesis. The structure of
science makes it impossible to totally confirm a theory's absolute “correctness” because scientists may still
devise a future experiment to disprove the theory. The strength of the experimental method lies in rejecting
hypotheses that have direct bearing on theories or predictions from theories. The notion of disproof
represents an important distinguishing feature of the scientific method.
Publishing Results of Experiments

Fact-finding, law formulation, and theory development represent fundamental aspects of science.
Allowing fellow scientists to critique one’s research findings prior to their distribution completes the process
of scientific inquiry. Most journals that disseminate research rely on the researcher’s peers to review and pass
judgment on the suitability and quality of methods, experimental design, appropriateness of conclusions, and
contribution to new knowledge. While this aspect of science often receives criticism for failing to achieve true
objectivity and freedom from professional bias, few would discount its importance; when executed properly,
peer review in refereed journals maintains a level of “quality control” in disseminating new information.
Imagine the many instances where an experimental outcome could be influenced by self-interest and/or
professional bias. Athletic shoe and nutrient supplement manufacturers sponsor sophisticated laboratories to
conduct detailed “research” on the efficacy of their products. To assure credibility, research from such
laboratories must be reviewed by experts having no affiliation (direct or indirect) with the company. Without
a system of “checks and balances,” such studies should be rightfully viewed with skepticism, and lack
trustworthiness as a legitimate source of new knowledge.
Empirical vs. Theoretical – Basic vs. Applied Research

Different approaches lead to successful
experimentation and knowledge acquisition.
Figure 3 shows two different continuum for
experimentation. The theoretical-empirical
research continuum has at its foundation
experimentation related to establishing laws
and testing theories. Scientists in theoretical
research maintain that fact finding alone
represents an unfocused waste of energy if the
process does not emanate from and contribute
Figure 3. Research continuum in science.
to theory building. Scientists at the opposite end of the continuum collect facts and make observations with
little regard for building theory. The influential psychologist B.F. Skinner exemplifies the proponent of the
empirical research (experience related) approach. His discoveries about reinforcement - a reward for
successful behavior increases the probability of success in subsequent trials - were uncovered by “accident.”
Skinnerian empiricists argue that theoretical scientists often do not uncover meaningful relationships because
they become too “locked into” theoretical formulations and abstract models.
Basic-applied research represents another continuum. Applied research incorporates scientific endeavors
to solve specific problems, the solution of which directly applies to medicine, business, the military, sports
performance, or society’s general well being. Applied research in exercise physiology might focus on methods
for improving training responsiveness, facilitating fluid replenishment and temperature regulation in
exercise, enhancing endurance performance, blunting the effects of fatigue by-products, and countering the
deterioration of physiologic function during prolonged exposure to a weightless environment.
Basic research lies at the other end of this continuum; no concern exists for immediate practical application
of research findings. Instead, the researcher pursues a line of inquire purely for the sake of discovering new
knowledge. Often times, uncovering facts that initially seem of little value fill a theoretical void – and like
magic, a wonderful new practical solution (or product) emerges. Nowhere has this taken place with more
regularity than with research related to the space program. Facts uncovered in a weightless environment
about fundamental biological and chemical processes have contributed to practical outcomes that benefit
humans. Experiments on how certain chemicals react in zero gravity, for example, have resulted in the
discovery of at least 25 new medicines. Manned space missions have provided fresh insights into almost
every facet of medicine and physiology, from the affects of weightlessness on bone dynamics, blood pressure,
and cardiac, respiratory, hormonal, neural, and muscular function, to growth of genetically engineered plants
and a new generation of polymers. Each new insight and observation spawns numerous new ideas and
additional facts that help to create products with practical applications.
Research can be generally classified into one of four categories depicted by the quadrants in Figure 6.
Basic-empirical research in Quadrant 1 has no immediate practical outcomes and little to do with theory.
Research without immediate practical implications, but motivated by theory (establishing laws and
conducting experiments that bear on theory), falls into Quadrant 2. Quadrant 3 contains theoretical-applied
research primarily focused on problem solving within the framework of an existing theoretical model, while
Quadrant 4 classifies empirical-applied research (not theory based), but aimed at solving problems. Often,
lines of demarcation are not as clear-cut as in the figure, and a particular research effort might qualify for
inclusion in multiple quadrants.
READING #1 STUDY GUIDE
Define Key Terms and Concepts
1. Applied research
2. Basic research
3. Casual relationships
4. Causal relationships
5. Continuous variables
6. Dependent variables
7. Laws
8. Disciplines
9. Discrete variables
10. Empirical research
11. Theories
12. Experimental studies
13. Field of study
14. Field studies
15. Science hierarchy
16. Independent variables
17. Operational definitions
18. Profession
19. Science
20. Theoretical research
STUDY QUESTIONS
The Scientific Method and Exercise Physiology

General Goals of Science
Give two goals of science.
1.
2.
Give four aims of science.

1. 3.
2. 4.
Hierarchy in Science
List the three levels of a science.
1.
2.
3.
Fact Finding
Give two ways to “find facts”.
1.
2.
Interpreting Facts
Describe an independent variable.
Describe a dependent variable.
Casual and Causal Relationships

Independent and Dependent Variables
List two methods to establish cause and effect relationships between independent and dependent
variables.
1.
2.
Nature of Experimental Studies

Give the main point of experimental studies.
Nature of Field Studies

Give the main point of field studies.
Establishing Laws
Explain a law.
Developing Theories
List the three aspects of a theory and give one fact about each.
1. 3.
2.
The Surety of Science

Briefly describe the notion of “disproof.”
Empirical vs. Theoretical – Basic vs. Applied Research

Describe differences between empirical v theoretical approaches to knowledge acquisition.
READING #2
ORIGINS OF EXERCISE PHYSIOLOGY
Introduction
Discussion of the origins of exercise physiology begins with acknowledgment of the early, but
tremendously influential Greek physicians of antiquity; along the way, we highlight some milestones
including many contributions from scholars in the United States and Nordic countries that fostered the
scientific assessment of sport and exercise as a respectable field of study.
From Ancient Greece to the United States

Earliest Development – The Age of Galen
The first real focus on the physiology of exercise most likely began in early Greece and Asia Minor. The
topics of exercise, sports, games, and health concerned even earlier civilizations; the Minoan and Mycenaean
cultures, the great biblical Empires of David and Solomon, Assyria, Babylonia, Media, and Persia, and the
Empires of Alexander. The ancient civilizations of Syria, Egypt, Macedonia, Arabia, Mesopotamia and Persia,
India, and China also recorded references to sports, games, and health practices (personal hygiene, exercise,
training). The greatest influence on Western Civilization, however, came from the Greek physicians of
antiquity - Herodicus (ca. 480 BC); Hippocrates (460-377 BC), and Claudius Galenus or Galen (AD 131-201).
Herodicus, a physician and athlete, strongly advocated proper diet in physical training. His early writings
and devoted followers influenced Hippocrates, the famous physician and “father of preventive medicine”
who contributed 87 treatises on medicine including several on health and hygiene.
Five centuries after Hippocrates, Galen emerged as perhaps the most wellknown and influential physician that ever
lived. Galen began studying medicine at about age 16. Over the next 50 years he enhanced current thinking about health
and scientific hygiene, an area that some might consider applied exercise physiology. Throughout his life, Galen taught
and practiced “laws of health” (Table 1).
Laws of health according to
Galen, circa A.D. 140
1. Breathe Fresh Air
2. Eat Proper Foods
3. Drink The Right Beverages
4. Exercise
5. Get Adequate Sleep
6. Have A Daily Bowel Movement
7. Control One’s Emotions
Galen produced about 80
treatises and 500 essays on
numerous topics related to human
anatomy and physiology,
nutrition, growth and
Figure 1. The early Greek influence of Galen’s famous essay, “Exercise With the Small Ball”; a
treatise about the many uses of exercise for preventive and therapeutic medical and health
benefit. Galen advocated muscle strengthening with rope climbing because it did not pose health
problems. He firmly believed in walking and climbing mountains.
development, the beneficial effects of exercise and deleterious consequences of sedentary living, and diverse
diseases and their treatment. One of the first laboratory-oriented physiologists, Galen conducted original
experiments in physiology, comparative anatomy, and medicine; he dissected animals (e.g., goats, pigs, cows,
horses, and elephants). As physician to the gladiators (probably the first in Sports Medicine), Galen treated
torn tendons and muscles using surgical procedures he invented, and recommended rehabilitation therapies
and exercise regimens. Galen followed the Hippocratic School of medicine that believed in logical science
grounded in observation and experimentation, not superstition or deity dictates.
Galen wrote detailed descriptions about the forms, kinds, and varieties of “swift,” vigorous exercises,
including their proper quantity and duration. Galen’s essays about exercise and its effects might be
considered the first formal “How To” manuals about such topics that remained influential for the next 15
centuries.
The beginnings of more “modern day” exercise physiology include the periods of Renaissance,
Enlightenment, and Scientific Discovery in Europe. During this time, Galen’s ideas impacted the writings of
the early physiologists, doctors, and teachers of hygiene and health. For example, in Venice in 1539, the Italian
physician Hieronymus Mercurialis (1530-1606) published De arte Gymnastica apud ancientes (The Art of
Gymnastics Among the Ancients). This text, heavily influenced by Galen and other Greek and Latin authors,
profoundly affected subsequent writings about gymnastics (physical training and exercise) and health
(hygiene), in Europe and 19th century America. The panel in Figure 1, redrawn from De arte Gymnastica,
acknowledges the early Greek influence of one of Galen’s famous essays, Exercise with the Small Ball, showing
his regimen of specific strength exercises that included discus throwing rope climbing.
The Early United States Experience

By the early 1800s in the United States, European science-oriented physicians and experimental anatomists
and physiologists strongly promoted ideas about health and hygiene. Prior to 1800, only 39 first-edition
American-authored medical books had been published, several medical schools were founded (e.g., Harvard
Medical School, 1782), seven medical societies existed (the first was the New Jersey State Medical Society in
1766), and only one medical journal existed (Medical Repository, initially published in 1797). Outside of the
United States, 176 medical journals were published; by 1850 the number in the U.S. had increased to 117.
Medical journal publications in the United States increased tremendously during the first half of the
nineteenth century. Steady growth in the number of scientific contributions from France and Germany
influenced the thinking and practice of American medicine. An explosion of information reached the
American public through books, magazines, newspapers, and traveling “health salesmen” who sold an
endless variety of tonics and elixirs promising to optimize health and cure disease. Many health reformers
and physicians from 1800 to 1850 used “strange” procedures to treat disease and bodily discomforts. To a
large extent, scientific knowledge about health and disease was in its infancy. Lack of knowledge and factual
information spawned a new generation of “healers” who fostered quackery and primitive practices on a
public thirsting for anything that seemed to work. If a salesman could offer a “cure” to combat gluttony
(digestive upset) and other physical ailments, the product would catch hold and become
a common remedy.
The “hot topics” of the early 19th century (also true today) included nutrition and
dieting (“slimming”), general information about exercise, how to best develop overall
fitness, training (gymnastic) exercises for recreation and preparation for sport, and all
matters relating to personal health and hygiene. While many health faddists actually
practiced “medicine” without a license (licensure was not required to “practice”), some
enrolled in newly created medical schools (without entrance requirements), obtaining
the M.D. degree in as little as 16 weeks! Despite this brief training, some pioneer
Figure 2. Austin Flint
physicians contributed in significant ways to medical practice and development of exercise physiology as we
know it today.
By the middle 19th century, fledgling medical schools began to graduate their own students, many of
whom assumed positions of leadership in academia and allied medical sciences. Interestingly, physicians
either taught in medical school and conducted research (and wrote textbooks) or affiliated with departments
of physical education and hygiene.
Austin Flint, Jr., M.D.: American Physician-Physiologist

Austin Flint, Jr., M.D. (1836-1915; Figure 2 right), a pioneer American physician-scientist, contributed
significantly to the burgeoning literature in physiology. A respected physician, physiologist, and successful
textbook author, he fostered the belief among 19th century American physical education teachers that
muscular exercise should be taught from a strong foundation of science and experimentation. Flint, professor
of physiology and physiological anatomy in the Bellevue Hospital Medical College of New York, chaired the
Department of Physiology and Microbiology from 1861 to 1897. In 1866, he published a series of five classic
textbooks, the first entitled The Physiology of Man; Designed to Represent the Existing State of Physiological Science
as Applied to the Functions of the Human Body. Vol. 1; Introduction; The Blood; Circulation; Respiration. Eleven years
later, Flint published The Principles and Practice of Medicine, a synthesis of his first five textbooks consisting of
987 pages of meticulously organized sections with supporting documentation. Dr. Flint, well trained in the
scientific method, received the American Medical Association’s prize for basic research on the heart in 1858.
He published his medical school thesis, “The phenomena of capillary circulation,” in an 1878 issue of the
American Journal of the Medical Sciences. His 1877 textbook included many exercise-related details about: (1)
Influence of posture and exercise on pulse rate; (2) Influence of muscular activity on respiration; and (3)
Influence of muscular exercise on nitrogen elimination.
Flint was well aware of scientific experimentation in France and England, and cited the experimental
works of leading European physiologists and physicians including the incomparable François Magendie
(1783-1855), Claude Bernard (1813-1878), and influential German physiologists Justis von Liebig (1803-1873),
Edward Pflüger (1829-1910), and Carl von Voit (1831-1908). He also discussed the important contributions to
metabolism of Antoine Lavoisier (1743-1784) and digestive physiology from American physician-physiologist
William Beaumont (1785-1853).
Through his textbooks, Austin Flint, Jr. influenced the first medically trained and science-oriented
professor of physical education, Edward Hitchcock, Jr., M.D. (see next section). Hitchcock quoted Flint about
the muscular system in his syllabus of Health Lectures, which became required reading for all students
enrolled at Amherst College between 1861 and 1905.
Amherst College Connection

Two physicians, father and son (Figure 3) pioneered the
American sports science movement (Figure 4). Edward Hitchcock,
D.D., LL.D. (1793-1864), served as professor of chemistry and
natural history at Amherst College and as president of the College
from 1845-1854. He convinced the college president in 1861 to allow
his son Edward [(1828-1911; Amherst undergraduate (1849);
Harvard medical degree (1853)] to assume the duties of his
Figure 3. Left; Dr Edward Hitchcock,
17931864. Right, Edward Hitchcock, Jr., anatomy course. On August 15, 1861 Edward Hitchcock, Jr. became
18281911 Professor of Hygiene and Physical Education with full academic
rank in the Department of Physical Culture at an annual salary of
$1,000 - a position he held almost continuously to 1911. Hitchcock’s professorship became the second such
appointment in physical education in an American college. The first, to John D. Hooker a year earlier at
Amherst College in 1860, was short lived due to Hooker’s poor health. Hooker resigned in 1861 with
Hitchcock appointed in his place.
William Augustus Stearns, D.D., the fourth President of Amherst College had proposed the original idea
of a Department of Physical Education with a professorship in 1854. Stearns considered physical education
instruction essential for the health of students and useful to prepare them physically, spiritually, and
intellectually. In 1860, the Barrett Gymnasium at Amherst College, was completed and served as the training
facility where all students were required to perform systematic exercises for 30 minutes daily, four days a
week A unique feature of the gymnasium included Dr. Hitchcock’s scientific laboratory that included
strength and anthropometric equipment, and a spirometer to measure lung function, which he used to
measure the vital statistics of all Amherst students. Dr. Hitchcock was first to statistically record basic data on
a large group of subjects on a yearly basis. These measurements provided Dr. Hitchcock with solid
information for his counseling duties concerning health, hygiene, and exercise training.
In 1860, the Hitchcock’s co-authored an anatomy and physiology textbook geared to college physical
education (Hitchcock, E., and Hitchcock, E., Jr.: Elementary Anatomy and Physiology for Colleges, Academies, and
Other Schools. New York, Ivison, Phinney & Co., 1860); 29 years earlier, the father had published a science-
oriented hygiene textbook. Interestingly, the anatomy and physiology book predated Flint’s similar text by
six years, illustrating that an American-trained physician, with strong allegiance to the implementation of
health and hygiene in the curriculum, helped set the stage for the study of exercise and training well before
the medical establishment focused on this aspect of the discipline. A pedagogical aspect of the Hitchcocks'
text included questions at the bottom of each page about topics under consideration. In essence, the textbook
also served as a “study guide” or “workbook.”
George Wells Fitz, M.D.: A Major Influence

George Wells Fitz, M.D. (1860-1934), early “exercise physiology” researcher
helped create the Department of Anatomy, Physiology, and Physical Training at
Harvard University in 1891. One year later, Fitz established the first formal exercise
physiology laboratory. Instructors in the initial undergraduate B.S. degree program
included distinguished Harvard Medical School physiologists Henry Pickering
Bowditch whose research produced the “all or none principle of cardiac
contraction” and “treppe” (staircase phenomenon of muscle contraction), and W. T.
Porter, internationally recognized physiologist. Both men were noted for their
rigorous scientific and laboratory training. The new major, grounded in the basic
sciences, included formal coursework in exercise physiology, zoology,
Figure 4. G.W. Fitz morphology (animal and human), applied anatomy, anthropometry, animal
mechanics, medical chemistry, comparative anatomy, remedial exercises, physics,
gymnastics and athletics, history of physical education, and English (see accompanying For Your Information,
below)

Exercise Physiology
Few of today’s undergraduate Physical Education [Kinesiology] major programs could match the strong
science core required at Harvard in 1893. Below is listed the 4-year course of study. Along with core
courses, Professor Fitz established an exercise physiology laboratory [Reference: Harvard University
Catalog: Lawrence Scientific School. Description of Course of Study. 1891-1892, page 222.]
Course of Study: Department of Anatomy, Physiology, and Physical Training, Lawrence Scientific
School, Harvard University, 1893.
First Year Second Year Third Year (at Harvard Medical) Fourth Year
Experimental Comparative Anatomy of Anatomy and Dissection Psychology
Physics Vertebrates General Physiology Anthropometry
Elementary Zoology Geology Histology Applied Anatomy and
Morphology of Physical Geography and Hygiene Animal Mechanics
Animals Meteorology Foods and Cooking (Kinesiology)
Morphology of Experimental Physics Medical Chemistry Physiology of Exercise
Plants General Descriptive Auscultation and Percussion Remedial Exercise
Elementary Physics Gymnastics and Athletics History of Physical
Physiology and Qualitative Analysis Education
Hygiene English Composition Forensics
General Chemistry Gymnastics and Athletics Gymnastics and
Rhetoric and English Athletics
Composition
Elementary German
Gymnastics and
Athletics
Prelude to Exercise Science: Harvard’s Department of

Anatomy, Physiology, and Physical Training (B.S.
Degree, 1891-1898)
Harvard’s physical education major and exercise physiology research laboratory focused on three
objectives:
 Prepare students, with or without subsequent training in medicine, to become directors of gymnasia or
instructors in physical training
 Provide necessary knowledge about the science of exercise
 Provide suitable academic preparation to enter Medical School
Physical education students took general anatomy and physiology courses in the medical school; after
four years of study, graduates could enroll as second-year medical students and graduate in three years with
an M.D. degree. Dr. Fitz taught the physiology of exercise course; thus, he may have been the first person to
formally teach such a course. It included experimental investigation and original work and thesis, including
six hours a week of laboratory study. The prerequisite for the “Physiology of Exercise” course included a
course in general physiology at the medical school or its equivalent. The course introduced students to the
fundamentals of physical education, and provided training in experimental methods related to exercise
physiology.
In addition to a remedial exercise course, students took a required course in “Applied Anatomy and
Animal Mechanics. Action of Muscles in different Exercises.” This thrice-weekly course taught by Dr. Dudley
Sergeant, was the forerunner of modern biomechanics courses. Its prerequisite was general anatomy at the
medical school, or its equivalent.
Nine men graduated with B.S. degrees from the Department of Anatomy, Physiology, and Physical
Training, before it’s dismantling in 1900. The aim of the major was to prepare students to become directors
of gymnasia or instructors in physical training, to provide students with the necessary knowledge about
the science of exercise, and to offer suitable training for entrance to medical school. The stated purpose of
the new exercise physiology research laboratory was as follows:
A large and well-equipped laboratory has been organized for the experimental study of the
physiology of exercise. The object of this work is to exemplify the hygiene of the muscles, the
conditions under which they act, the relation of their action to the body as a whole affecting
blood supply and general hygienic conditions, and the effects of various exercises upon
muscular growth and general health.
Coinciding with Fitz’s untimely departure from Harvard in 1899 (no one is quite sure why Fits left
Harvard), the department changed its curricular emphasis (the term physical training was dropped from the
department title), thus terminating at least temporarily this unique experiment in higher education, and
depriving the next generation of students in exercise physiology of a visionary to propel the field forward.
One of the legacies of the Fitz-directed “Harvard experience” between 1891 and 1899 was the mentoring it
provided specialists who began their careers with a strong scientific basis in exercise and training and its
relationship to health. They were taught that experimentation and discovery of new knowledge about
exercise and training played a crucial role in furthering development of a science based curriculum.
Unfortunately, it would take another six decades before the next generation of science-oriented physical
educators (led by physiologists like A.V. Hill and D.B. Dill, not educators) would once again exert strong
influence on physical education and propel exercise physiology to the forefront of scientific investigation.
By 1927, 135 institutions in the U.S. offered bachelors degree programs in Physical Education with
coursework in the basic sciences; this included four masters degree programs and two doctoral programs
(Teachers College-Columbia University and New York University). Since then, programs of study [with
emphasis in exercise physiology] have proliferated. Currently, about 172 programs in the United States and
19 in Canada offer the masters or doctoral degrees with specialization in some aspect of exercise physiology.
Exercise Studies in Research Journals

A notable event in the growth of exercise physiology occurred in 1898 when three articles on physical
activity appeared in the first volume of the American Journal of Physiology. Other articles and reviews
subsequently appeared in prestigious journals, including the first published review in Physiological Reviews
(2: 310, 1922) on the mechanisms of muscular contraction by Nobel laureate A.V. Hill. The German applied
physiology publication, Internationale Zeitschrift fur angewandte Physiologie einschliesslich Arbeitsphysiologie
(1929-1940; now European Journal of Applied Physiology and Occupational Physiology), became a significant
journal for research about exercise physiology-related topics. The Journal of Applied Physiology, first published
in 1948 is a must reading for exercise physiologists. The official journal of the American College of Sports
Medicine, Medicine and Science in Sports, first appeared in 1969. It aimed to integrate both medical and
physiological aspects of the emerging fields of sports medicine and exercise science. The official name of this
journal changed in 1980 to Medicine and Science in Sports and Exercise. Publications emphasizing applied and
basic exercise physiology research have increased as the field expands into different areas. The World Wide
Web offers unique growth potential in this regard.
The Harvard Fatigue Laboratory (1927-1946)

The real impact of laboratory research in exercise physiology (along with many other
research specialties) occurred in 1927, again at Harvard University, 27 years after
Harvard closed the first exercise physiology laboratory in the United States. The 800-
square foot Harvard Fatigue Laboratory in the basement of Morgan Hall of Harvard
University’s Business School established the legitimacy of exercise physiology on its
own merits as an important area of research and study.
Many of the great scientists of the 20th century with an interest in exercise affiliated
with the Fatigue Laboratory. Established by renowned Harvard chemist and professor
of biochemistry, J. Henderson, M.D. (1878-1942). David Bruce Dill (1891-1986), a
Figure 5. David Bruce
Stanford Ph.D. in physical chemistry became the first and only scientific director of
Dill (18911986)
the Laboratory. While at Harvard, Dill refocused his efforts from biochemistry to
experimental physiology and became the driving force behind the Laboratory’s numerous scientific
accomplishments.
Similar to the legacy of the first exercise physiology laboratory established in 1891 at Harvard’s Lawrence
Scientific School 31 years earlier, the Harvard Fatigue Laboratory demanded excellence in research and
scholarship. Cooperation among scientists from around the world fostered lasting collaborations. Many its
charter scientists profoundly influenced a new generation of exercise physiologists worldwide.

The Harvard Fatigue Laboratory
Over a 20-year span, Harvard Fatigue Laboratory scientists published 352 research papers, monographs, and
a book dealing with basic and applied exercise physiology, including methodological refinements in blood
chemistry analysis, and methods for analyzing fractional concentrations of expired air. Other research
included acute responses and chronic adaptations to exercise under the environmental stress of altitude,
heat, and cold exposure. Most of the experiments used humans exercising on a treadmill or bicycle
ergometer. These studies formed the cornerstone for future research efforts in exercise physiology; they
included assessment of working capacity and physical fitness, cardiovascular and hemodynamic responses
during maximal exercise, oxygen uptake and substrate utilization kinetics, exercise and recovery
metabolism.
Other Early Exercise Physiology Research Laboratories

Other notable research laboratories helped exercise physiology become an established field of study at
colleges and universities. These included the Nutrition Laboratory at the Carnegie Institute in Washington,
D.C. (established 1904) that initiated experiments in nutrition and energy metabolism. The first research
laboratories established in a department of physical education in the United States originated at George
Williams College (1923), University of Illinois (1925), Springfield College (1927), and Laboratory of
Physiological Hygiene at the University of California, Berkeley (1934). The syllabus for the Physiological
Hygiene course contained 12 laboratory experiments. In 1936, Dr. Franklin M. Henry assumed responsibility
for the laboratory; shortly thereafter, his research appeared in various physiology-oriented journals.
Nordic Connection (Denmark, Sweden, Norway and

Finland)
Denmark and Sweden played an important historical role in developing the field of exercise physiology.
In 1800, Denmark became the first European country to require physical training (military-style gymnastics)
in the school curriculum. Since then, the Danish and Swedish scientists continue to make outstanding
contributions to research in both traditional physiology and exercise physiology.
Danish Influence
In 1909, the University of Copenhagen
endowed the equivalent of a Chair in Anatomy,
Physiology, and Theory of Gymnastics. The
first Docent, Johannes Lindhard, M.D. (1870-
1947), later teamed with August Krogh, Ph.D.
(1874-1949), an eminent scientist specializing in
physiological chemistry and research
instrument design and construction, to conduct
many of the classic experiments in exercise
physiology.
Figure 6. The “three musketeers”; Dr. Erling Assmusen (left), Erik
By 1910, Krogh and his physician-wife Marie
HohwuChristensed (center), and Marius Nielson (right), 1988.
had proven through a series of ingenious,
experiments that diffusion governed pulmonary gas exchange during exercise and altitude exposure, not
oxygen secretion from lung tissue into the blood as postulated by British physiologists Sir John Scott Haldane
and James Priestley. Krogh won the Nobel Prize in Physiology or Medicine in 1920 for discovering the
mechanism for capillary control of blood flow in resting and exercising muscle. To honor Krogh’s
achievements the institute for physiological research in Copenhagen bears his name (August Krogh Institute).
Three other Danish researchers - physiologists Erling Asmussen (1907-1991; ACSM Citation Award, 1976
and ACSM Honor Award, 1979), Erik Hohwü-Christensen (b. 1904-1996; ACSM Honor Award, 1981), and
Marius Nielsen (b. 1903) - conducted significant exercise physiology studies (Figure 6, above). These “three
musketeers,” as Krogh called them, published voluminously during the 1930s to 1970s.
Swedish Influence
Modern exercise physiology in Sweden can be traced to Per Henrik Ling (1776-
1839), who in 1813 became the first director of Stockholm’s Royal Central Institute of
Gymnastics. Ling, a specialist in fencing, developed a system (incorporating his
studies of anatomy and physiology) of “medical gymnastics,” which became part of
Sweden’s school curriculum in 1820. Ling’s son, Hjalmar, published a book on the
kinesiology of body movements in 1866. As a result of the Lings’ philosophy and
influence, physical education graduates from the Stockholm Central Institute were
well schooled in the basic biological sciences, in addition to proficiency in sports
Figure 7. PerOlof
and games. Currently, the College of Physical Education (Gymnastik-Och Idrotts-
Astrand, Stockholm,
Sweden. skolan) and the Department of Physiology in the Karolinska Institute Medical
School in Stockholm continue to sponsor studies in exercise physiology.
Per-Olof Åstrand, M.D., Ph.D. (b. 1922) is the most famous graduate of the College of Physical Education
(1946); in 1952 he presented his doctoral thesis at the Karolinska Institute Medical School (Figure 7) Åstrand
taught in the Department of Physiology in the College of Physical Education from 1946-1977; it then became a
department at the Karolinska Institute where he served as professor and department head from 1977 to 1987.
Christensen, Åstrand’s mentor, supervised his thesis, which evaluated physical working capacity of men and
women aged 4 to 33 years. This important study, among others, established a line of research that propelled
Åstrand to the forefront of experimental exercise physiology for which he achieved worldwide fame. Four of
his papers, published in 1960 with Christensen as co-author, stimulated further studies on the physiological
responses to intermittent exercise. Åstrand has mentored an impressive group of exercise physiologists,
including “superstar” Bengt Saltin.
Norwegian and Finnish Influence

The new generation of exercise physiologists trained in the late 1940s analyzed respiratory gases with a
highly accurate sampling apparatus that measured minute quantities of CO2 and O2 in expired air.
Norwegian scientist Per Scholander (1905-1980) developed the method of analysis and analyzer in 1947.
Another prominent Norwegian researcher, Lars A. Hermansen (1933-1984; ACSM Citation Award, 1985)
made many contributions including a classic 1969 article entitled “Anaerobic energy release,” that appeared
in the first issue of the ACSM journal, Medicine and Science in Sports).
In Finland, Martti Karvonen, M.D., Ph.D. (ACSM Honor Award, 1991) from the Physiology Department of
the Institute of Occupational Health, Helsinki, achieved notoriety for a method to predict optimal exercise
training heart rate, now called the “Karvonen formula”. Paavo Komi, Department of Physical Activity,
University of Jyvaskyla, has been Finland’s most prolific researcher with numerous experiments published in
the combined areas of exercise physiology and sport biomechanics.
The University of Michigan Experience

In 1870 the University of
Michigan Senate recommended
the establishment of a
Department of Hygiene and
Physical Culture, the
appointment of a professor to
run it, and the construction of a
gymnasium costing about
$25,000. No action was taken on
these recommendations, but the
seed were sewn. Nearly 25 years
later the gymnasium and the
program became a reality.
Figure 7. Barbour (Women’s) Gym [circa, 1900] attached to Waterman (Men’s) gym The roots of today’s

Kinesiology program date back
(not shown [circa 1894] on the site of the current chemistry building. Barbour/
Waterman was the long time home of Kinesiology. It was demolished in 1977. earlier than the Senate’s 1870
statement and the 1894 completion of Waterman gym (150 feet long and 90 feet wide with a running track in
the balcony of 14 laps to the mile was located on the site of Chemistry building, but razed in 1977). Students
formed the first gymnasium in 1858 from an old military barracks on the site of the original Engineering
building on the Diag. This makeshift facility rested on poles, open to weather, and was furnished only with a
few ropes and rings. Students made various attempts at fundraising to build a “proper” gym, but most of the
money ($20,000) came from Joshua W. Waterman, a Detroit attorney and sports enthusiast. The university
added the rest and Waterman Gym were completed at a cost of $51,874.49. The gym opened in 1894 and Dr.
James Fitzgerald was named the first director. Dr. George A. May, hired in 1901 to teach classes served as
director of the gym from 1910 to 1942. “Doc” May was a well-known personality on campus and was
instrumental in convincing the university senate to offer physical education instruction on a required bases to
all students (men and women) to “counteract the strain placed on students by extensive study”. Women were
permitted to use Waterman gym, “on occasion during mornings”. University President Dr. James Angell
supported coeducational instruction, including use of the gym, and authorized the building of Barbour
Gymnasium (Regent Levi Barbour offered the land adjacent to Waterman Gym valued at $25,000) in 1894 (full
use occurred in 1896.) President Angell, seeing the need for a women’s physical education program hired Dr.
Eliza M. Mosher, a UM medical student in the early ‘70s and a practicing physician in New York, to become
the first Professor of Hygiene and Women’s Dean of the Department of Literature, Science and Arts
(becoming the first women to head Physical Education for women.)
In 1894 men’ and women’s physical education began as electives, but four years later the Regents passed a
resolution making the classes compulsory for all freshman (in the hope that the students would continue to
take systematic exercise on a regular basis thereafter). By this time Physical Education was an integral part of
campus life, but a professional four-year program to train teachers in physical education, leading to a B.S.
degree would not be started until the early 1920s.
In March, 1920, University President Marion L. Burton brought before the UM Regents message from the
Michigan State Department of Public Instruction on the growing need for physical education teachers. The
following February, the Regents took the following action:
“There is herby created and established a University Department of Physical Education….

“The Director of Physical Education shall be in primary charge of all athletic fields for men
and women, of both gymnasium, of all sports, indoor, outdoor, intercollegiate and
intramural.”
In June, the plan was revised to create two units: A Department of Intercollegiate Athletics, headed by
Fielding Yost, and a Department of Hygiene and Public Health, including Physical Education. Dr. John M.
Sudwall was named to the latter post in September, 1921. Physical Education was placed in the newly formed
School of Education. With no budget for new faculty, the four-year curriculum was inaugurated in fall, 1921.
It was designed to prepare men and women to:
 Supervise the physical health of children in the public schools
 Provide recreation for growing youth
 Instruct prospective coaches in scientific methods and training of teams
The program emphasized two areas: training individuals in gymnastics, recreation, health and games for
people of all ages; and prepare future coaches in various sports.
Among the many faculty whose contributions shaped the Men’s and Women’s programs through and
beyond the 20s, two deserve special mention: Margaret Bell, who chaired the Women’s Physical Education
Department, 1923-1957, and Elmer Mitchell, Director of Intramural Sports from 1919-1958, and Chair of the
Department of Physical Education for Men, 1942-1958.
With the beginning of the program in 1921, the departments essentially had two parts: the required
program that provided non-credit physical education (sports and games) courses for all students, and the
four-year professional program leading to teacher certification.
With the undergraduate program well established by the 1930s, the PE faculty introduced a graduate
curriculum in Physical Education leading to an M.A. degree in 1931 (there were 3 areas of specialization:
administration, supervision and teaching; school health education, and teacher education). The Ph.D. or
Ed.D. was established in 1938, and first two doctoral degrees were awarded in 1940. By the end of the 1930s,
undergraduate enrollment in Physical Education stood at about 75 men and 50 women.
In 1941, the Physical Education Departments (men’s and women’s) were reorganized and renamed
Physical Education and Athletics, and by 1942 all academic titles (professor, associate professor, assistant
professor) were taken away and changed to director, associate supervisor, assistant supervisor. The
departments were removed from education and stood as a solitary unit on campus, yet were permitted to
continue to grant university degrees and offer required physical training classes.
In 1949 Paul Hunsicker, a recent graduate of T.K. Cureton’s Illinois program in Physical Education
(emphasis in Exercise Physiology) came to Michigan and established the first experimental exercise
physiology laboratory (housed in the old Physical Education Building – now the Athletic Ticket Office on
South State Street). Dr. Hunsicker established the laboratory with a primary interest in physical fitness testing
of youth throughout the country.
Upon the retirement of Dr. Mitchell in 1958, Dr. Hunsicker became head of the Men’s Department of
Physical Education. Dr. Esther French succeeded Margaret Bell as Chair of the Women’s Physical Education
Department in 1957. In 1967 the University reversed its stance of 25 years earlier and returned the professorial
titles to the men’s and women’s faculties, following an academic review.
In 1970 the Physical Education requirement was abolished. Thus, the 72-year tradition of required Physical
Education was ended; in its place, a coeducational elective program continued to offer students the
opportunity to acquire sports sills. This elective program has evolved into today’s Adult Lifestyle Program.
In 1971 the Men’s and Women’s Departments were merged, with Dr. Paul Hunsicker serving as Chair. At
the height of his career, in January, 1976, Paul Hunsicker died of a heart attack. Dr. D.W. Edington, a
professor from the University of Massachusetts was recruited as chair with the mandate to establish a first-
rate research department. During the mid ‘70s Physical Education severed ties with Athletics to become an
independent unit within the School of Education. The undergraduate and graduate programs focused on
research with little emphasis on teacher preparation. New faculty was recruited with emphasis in motor
control, biomechanics and exercise physiology and new laboratories were established.
On September 21, 1984 the UM Regents created an independent Division of Physical Education,
completely separated from Education. On July 20, 1990 the Michigan Board of Regents agreed that Physical
Education no longer accurately described the field of study and officially changed the name to the Division
of Kinesiology. Kinesiology is now one of the 17 schools and colleges within the university.
Other Contributors to Exercise Physiology

In addition to the American and Nordic scientists who achieved distinction in the study of exercise, many
other “giants” in the fields of physiology and experimental science made monumental contributions that
indirectly contributed to the knowledge base in exercise physiology. These include physiologists Antoine
Laurent Lavoisier (1743-1794; fuel combustion), Sir Joseph Barcroft (1872-1947; altitude), Christian Bohr (1855-
1911; oxygen-hemoglobin dissociation curve), John Scott Haldane (1860-1936; respiration), Otto Myerhoff,
1884-1951; Nobel Prize, cellular metabolic pathways), Nathan Zuntz (1847-1920; portable metabolism
apparatus), Carl von Voit (1831-1908) and his student, Max Rubner (1854-1932; direct and indirect
calorimetry, and specific dynamic action of food), Max von Pettenkofer (1818-1901; nutrient metabolism),
Eduard F.W. Pflüger (1829-1910; tissue oxidation).
Closer to home, the field of exercise physiology owes a debt of gratitude to the pioneers of the physical
fitness movement in the United States, notably Thomas K. Cureton (1901-1993; ACSM charter member, 1969
ACSM Honor Award) at the University of Illinois, Champaign. Cureton, a prolific researcher, trained four
generations of students beginning in 1941 who later established their own research programs and influenced
many of today's top exercise physiologists. These early graduates with an exercise physiology specialty soon
assumed leadership positions as professors of physical education with teaching and research responsibilities
in exercise physiology at numerous colleges and universities in the United States and throughout the world.
Reading #2 Study Guide

1. Archibald Vivian Hill
2. August Krogh
3. Austin Flint, Jr., M.D.
4. D.W. Edington
5. David Bruce Dill
6. Eliza M. Mosher
7. Fielding Yost
8. Galen
9. George Wells Fitz.
10. Harvard Fatigue Laboratory
11. Hippocrates
12. Margaret Bell

13. Paul Hunsicker
14. Per-Olof Åstrand
15. The Hitchcock’s
16. Thomas K. Cureton
STUDY QUESTIONS
From Ancient Greece to the United States, circa 1850
Earliest Development
Name of the Greek physician-athlete who many consider the “father of preventive medicine.
The Early United States Experience

Name the first US medical school.
List two “hot” topics of interest to medicine and exercise physiology in the early 19th century.
1.
2.
Austin Flint, Jr., M.D.: American Physician-Physiologist

Give two reasons for Austin Flint’s importance in the history of exercise physiology.
1.
2.
Amherst College Connection

Name the father and son pioneer sport science professors.
1.
2.
George Wells Fitz, M.D.: A Major Influence

List two reasons for G.W. Fitz importance in the history of exercise physiology.
1.
2.
Prelude to Exercise Science: Harvard’s Department of Anatomy, Physiology, and

Physical Training (B.S. Degree, 1891-1898)
List one unique aspect of the academic major in Harvard’s Department of Anatomy, Physiology,
and Physical Training.
List three objectives of Harvard’s new physical education major and exercise physiology research
laboratory.
1. 3.
2.
The Harvard Fatigue Laboratory (1927-1946)

Name the first director of the Harvard Fatigue Laboratory.
Other Early Exercise Physiology Research Laboratories

Name an “exercise physiology” department in the United States before 1935.
The Nordic Connection (Denmark, Sweden, Norway and Finland)

Which of the Nordic countries first required physical training in the school curriculum?
Danish Influence
Name one famous Danish exercise physiologist.
Swedish Influence
Name one famous Swedish exercise physiologist.
Norwegian and Finnish Influence

Name one famous Norwegian exercise physiologist.
Other Contributors to Exercise Physiology Knowledge

Name the most famous “physical fitness” researcher from the U.S.
The University of Michigan Experience

Give four important dates and their significance in the development of the Division of Kinesiology
at the University of Michigan.
Date Significance
1.
2.
3.
4.
Name four important people and briefly describe their contributions to shaping the history of the
Division of Kinesiology at the University of Michigan.
1. 3.
2. 4.
READING #3
PROFESSIONAL EXERCISE PHYSIOLOGY
Introduction: The Exercise Physiologist
Many individuals view exercise physiology as representing an undergraduate or graduate academic major
(or concentration) completed at an accredited college or university. In this regard, only those who complete
this academic major have the “right” to be called “exercise physiologist.” However, many individuals
complete undergraduate and graduate degrees in related fields with considerable coursework and practical
experience in exercise physiology (or related areas). Consequently, the title exercise physiologist could also
apply so long as their academic preparation is adequate. Resolution of this dilemma becomes difficult
because no national consensus exists as to what constitutes an acceptable (or minimal) academic program of
course work in exercise physiology. In addition, there are no universal standards for hands-on laboratory
experiences (anatomy, kinesiology, biomechanics, and exercise physiology), demonstrated level of
competency, and internship hours that would stand the test of national certification or licensure. Moreover,
with areas of concentration within the field are so broad, consensus certification testing indeed becomes
challenging.
No national accreditation or licensure exists to certify exercise physiologists. Only one state, Louisiana,
currently requires individuals to pass a state certification exam for the position of “clinical exercise
physiologist.” Many states are in various stages of similar legislation.
What Do Exercise Physiologists Do?

Exercise physiologists assume diverse careers. Some use their research skills in colleges, universities, and
private industry settings. Others are employed in health, fitness, and rehabilitation centers, while others serve
as educators, personal trainers, managers, and entrepreneurs in the health/fitness industry.
Exercise physiologists also own health and fitness companies or are hands-on practitioners who teach and
service the community including corporate, industrial, and governmental agencies. Some specialize in other
types of professional work like massage therapy while others go on to pursue professional degrees in
physical therapy, occupational therapy, nursing, nutrition, medicine, and chiropractic.
Table 1 presents a partial list of different employment descriptions for a qualified exercise physiologist in
one of six areas.
Table 1. Partial list of different employment opportunities for qualified exercise physiologists.
College/ Gov/
Sports Community Clinical Business Private
University Military
Manage/direct Test/supervise Fitness Sports Personal
Sports director Professor health/wellness cardiopulmonary director/man- manage- health/fitness
programs patients ager ment consultant
Evaluate/supervise
special populations
(diabetes; obesity;
Health/fit-
arthritis; dyslipi- Health/fit-
Strength/con- Community ness directory
Researcher demia; cystic fibro- ness Own business
ditioning coach education in correctional
sis; cancer, hyper- promotion
institutions
tension; children;
low functional capa-
city; pregnancy)
Director, Administrator Exercise Sport
manager of technologies in psycholo-
state/national
cardiology practice gist
teams
Sports
Teacher Occupational
Consultant nutrition
Instructor rehabilitation
programs
Health/fit-
Researcher ness club
instructor
The Exercise Physiologist/Health-Fitness Professional in the

Clinical Setting
The well-documented health benefits of regular physical activity have enhanced the exercise physiologist’s
role beyond traditional lines. A clinical exercise physiologist becomes part of the health/fitness professional
team. This team approach to preventive and rehabilitative services requires different personnel depending on
program mission, population served, location, number of participants, space availability, and funding level. A
comprehensive clinical program can include the following personnel, in addition to the exercise physiologist:
 Physicians  Dietitians
 Nurses  Physical therapists
 Occupational  Social workers

therapists
 Respiratory therapists  Psychologists
 Health educators  Certified personnel (exercise leaders, health-
fitness instructors, directors, exercise test
technologists, preventive and rehabilitative
exercise specialists, preventive and rehabilitative
exercise directors)
The health professional team works in harmony to restore a patient’s mobility, functional capacity, and
overall health. Issues about available funding, specific client needs, and programmatic direction dictate the
extent of part-time and full-time personnel.
Sports Medicine and Exercise Physiology: A Vital Link

The traditional view of sports medicine involves rehabilitating athletes from sports injuries. A more
contemporary view relates sports medicine to the scientific and medical aspects of physical activity, physical
fitness, and sports. Thus, a close link ties sports medicine to clinical exercise physiology. The sports medicine
professional and exercise physiologist work hand-in-hand with similar populations including the sedentary
person, the athlete and those requiring special needs (e.g., disabled athlete).

Partial Listing of Research Journals publishing exercise physiology research
articles.
Biomedical Databases Exercise Immunology Review
British Journal of Sports Medicine Health Sciences Library
British Medical Journal Human Performance
Canadian Journal of Applied Physiology International Journal of Psychophysiology
Clinical Exercise Physiology International Journal of Sport Nutrition
Coaching Science Abstracts Journal of Applied Biomechanics
Human Movement Science Journal of Aging and Physical Activity
International Journal of Epidemiology Journal of Applied Physiology
Internet Journal of Health Promotion Journal of Health Communication
Journal of the American Medical Association Motor Control
Journal of Applied Biomechanics Journal of Sport Management
Journal of Exercise Physiology online Journal of Sport Rehabilitation
Journal of Performance Enhancement Journal of Sport and Exercise Psychology
Journal of Science and Medicine in Sport Kinesiology Online
Journal of Athletic Training Pediatric Exercise Science
Medicine & Science in Sports & Exercise New Zealand Journal of Physiotherapy
Carefully prescribed exercise contributes to overall health and quality of life. In conjunction with sports
medicine professionals, the clinical exercise physiologist tests, treats, and rehabilitates individuals with
diverse diseases and disabilities. In addition, prescription of physical activity and athletic competition for the
physically challenged plays an important role in sports medicine and exercise physiology, providing unique
opportunities for research, clinical and professional advancement.
Training and Certification by Professional Organizations

To fulfill responsibilities in the exercise setting, the health-fitness professional integrates unique
knowledge, skills, and abilities related to exercise, physical fitness, and health. Different professional
organizations provide leadership in training and certifying health-fitness professionals. Table 2 lists
organizations offering training/certification programs with diverse emphases and specializations.
Table 2. Organizations offering training/certification programs related to physical activity.
Organization Areas of Specialization and Certification

AFP Fitness Practitioner, Primary Aerobics Instructor,
Aerobics and Fitness Association of America (AFAA)
Personal Trainer & Fitness Counselor, Step Reebok
15250 Ventura Blvd., Suite 200
Certification, Weight Room/Resistance Training
Sherman Oaks, CA 91403
Certification, Emergency Response Certification
American College Sports Medicine (ACSM) Exercise Leader, Health/Fitness Instructor, Exercise Test
401 West Michigan Street Technologist, Health/Fitness Director, Exercise Specialist,
Indianapolis, IN 46202 Program Director
American Council on Exercise (ACE)
Group Fitness Instructor, Personal Trainer, Lifestyle &
5820 Oberlin Drive, Suite 102
Weight Management Consultant
San Diego, CA 92121
Canadian Aerobics Instructors Network (CAIN)
2441 Lakeshore Road West, P.O. Box 70029 CIAI Instructor, Certified Personal Trainer
Oakville, ON L6L 6M9
Canadian Personal Trainers Network (CPTN) CPTN/OFC Certified Personal Trainer, CPTN Certified
Ontario Fitness Council (OFC) Specialty Personal Trainer, CPTN/OFC Assessor of
1185 Eglington Ave. East, Suite 407 Personal Trainers, CPTN/OFC Course Conductor for
North York, ON M3C 3C6 Personal Trainers
Canadian Society for Exercise Physiology CFC-Certified Fitness Consultant, PFLC-Professional
1600 James Naismith Drive, Suite 311 Fitness and Lifestyle Consultant, AFAC-Accredited Fitness
Gloucester, ON K1B 5N4 Appraisal Center
PFS-Physical Fitness Specialists (Personal Trainer), GEL-
The Cooper Institute for Aerobics Research Group Exercise Leadership (Aerobic Instructor), ADV.PFS-
12330 Preston Road Advanced Physical Fitness Specialist, Biomechanics of
Dallas, TX 75230 Strength Training, Health Promotion Director
Disabled Sports USA

451 Hungerford Drive, Suite 100 Adapted Fitness Instructor
Rockville, MD 20850
International Weightlifting Association (IWA)
P.O. Box 444 CWT-Certified Weight Trainer
Hudson, OH 44236
Jazzercise
2808 Roosevelt Blvd. Certified Jazzercise Instructor
Carlsbad, CA 92008
National Federation of Personal Trainers (NFPT)
P.O. Box 4579 Certified Personal Fitness Trainer
Lafayette, IN, 47903
National Strength & Conditioning Association
(NSCA) Certified Strength and Conditioning Specialist, Certified
P.O. Box 38909 Personal Trainer
Colorado Springs, CO 80937
YMCA of the USA Certified Fitness Leader (Stage I-Theory, II-Applied Theory,
101 North Wacker Drive III-Practical, Certified Specialty Leader, Trainer of Fitness
Chicago, IL 60606 Leaders, Trainer of Trainers
The American College of Sports Medicine (ACSM) has emerged as the preeminent academic organization
offering comprehensive programs in areas related to the health-fitness profession. ACSM certifications
encompass cognitive and practical competencies that are evaluated by written and practical examinations.
The candidate must successfully complete each of these components (scored separately) to receive the world-
recognized ACSM certification. ACSM offers a wide variety of certification programs throughout the United
States and in other countries <http://www.acsm.org/index.asp>.
ACSM Qualifications and Certifications

Health and fitness professionals need to be knowledgeable and competent in different areas, including
first-aid and CPR certification, depending on personal interest. Table 3 presents content areas for different
ACSM certifications. Each of these areas has general and specific learning objectives.
Table 3. Major knowledge/competency areas required for individuals interested in

ACSM certifications
Functional anatomy and biomechanics
Exercise physiology
Pathophysiology and risk factors
Human development and aging
Human behavior and psychology
Health appraisal and fitness testing
ECG
Emergency procedures and safety
Exercise programming
Program administration
From ACSM’s Guidelines for Exercise Testing and Prescription, 5th Ed. Baltimore, MD: Williams
& Wilkins, 1995.
Health and Fitness Track

The Health and Fitness Track encompasses the Exercise Leader, Health/Fitness Instructor, and
Health/Fitness Director categories.
Exercise Leader
An Exercise Leader must know about physical fitness (including basic motivation and counseling
techniques) for healthy individuals and those with cardiovascular and pulmonary diseases. This category
requires at least 250 hours of hands-on leadership experience, or an academic background in an appropriate
allied health field. Examples of general objectives for an Exercise Leader in exercise physiology include to:
1. Define aerobic and anaerobic metabolism
2. Describe the role of carbohydrates, fats, and proteins as fuel for aerobic and anaerobic exercise
performance
3. Define the relationship of METs and kilocalories to levels of physical activity
Health/Fitness Instructor
An undergraduate degree in exercise science, kinesiology, physical education, or appropriate allied health

THE AMERICAN COLLEGE OF SPORTS MEDICINE
The American College of Sports Medicine (ACSM) has more than 20,000 International, National, and Regional
Chapter members. ACSMs Mission promotes and integrates scientific research, education, and practical
applications of sports medicine and exercise science to maintain and enhance physical performance, fitness,
health, and quality of life. The ACSM was founded in 1954. Since then, members have applied their
knowledge, training and dedication in sports medicine and exercise science to promote healthier lifestyles for
people around the globe. In 1984, the National Center relocated to its current headquarters in Indianapolis,
Indiana. The ACSM continues to grow and prosper both nationally and internationally. Working in a wide
range of medical specialties, allied health professions and scientific disciplines, ACSM is committed to the
diagnosis, treatment, and prevention of sports-related injuries and the advancement of the science of exercise.
The ACSM represents the largest, most respected sports medicine and exercise science organization in the
world.
field represents the minimum education prerequisite for a Health/Fitness Instructor. These individuals must
demonstrate competency in physical fitness testing, designing and executing an exercise program, leading
exercise, and organizing and operating fitness facilities. The Health/Fitness Instructor has added
responsibility for (a) training and/or supervising exercise leaders during an exercise program, and (b) serving
as an exercise leader. Health/Fitness Instructors also function as health counselors to offer multiple
intervention strategies for lifestyle change.
Health/Fitness Director
The minimum educational prerequisite for Health/Fitness Director certification requires a postgraduate
degree in an appropriate allied health field. Health/Fitness Directors must acquire a Health/Fitness Instructor
or Exercise Specialist certification. This level requires supervision by a certified program director and
physician during an approved internship, or at least 1 year of practical experience. Health/Fitness Directors
require leadership qualities that ensure competency in training and supervising personnel, and proficiency in
oral presentations.
ACSM Clinical Track

The title “clinical” indicates that certified personnel in these areas
provide leadership in health and fitness and/or clinical programs.
These professionals possess added clinical skills and knowledge that
allow them to work with higher risk, symptomatic populations.
Exercise Test Technologist
Exercise Test Technologists administer exercise tests to individuals

in good health and various states of illness. They need to demonstrate
appropriate knowledge of functional anatomy, exercise physiology,
pathophysiology, electrocardiography, and psychology. They must
know how to recognize contraindications to testing during
preliminary screening, administer tests, record data, implement emergency procedures, summarize test data,
and communicate test results to other health professionals. Certification as an Exercise Test Technologist does
not require prerequisite experience or special level of education.

What’s in a Name?
A lack of unanimity exists for the name of departments offering degrees (or even coursework) in exercise
physiology. The list below presents 45 examples of different names of departments in the United States
that offer essentially the same area of study. Each provides some undergraduate or graduate emphasis in
exercise physiology (e.g., one or several courses, internships, work-study programs, laboratory rotations,
or in-service programs.
Allied Health Leisure Science
Allied Health Sciences Movement and Exercise Science
Exercise and Movement Science Movement Studies
Exercise and Sport Science Nutrition and Exercise Science
Exercise and Sport Studies Nutritional and Health Sciences
Exercise Science Performance and Sport Science
Exercise Science and Human Movement Physical Culture
Exercise Science and Physical Therapy Physical Education
Health and Human Performance Physical Education and Exercise Science
Health and Physical Education Physical Education and Human Movement
Health, Physical Education, Recreation & Dance Physical Education and Sport Programs
Human Biodynamics Physical Education and Sport Science
Human Kinetics Physical Therapy
Human Kinetics and Health Recreation
Human Movement Recreation and Wellness Programs
Human Movement Sciences Science of Human Movement
Human Movement Studies Sport and Exercise Science
Sport Management Human Movement Studies and PE
Human Performance Sport, Exercise, and Leisure Science
Human Performance and Health Promotion Sports Science
Human Performance and Leisure Studies Sport Science and Leisure Studies
Human Performance and Sport Science Sport Science and Movement Education
Interdisciplinary Health Studies Sport Studies
Integrative Biology Wellness and Fitness
Kinesiology Wellness Education
Kinesiology and Exercise Science
Preventive/Rehabilitative Exercise Specialist

Unique competencies for the category Preventive/Rehabilitative Exercise Specialist include the ability to
lead exercises for persons with medical limitations (particularly cardiorespiratory and related diseases) and
healthy populations. The position requires a bachelors or graduate degree in an appropriate allied health field
and an internship of six months or more (800 hours), largely with cardiopulmonary disease patients in a
rehabilitative setting. The preventive/rehabilitative exercise specialist conducts and administers exercise tests,
evaluates and interprets clinical data and formulates an exercise prescription, conducts exercise sessions, and

SEARCHING FOR EXERCISE SCIENCE INFORMATION: THE WEB OF
SCIENCE
Professionals in the field continually need to research information about a specific topic or must locate
research articles by specific scientists. The Web of Science <http://www.isinet.com/products/citation/wos/>
provides a unique web based search tool, permitting extra-ordinary searching of many different
databases. The Web of Science accesses multidisciplinary databases of bibliographic information gathered
from thousands of scholarly journals. Each database is indexed so as to enable a search for a specific
article by subject, author, journal, and/or author address. The information stored about each article
includes the article's cited reference list (often called its bibliography), and searches can include the
databases for articles that cite a known author or work. With the Web of Science you can: (1) search the
databases for published works, (2) view full bibliographic records and add them to your Marked List for
export to bibliographic management software, (3) save them to a file, (4) format them for printing, (5) e-
mail them, (6) order the full text,(7) link directly to other articles on the same topic as the one you are
viewing, even articles that have been published after the article you are viewing, and (8) save your search
statements, which can be opened later and run again. Use the following URL for a tutorial on using the
Web of Science: http://www.isinet.com/tutorials/webofscience/.
demonstrates leadership, enthusiasm, and creativity. This person can respond appropriately to complications
during exercise testing and training, and can modify exercise prescriptions for patients with specific needs.
Preventive/Rehabilitative Program Director
The Preventive/Rehabilitative Program Director holds an advanced degree in an appropriate allied health-
related area. The certification requires an internship or practical experience of at least 2 years. This health
professional works with cardiopulmonary disease patients in a rehabilitative setting, conducts and
administers exercise tests, evaluates and interprets clinical data, formulates exercise prescriptions, conducts
exercise sessions, responds appropriately to complications during exercise testing and training, modifies
exercise prescriptions for patients with specific limitations, and makes administrative decisions regarding all
aspects of a specific program.
Selected References
ACSM,s Guidelines for Exercise Testing and Prescription, sixth edition, Baltimore, Lippincott Williams & Wilkins,
2000
ASCM’s Guidelines to Exercise Testing and Prescription. 5th Ed. Baltimore, MD: Williams & Wilkins, 1995.
Blair, S., et al. (eds.) Resource Manual for Guidelines for Exercise Testing and Prescription. Philadelphia: Lea
& Febiger, 1988.
Reading #3 Study Guide

17. Exercise physiologist
18. Clinical setting
19. Sports medicine and exercise physiology
20. Sports medicine professional
21. ACSM certification.
22. Health and fitness track
23. Exercise leader
24. Health/fitness instructor
25. Health/fitness director
26. ACSM
27. Clinical track
28. Exercise test technologist

29. Preventive/rehabilitative exercise specialist
30. Preventive/rehabilitative program director
31. The Web of Science
STUDY QUESTIONS
Introduction: The Exercise Physiologist
Do all states require accreditation to become an exercise physiologist?
What Do Exercise Physiologists Do?

Name three different careers that an exercise physiologist can do.
1.
2.
The Exercise Physiologist/Health-Fitness Professional in the Clinical Setting

Name three different health-care professionals that typically work with an exercise physiologist.
1.
2.
3.
Sports Medicine and Exercise Physiology: A Vital Link

Name two types of populations that sports medicine and exercise physiologists typically work
with.
1.
2.
Name three different journals that publish exercise physiology research articles
1.
2.
3.
Training and Certification by Professional Organizations

Name four organizations that certify different types of health-care professionals.
1. 3.
2. 4.
ACSM Qualifications and Certifications

List four different competencies required for individuals interested in ACSM certifications.
1. 3.
2. 4.
Health and Fitness Track

Name three categories of ACSMs health and fitness track.
1.
2.
3.
ACSM Clinical Track

Name three categories of ACSMs health and fitness track.
1.
2.
3.
LECTURE #4
MEASUREMENT OF HUMAN ENERGY EXPENDITURE
Introduction
In this lecture I introduce concepts related to the measurement of energy expenditure in humans. These
procedures form the basis for accurately quantifying differences among individuals in energy metabolism at
rest and during physical activity.
The Energy Content of Food
The Calorie – A Measurement Unit of Food Energy

One calorie expresses the quantity of heat to raise the temperature of 1 kg (1 L) of water 1°C
(specifically, from 14.5 to 15.5°C). For example, if a particular food contains 300 kCal, then releasing the
potential energy trapped within this food's chemical structure increases the temperature of 300 L of water
1°C. Different foods contain different amounts of potential energy. One-half cup of peanut butter, for
example, with a caloric value of 759 kCal contains the equivalent heat energy to increase the temperature of
759 L of water 1°C.
Gross Energy Value of Foods

Laboratories use a bomb calorimeter, similar to the one illustrated in Figure 1, to measure the total (gross)
energy value of a food macronutrient. Bomb calorimeters operate on the principle of direct calorimetry,
measuring the heat liberated as the food burns completely.
The bomb calorimeter works as
follows:
 A small, insulated chamber
filled with oxygen under
pressure contains a weighed
portion of food.
 The food ignites and literally
explodes and burns when an
electric current ignites a fuse
inside the chamber.
 A surrounding water bath
absorbs the heat released as the
food burns (termed the heat of
Figure 1. Bomb calorimeter directly measures the energy value of food. combustion). Insulation
prevents loss of heat to the
outside.
 A sensitive thermometer measures the amount of heat absorbed by the water. For example, the combustion
of one 4.7 oz, 4-inch sector of apple pie liberates 350 kCal of heat energy. This would raise 3.5 kg (7.7 lb) of
ice water to the boiling point.
Heat of Combustion
The heat liberated by burning or oxidizing food in a bomb calorimeter represents its heat of combustion
or the total energy value of the food. Burning 1 g of pure carbohydrate yields a heat of combustion of 4.20
kCal, 1 g of pure protein releases 5.65 kCal, and 1 g of pure lipid yields 9.45 kCal. Because most foods in the
diet consist of various proportions of the three macronutrients, the caloric value of a given food reflects the
sum of the heats of combustion of each of the macronutrients in the food.
The average heats of combustion for the three nutrients (carbohydrate = 4.2 kCal•g -1; lipid = 9.4 kCal
kCal•g-1; protein = 5.65 kCal kCal•g-1) demonstrates that the complete oxidation of lipid in the bomb
calorimeter liberates about 65% more energy per gram than protein oxidation, and 120% more energy than
the oxidation of 1 g carbohydrate.
Net Energy Value of Foods

Differences exist in the energy value of foods when comparing their heat of combustion (gross energy
value) determined by direct calorimetry to the net energy actually available to the body. This pertains
particularly to proteins because the nitrogen component of this nutrient cannot be oxidized. In the body,
nitrogen atoms combine with hydrogen to form urea, which excrets in urine. Elimination of hydrogen
represents a loss of about 19% of the protein's potential energy. The hydrogen loss reduces protein's heat of
combustion in the body to approximately 4.6 kCal per gram instead of 5.65 kCal per gram from oxidation in a
bomb calorimeter. In contrast, identical fuel values determined by bomb calorimetry exist for carbohydrates

MORE LIPID EQUALS MORE CALORIES
Lipid-rich foods contain a higher energy content than fat-free foods. One
cup of whole milk, for example, contains 160 kCal, whereas the same
quantity of skimmed milk (without fat) contains only 90 kCal. If a person
who normally consumes one quart of whole milk each day switches to
skimmed milk, the total calories ingested each year would be reduced by
the equivalent calories in 25 lbs of body fat. In three years, all other
things remaining constant, the loss of body fat would equal 75 lbs!
and lipids (which contain no nitrogen) compared to their heats of combustion in a bomb calorimeter.
DIGESTIVE EFFICIENCY
The “availability” to the body of the ingested macronutrients determines their ultimate caloric yield.
Availability refers to completeness of digestion and absorption. Normally about 97% of carbohydrates,
95% of lipids, and 92% of proteins become digested, absorbed, and available to the body for energy. Large
variation exists for protein ranging from a high of 97% for animal protein to a low 78% for dried peas and
beans. Furthermore, less energy becomes available from a meal with high fiber content. Considering average
digestive efficiencies, the net kCal value per gram for carbohydrate equals 4.0, 9.0 for lipid, and 4.0 for
protein. These corrected heats of combustion comprise the “Atwater Factors,” named after the scientist who
first studied the energy release from food in the calorimeter, and in the body.
Energy Value of a Meal

If the composition and weight of
Table 1. Method of calculating the caloric value of a food from its a food are known, the caloric
composition of nutrients. content of any portion of food or an
Composition entire meal can be termed using the
Atwater factors. Table 1 illustrates
Protein Fat Carbohydrate
the method for calculating the kCal
Atwater Factor
(kCal•g1) value of 100 g (3.l5 oz) of vanilla ice
4 9 4
Percentage 4% 13% 21% cream. Based on laboratory
Total grams 4.0 13.0 21.0 analysis, vanilla ice cream contains
In one gram 0.04 g 0.13 g 0.21 g about 4% protein, 13% lipid, and
KCal• g1 0.16 1.17 0.84 21% carbohydrate, with the
(0.04 x 4.0=0.16) (0.13 x 9.0=1.17) (0.21 x 4.0=0.84) remaining 62% water. Thus, each
Total kCal per gram: 0.16 + 1.17 + 0.84 = 2.17 kCal gram of ice cream contains 0.04 g
Total kCal per 100 grams: 2.17 x 100 = 217 kCal protein, 0.13 g lipid, and 0.21 g
carbohydrate. Using these compositional values and the Atwater factors the kCal value per gram of ice cream
is determined as follows: The net kCal value indicate that 0.04 g of protein contains 0.16 kCal (0.04 x 4.0
kCal•g-1), 0.13 g of lipid contains 1.17 kCal (0.13 x 9 kCal•g-1, and 0.21 g of carbohydrate contains 0.84 kCal
(0.21 g x 4.0 kCal•g-1. Combining the separate values for the nutrients yields a total energy value for each
gram of vanilla ice cream equal to 2.17 kCal (0.16 + 1.17 + 0.84). A 100-g serving yields a caloric value 100
times as large, or 217 kCal. Increasing or decreasing portion sizes or adding rich sauces or candies, or,
conversely, adding fruits or calorie-free substitutes will affect the kCal content accordingly. Fortunately, the
need seldom exists to compute the kCal value of foods because the United States Department of Agriculture
(USDA) has already made these determinations for most foods.
Calories Equal Calories

When examining the energy value of various foods, one makes a rather striking observation with regard to
a food’s energy value. Consider, for example, five common foods: raw celery, cooked cabbage, cooked
asparagus spears, mayonnaise, and salad oil. To consume 100 kCal of each of these foods, one must eat 20
stalks of celery, 4 cups of cabbage, 30 asparagus spears, but only 1 tablespoon of mayonnaise or 4/5
tablespoon of salad oil. The point is that a small serving of some foods contains the equivalent energy
value as a large quantity of other foods. Viewed from a different perspective, to meet daily energy needs a
sedentary young adult would have to consume more than 4000 stalks of celery, 800 cups of cabbage, or 30
eggs, yet only 1.5 cups of mayonnaise or about 8 ounces of salad oil! The major difference among these foods
is that high-fat foods contain more energy with little water. In contrast, foods low in fat or high in water tend
to contain relatively little energy. An important concept, however, is that 100 kCal from mayonnaise and 100
kCal from celery are exactly the same in terms of energy.
Also note that a calorie reflects food energy regardless of the food source. Thus, from an energy
standpoint, 100 calories from mayonnaise equals the same 100 calories in 20 celery stalks. The more one eats
of any food, the more calories one consume. However, a small quantity of fatty foods represents a
considerable quantity of calories; thus, the term “fattening” often misdescribes these foods. An individual's
caloric intake equals the sum of all energy consumed from either small or large quantities of foods. Celery
would become a “fattening” food if consumed in excess!

EQUIVALENTS FOR 100 CALORIES
• 20 stalks of celery • 2 bites (1/16) of a Big Mac
• 4 cups cooked cabbage • 9 oz skim mile
• 1-tablespoon mayonnaise • 5 oz whole milk
Heat Produced by the Body

Calorimetry
The principles of human heat production is summarized below:
FOODSTUFF + OXYGEN –––––> HEAT + CO2 +
H2O
INDIRECT DIRECT
CALORIMETRY CALORIMETR
Y
MEASURE
EITHER HEAT
OR O2
Calorimetry involves the measurement of heat dissipation, which is a direct measure of Calorie
expenditure. One can measure heat directly (direct calorimetry) or the amount of oxygen consumed (indirect
calorimetry) to indicate caloric expenditure by the body.
METABOLI CALORIME
SM TRY
Direct Indirec
t
CO2 +
Oxygen
Consumption N2 Balance
Open Circuit Closed

Circuit
Direct Calorimetry
All of the body's metabolic processes ultimately result in heat production. Consequently, we can
measure human heat production similarly to the method used to determine the caloric value of foods in the
bomb calorimeter (refer to Figure 1, above).
The human calorimeter
illustrated in Figure 2 consists of
an airtight chamber where a
person lives and works for
extended periods. A known
volume of water at a specified
temperature circulates through a
series of coils at the top of the
chamber. Circulating water
absorbs the heat produced and
radiated by the individual.
Insulation protects the entire
chamber so any change in
water temperature relates
directly to the individual’s
energy metabolism. For
adequate ventilation, chemicals
continually remove moisture
and absorb carbon dioxide
from the person’s exhaled air.
Oxygen added to the air
recirculates through the
chamber.
Professors Atwater (a
chemist) and Rosa (a Figure 2. Directly measuring the body’s heat production in a human calorimeter.
physicist) in the 1890s built
and perfected the first human calorimeter of major scientific importance at Wesleyan University
(Connecticut). Their elegant human calorimetric experiments relating energy input to energy expenditure
successfully verified the law of the conservation of energy and validated the relationship between direct and
indirect calorimetry. The Atwater-Rosa Calorimeter consisted of a small chamber where a subject lived, ate,
slept, and exercised on a bicycle ergometer or treadmill. Experiments lasted from several hours to 13 days;
during some experiments, subjects performed cycling exercise continuously for up to 16 hours expending
more than 10,000 kCal! The calorimeter's operation required 16 people working in teams of eight for 12-hour
shifts.
Direct measurement of heat production in humans has considerable theoretical implications, but limited
practical application. Accurate measurements of heat production in the calorimeter require considerable time,
expense, and formidable engineering expertise. Thus, the calorimeters use remains generally inapplicable for
human energy determinations for most sport, occupational, and recreational activities. Also, direct
calorimetry cannot be applied for large-scale studies in underdeveloped and poor countries. Great need exists
for total nutritional and energy balance assessments under a variety of deprivation conditions, particularly
undernutrition and starvation. In the 90 years since Atwater and Rosa published their papers on human
calorimetry, other methodology evolved to infer energy expenditure indirectly from metabolic gas exchanges
(see next section). For example, the modern space suit worn by astronauts, in reality a “suit-calorimeter,”
maintains respiratory gas exchange and thermal balance while the astronaut works outside an orbiting space
vehicle.
Indirect Calorimetry
All energy-releasing reactions in the body ultimately depend on oxygen utilization. By measuring a
person’s oxygen uptake during steady-rate exercise, researchers obtain an indirect yet accurate estimate of
energy expenditure. Indirect calorimetry remains relatively simple and less expensive to maintain and staff
compared to direct calorimetry. Closed-circuit and open-circuit spirometry represent the two common
methods of indirect calorimetry.
Closed-Circuit Spirometry
Figure 3 illustrates the technique of closed-circuit
spirometry developed in the late 1800's and now
used in hospitals and research laboratories to
estimate resting energy expenditure. The subject
breathes 100% oxygen from a prefilled container
(spirometer). The equipment consists of a "closed
system" because the person rebreathes only the gas in
the spirometer. A canister of soda lime (potassium
hydroxide) placed in the breathing circuit absorbs the
carbon dioxide in the exhaled air. A drum attached to
the spirometer revolves at a known speed and
records oxygen uptake from changes in the system's
volume.
During exercise, oxygen uptake measurement
using closed-circuit spirometry becomes problematic.
The subject must remain close to the equipment, the
breathing circuit offers great resistance to the large
gas volumes exchanged during exercise, and the
relatively slow speed of carbon dioxide removal
becomes inadequate during heavy exercise.
Open-Circuit Spirometry Figure 3. Closedcircuit method uses a spirometer prefilled

with 100% oxygen. This method works well for rest or light
The open-circuit method remains the most exercise, but not for intense exercise.
widely used technique to measure oxygen uptake
during exercise. A subject inhales ambient air with a constant composition of 20.93% oxygen, 0.03% carbon
dioxide, and 79.04% nitrogen. The nitrogen fraction also includes a small quantity of inert gases. Changes in
oxygen and carbon dioxide percentages in expired air compared to inspired ambient air indirectly reflect the
ongoing process of energy metabolism. Thus, analysis of two factors volume of air breathed during a
specified time period, and composition of exhaled air provide a useful way to measure oxygen uptake and
infer energy expenditure.
Three common open-circuit, indirect calorimetric procedures measure oxygen uptake during physical
activity:
 Portable spirometry
 Bag technique
Figure 4. Portable spirometer.
 Computerized instrumentation
Portable Spirometry
German scientists in the early 1940’s perfected a lightweight, portable
system to determine indirectly the energy expended during physical activity.
The activities included war-related operations  traveling over different
terrain with full battle gear, operating transportation vehicles, and tasks
soldiers would encounter during combat operations. The person carries the 3- kg
box-shaped apparatus (Figure 4) on the back. Air passes through a two-way
valve, and expired air exits through a gas meter. The meter measures expired air
volume and collect a small gas sample for later analysis of O2 and CO2
content, and thus determination of oxygen uptake and energy expenditure.
Carrying the portable spirometer allows considerable freedom of
movement for estimating energy expenditure in diverse activities like
mountain climbing, downhill skiing, sailing, golf, and common household
activities. The equipment becomes cumbersome during vigorous activity;
with rapid breathing, the meter under-records airflow measurements during
heavy exercise.
Bag Technique
Figure 5 depicts the bag technique. The subject rides a stationary cycle ergometer wearing headgear
containing a two-way, high-velocity, low-resistance breathing valve. He breathes ambient air through one
side of the valve and expels it out the other side. The air then passes into either large canvas or plastic bags or
rubber meteorological balloons, or directly through a gas meter,
which continually measures expired air volume. The meter
collects a small sample of expired air for analysis of oxygen and
carbon dioxide composition. Assessment of oxygen uptake (as
with all indirect calorimetric techniques) uses an appropriate
calorific transformation to convert measures of oxygen uptake to
energy expenditure. Figure 6 illustrates oxygen uptake measured
by the bag technique while lifting boxes of different weight and
size to evaluate the energy requirements of a specific
occupational task.
Computerized Instrumentation
With advances in computer and microprocessor technology, the
exercise scientist can accurately and rapidly measure metabolic
and cardiovascular response to exercise. A computer interfaces
with different instruments to measure oxygen uptake.
The computer performs metabolic calculations based on
electronic signals it receives from the instruments. A printed or
graphic display of the data appears during the measurement
Figure 5. Bag technique to measure oxygen period. More advanced systems include automated blood
consumption. pressure, heart rate, and temperature monitors, and preset
instructions to regulate speed, duration, and workload of a treadmill, bicycle ergometer, stepper, rower, swim
flume, or other exercise apparatus.
Caloric Transformation for Oxygen

Bomb calorimeter studies show that approximately 4.82 kCal release when a blend of carbohydrate, lipid,
and protein burns in one liter of oxygen. Even with large variations in metabolic mixture, this calorific value
for oxygen varies only slightly (generally within 2 to 4%). Assuming the combustion of a mixed diet, a
rounded value of 5.0 kCal per liter of oxygen consumed designates the appropriate conversion factor for
estimating energy expenditure under steady-rate conditions of aerobic metabolism. An energy-oxygen
equivalent of 5.0 kCal per liter provides a convenient yardstick for transposing any aerobic physiologic
activity to a caloric (energy) frame of reference. In fact, indirect calorimetry through oxygen uptake
measurement serves as the basis to quantify the caloric stress of most physical activities.
The Respiratory Quotient (RQ)

Complete oxidation of a molecule's carbon and hydrogen atoms to the carbon dioxide and water end-
products requires different amounts of oxygen due to inherent chemical differences in carbohydrate, lipid,
and protein composition. Thus, the substrate metabolized determines the quantity of carbon dioxide
produced in relation to oxygen consumed. The respiratory quotient (RQ) refers to the following ratio of
metabolic gas exchange:
RQ = CO2 produced  O2 uptake
The RQ provides a convenient guide for approximating the nutrient mixture catabolized for energy during
rest and aerobic exercise. Also, because the caloric equivalent for oxygen differs somewhat depending on the
nutrients oxidized, precisely determining the body's heat production requires knowledge of both RQ and
oxygen uptake.
RQ For Carbohydrate, Lipid and Protein

Because the ratio of hydrogen to oxygen atoms in carbohydrates is always the same as in water, that is 2:1,
the complete oxidation of a glucose molecule consumes six molecules of oxygen and six carbon dioxide
molecules as follows:
C6H12O6 + 6 O2 6 CO2 + 6 H2O
Gas exchange during glucose oxidation produces an equal number of CO2 molecules to O2 molecules
consumed; therefore, the RQ for carbohydrate equals 1.00:
RQ = 6CO2 6O2 =1.00
The chemical composition of lipids differs from carbohydrates because lipids contain considerably fewer
oxygen atoms in proportion to carbon and hydrogen atoms. Consequently, when a lipid catabolizes for
energy, additional oxygen is required for the oxidation of the hydrogen atoms in excess of their 2 to 1 ratio
with oxygen. Palmitic acid, a typical fatty acid, oxidizes to carbon dioxide and water, producing 16 carbon
dioxide molecules for every 23 oxygen molecules consumed. The following equation summarizes this
exchange to compute RQ:
C16H32O2 + 23O2  16CO2 + 16H2O
RQ = 16CO2  23O2 = 0.696
Generally, a value of 0.70 represents the RQ for lipid with variation ranging between 0.69 and 0.73,
depending on the oxidized fatty acid's carbon chain length.
Proteins do not simply oxidize to carbon dioxide and water during energy metabolism in the body.
Rather, the liver first deaminates the amino acid molecule; then the body excretes the nitrogen and sulfur
fragments in the urine, sweat, and feces. The remaining “keto acid” fragment oxidizes to carbon dioxide and
water to provide energy for biologic work. Short-chain keto acids, as in fat catabolism, require more oxygen
in relation to carbon dioxide produced to achieve complete combustion. The protein albumin oxidizes as
follows:
C72H112N2O22S + 77O2  63CO2 + 38H2O + SO3 + 9CO(NH2)2
RQ = 63CO2  77O2 = 0.818
The general value 0.82 characterizes the RQ for protein.
RQ For a Mixed Diet

During activities ranging from complete bed rest to mild aerobic exercise (walking or slow jogging), the
RQ seldom reflects the oxidation of pure carbohydrate or pure fat. Instead, metabolism of a mixture of these
nutrients occurs with an RQ intermediate between 0.70 and 1.00. Assume an RQ of 0.82 from the metabolism
of a mixture of 40% carbohydrate and 60% fat, applying the caloric equivalent of 4.825 kCal per liter of
oxygen for the energy transformation. Using 4.825 kCal, the maximum error in estimating energy metabolism
from steady-rate VO2 would equal about 4%.
Thermal Equivalents of Oxygen: The RQ Table

Table 2 (next page) presents the energy expenditure per liter VO2 for different non-protein RQ values,
including corresponding percentages and grams of carbohydrate and fat used for energy. The non-protein
value assumes that the metabolic mixture comprises only carbohydrate and fat. Interpret the table as follows:
Suppose oxygen uptake during 30 min of exercise averages 3.22 L•min–1 with CO2 production of 2.78 L .
min-1. The RQ, computed as VCO2/VO2 (2.78/3.22), equals 0.86. From Table 1, this RQ value (left column)
corresponds to an energy equivalent of 4.875 kCal per liter of oxygen uptake, or an energy output of 15.7
kCal•min–1 (2.78 L O2•min–1 x 4.875 kCal). Based on a non-protein RQ, 54.1% of the calories come from the
combustion of carbohydrate and 45.9% from fat. The total calories expended during the 30-minute exercise
period equal 471 kCal (15.7 kCal•min–1 x 30).

Liters of Oxygen and Calories
• 1 Liter per minute Oxygen Consumed = 5 kCal per minute heat liberated
• Rest oxygen consumption during rest = 250 mL (0.25 L) per minute
• 5 kCal per Liter x 0.25 Liters = 1.25 kCal per minute (5 x 0.25 = 1.25)
• kCal per hour = 60 minutes x 1.25 kCal per minute = 75 kCal per hour
• kCal per 24 hour = 24 h x 75 kCal per h = 1800 kCal per 24 h
Table 2. Thermal equivalents of oxygen for the non-protein respiratory quotient, including percent kCal
and grams derived from carbohydrate and fat.
Non-Protein kCal per Liter % kCal Derived %kCal Derived Grams per Grams per
RQ O2 Uptake from CHO From Fat Liter O2 CHO Liter O2 Fat
0.7 4.686 0.0 100.0 0.000 0.496
0.71 4.69 0.1 98.9 0.120 0.491
0.72 4.702 4.8 95.2 0.510 0.476
0.73 4.714 8.4 91.6 0.900 0.460
0.74 4.727 12.0 88.0 0.130 0.444
0.75 4.739 15.6 84.4 0.170 0.428
0.76 4.75 19.2 80.8 0.211 0.412
0.77 4.764 22.8 77.2 0.250 0.396
0.78 4.776 26.3 73.7 0.290 0.380
0.79 4.788 29.9 70.1 0.330 0.363
0.8 4.801 33.4 66.6 0.371 0.347
0.81 4.813 36.9 63.1 0.413 0.330
0.82 4.825 40.3 59.7 0.454 0.313
0.83 4.838 43.8 56.2 0.496 0.297
0.84 4.85 47.2 52.8 0.537 0.280
0.85 4.862 50.7 49.3 0.579 0.263
0.86 4.875 54.1 45.9 0.621 0.247
0.87 4.887 57.5 42.5 0.663 0.230
0.88 4.889 60.8 39.2 0.705 0.213
0.89 4.911 64.2 35.8 0.749 0.195
0.9 4.924 67.5 32.5 0.791 0.178
0.91 4.936 70.8 29.2 0.834 0.160
0.92 4.948 74.1 25.9 0.877 0.143
0.93 4.961 77.4 22.6 0.921 0.125
0.94 4.973 80.7 19.3 0.964 0.108
0.95 4.985 84.0 16.0 1.008 0.090
0.96 4.998 87.2 12.8 1.052 0.072
0.97 5.01 90.4 9.6 1.097 0.054
0.98 5.022 93.6 6.4 1.142 0.036
0.99 5.035 96.8 3.2 1.186 0.018
1 5.047 100.0 0.0 1.231 0.000
RREADING #4 STUDY GUIDE
1. 4.2 kcal•gm-1
2. 5.65 kcal•gm-1
3. 9.4 kcal•gm-1
4. Atwater factors
5. Bomb calorimeter
6. Calorie
7. Direct calorimetry
8. Closed-circuit spirometry
9. Digestive efficiency
10. Direct calorimetry
11. Heat of combustion

12. Indirect calorimetry
13. Open-circuit spirometry
14. Respiratory exchange ratio
STUDY QUESTIONS
The Calorie – A Measurement Unit of Food Energy

Describe the difference between a calorie and a kilocalorie.
Gross Energy Value of Foods

Describe the instrument in direct calorimetry to measure a food’s energy content?
Heat of Combustion
Give the heats of combustion for the three macronutrients>
Carbohydrate
Lipid
Protein
Why is the heat of combustion for protein less in the body than in a bomb calorimeter?
Net Energy Value of Foods

Compare the heat of combustion of carbohydrates and lipids in the body and determined by bomb
calorimetry.
In the body
Bomb calorimetry
Digestive Efficiency
List one effect that dietary fiber has on the energy availability of ingested foods?
Energy Value of a Meal

Calculate the caloric content of 100 grams of a food containing 5% protein, 14% lipid, and 20%
carbohydrate. (Hint: Use the Atwater general factors.)
Calories Equal Calories

From an energy standpoint, explain why 100 calories from a piece of cake is no more fattening that
100 kcal from celery?
Heat Produced by the Body

List two methods to determine heat production by the body.
1.
2.
Calorimetry
Briefly describe the principle of calorimetry.
Direct Calorimetry
Describe direct calorimetry to measure human heat production.
Indirect Calorimetry
List the two methods of indirect calorimetry.
1.
2.
Closed-Circuit Spirometry
Give one disadvantage of closed-circuit spirometry during exercise studies
Open-Circuit Spirometry
List one positive aspect of each of the following procedures of indirect calorimetry during exercise
studies.
Portable Spirometry
Bag Technique
Portable Spirometry
Who were the first scientists to use portable spirometry?
Bag Technique
What kind of breathing valve must be used with the bag technique for open-circuit spirometry?
Lists three instruments that need to be interfaced with a computer for on-line measurement of
oxygen uptake.
1. 3.
2.
Direct Versus Indirect Calorimetry

Give an example of the degree of agreement between energy expenditure obtained by direct and
indirect calorimetry.
Caloric Transformation for Oxygen

Assuming combustion of a mixed diet, give the rounded value for the number of calories released
per liter of oxygen consumed?
The Respiratory Quotient (RQ)

Write the RQ formula.
RQ For Carbohydrate, lipid and protein

Write the RQ for carbohydrate?
Write the RQ for lipid?
Write the RQ for protein?
RQ for A Mixed Diet

Give the RQ for a diet of approximately 40% carbohydrate and 60% lipid. What is the
corresponding caloric equivalent?
RQ
Caloric equivalent
READING #5
HUMAN ENERGY TRANSFER BASICS
Introduction
In this lecture, I present an overview of how the body obtains energy to power its diverse functions. A
basic understanding of carbohydrate, fat, and protein catabolism and subsequent anaerobic and aerobic
energy transfer forms the basis for much of the content of exercise physiology. Knowledge about human
bioenergetics provides the practical basis for formulating sport-specific exercise training regimens,
recommending activities for physical fitness and weight control, and advocating prudent dietary
modifications for specific sport requirements.
The body’s capacity to extract energy from food nutrients and transfer it to the contractile elements in
skeletal muscle determines the capacity to swim, run, bicycle, and ski long distances at high intensity. Energy
transfer occurs through thousands of complex chemical reactions that require the proper mixture of macro-
and micronutrients continually fueled by oxygen. The term aerobic describes such oxygen-requiring energy
reactions. In contrast, anaerobic chemical reactions generate energy rapidly for short durations without
oxygen. Rapid energy transfer allows for a high standard of performance in maximal short-term sprinting in
track and swimming, or repeated stop-and-go sports like soccer, basketball, lacrosse, water polo, volleyball,
field hockey, and football. The following point requires emphasis: The anaerobic and aerobic breakdown of
ingested food nutrients provides the energy source for synthesizing the chemical fuel that powers all
forms of biologic work.
Part 1. ATP and Phosphate Bond Energy

The human body receives a continual supply of chemical energy to perform its many functions. Energy
derived from the oxidation of food does not release suddenly at some kindling temperature because the body,
unlike a mechanical engine, cannot use heat energy directly. Rather, complex, enzymatically-controlled
reactions within in the relatively cool, watery medium of the cell extract the chemical energy trapped within
the bonds of carbohydrate, fat, and protein molecules. This relatively slow extraction process reduces energy
loss and provides for enhanced efficiency in energy transformations. In this way, the body makes direct use of
chemical energy for biologic work. In a sense, energy becomes available to the cells as needed. The body
maintains a continuous energy supply through the use of adenosine triphosphate, or ATP, the special carrier
for free energy.
ATP – The Energy Currency

The energy in food does not transfer directly to cells for biologic work. Rather, this “macronutrient
energy” becomes released and funneled through the energy-rich compound ATP to power cellular needs.
Figure 1 shows how an ATP molecule forms from a molecule of adenine and ribose (called adenosine), linked
to three phosphate molecules. The bonds linking the two outermost phosphates, termed high-energy bonds,
represent a considerable stored energy within the ATP molecule.
A tight linkage or coupling exists between the
breakdown of the macronutrient energy molecules
and ATP synthesis, which “captures” a significant
portion of the released energy within its bonds.
Coupled reactions occur in pairs; the breakdown of
one compound provides energy for building another
compound. To meet energy needs, ATP joins with
water (in a process termed hydrolysis) splitting the
outermost phosphate bond from the ATP molecule.
Figure 1. ATP and it’s high energy bonds. The enzyme adenosine triphosphatase accelerates this
process forming a new compound adenosine
diphosphate or ADP. These reactions, in turn, couple to other reactions that use the “freed” phosphate-bond
chemical energy. The body uses ATP to transfer the energy produced during catabolic reactions to power
reactions that synthesize new materials. In essence, this energy receiver – energy donor cycle represents the
cells' two major energy-transforming activities:
 Form and conserve ATP from food's potential energy
 Use energy extracted from ATP to power biologic work
Figure 2 illustrates examples of the anabolic and catabolic reactions that involve the coupled transfer of
chemical energy. All of the energy released from catabolizing one compound does not dissipate as heat;
rather, a portion becomes harvested and conserved within the chemical structure of the newly formed
compound. ATP represents the common energy transfer “vehicle” in most coupled biologic reactions.
Anabolism requires energy for synthesizing new compounds. For example, several glucose molecules join
together, much like the links in a chain of sausages to form the larger more complex glycogen molecule;
similarly, glycerol and fatty acids combine to make triglycerides, and amino acids link forming proteins. Each
reaction starts with simple compounds and uses them as building blocks to form larger, more complex
compounds. Catabolic reactions release energy; in many instances, this process couples to ATP formation.
During ATP catabolism, the enzyme adenosine triphosphatase catalyzes the reaction when ATP joins with
water. For each mole of ATP degraded to adenosine diphosphate (ADP), the outermost phosphate bond
splits, liberating approximately 7.3 kCal of free energy (i.e., energy available for work).
ATP + H2O ––––>ATP + P -7.3 kCal
The free energy liberated in ATP hydrolysis reflects
energy differences between reactants and end-
products. Because this reaction generates considerable
energy, ATP is referred to as a high-energy
phosphate compound. Additional energy releases
when another phosphate splits from ADP. In some
reactions of biosynthesis, ATP donates its two terminal
phosphates simultaneously to construct new cellular
material. Adenosine monophosphate or AMP becomes
the new molecule with a single phosphate group.
The energy liberated during ATP breakdown
directly transfers to other energy-requiring molecules.
In muscle, this energy activates specific sites on the
contractile elements causing muscle fibers to shorten.
Because energy from ATP powers all forms of
biologic work, ATP constitutes the cell’s “energy
currency.”
The splitting of an ATP molecule immediately takes
place without oxygen. The cell’s capability for ATP
breakdown generates energy for rapid use; this would
not occur, however, if energy metabolism required
oxygen at all times. Think of anaerobic energy release
as a back-up power source, called upon to deliver
energy in excess of what can be generated aerobically.
For this reason, any form of activity can take place
immediately without instantaneously consuming
oxygen; examples include sprinting for a bus, lifting a
fork, driving a golf ball, spiking a volleyball, doing a
Figure 2. Examples of anabolic and catabolic reactions pushup, or jumping up in the air. The well known
that involve coupled energy transfer. practice of holding one’s breathe while sprint
swimming provides a clear example of ATP splitting
without reliance on atmospheric oxygen. Withholding air (oxygen), although not advisable, can be done
during a 100-yard sprint on the track, lifting a barbell, a dash up several flights of stairs, or simply holding
one's breath while rapidly flexing and extending the arms or fingers. In each case, energy metabolism
proceeds uninterrupted because the energy for performing the activity comes almost exclusively from
intramuscular anaerobic sources.
ATP Resynthesis
Because cells store only a small quantity of ATP, it must continually be resynthesized at its rate of use. This
provides a biologically useful mechanism for regulating energy metabolism. By maintaining only a small
amount of ATP, its relative concentration (and corresponding concentration of ADP) changes rapidly with
any increase in a cell’s energy demands. An ATP:ADP imbalance at the start of exercise immediately
stimulates the breakdown of other stored energy-containing compounds to resynthesize ATP. As one might
expect, increases in cellular energy transfer depend on exercise intensity. Energy transfer increases about
four-fold in the transition from sitting in a chair to walking. However, changing from a walk to an all-out
sprint almost immediately accelerates energy transfer rate about 120 times! Generating significant energy
output almost instantaneously demands ATP availability and a means for its rapid resynthesis.
ATP: A Limited Currency

As previously pointed out, a limited quantity of ATP serves as the energy currency for all cells. In fact, at
any one time the body stores only about 80 to 100 g (3.5 oz.) of ATP. This provides enough intramuscular
stored energy for several seconds of explosive, all-out exercise. A limited quantity of “stored” ATP represents
an advantage due to the molecule's heaviness. Biochemists estimate that sedentary persons each day use an
amount of ATP approximately equal to 75% of their body mass. For an endurance athlete running a marathon
race and generating about 20 times the resting energy expenditure over 3 hours, total ATP usage could
amount to 80 kg! Thus, with limited supplies and with high demand, ATP must be continually resynthesized
to meet energy requirements.
Phosphocreatine (PCr):
The Energy Reservoir
Some energy for ATP resynthesis
comes directly from the splitting
(hydrolysis) of a phosphate from another
intracellular high-energy phosphate
compound – phosphocreatine (PCr), also
known as creatine phosphate or CP. PCr,
similar to ATP, releases a large amount of
energy when the bond splits between the
creatine and phosphate molecules. The
hydrolysis of PCr for energy begins at the
onset of intense exercise, does not require
oxygen, and reaches a maximum in about
Figure 3. ATP and PCr are anaerobic sources of phosphate-bond 10 seconds. Thus, PCr can be considered a
energy. The energy liberated from the hydrolysis (splitting) of “reservoir” of high-energy phosphate
PCr powers the union of ADP to reform ATP. bonds. Figure 4 schematically illustrates the
release and use of phosphate-bond energy in ATP and PCr. The term high-energy phosphates describe these
stored intramuscular compounds. ATP and PCr are anaerobic sources of phosphate-bond energy. The energy
liberated from the hydrolysis (splitting) of PCr powers the union of ADP and P to reform ATP.
In both reactions in Figure 3, the arrows point in opposite directions to indicate reversible reactions. In
other words, creatine (C) and phosphate (P) can join again to reform PCr. This also holds true for ATP where
the union of ADP and P reforms ATP (see top part of figure). ATP resynthesis occurs if sufficient energy exists
to rejoin an ADP molecule with one P molecule. Hydrolysis of PCr supplies this energy.
Cells store PCr in considerably larger quantities than ATP. Mobilization of CP for energy takes place
almost instantaneously and does not require oxygen. For this reason, PCr is considered a “reservoir” of high-
energy phosphate bonds.
Cellular Oxidation
A molecule becomes reduced when it accepts electrons from an electron donor. In turn, the molecule that
gives up the electron becomes
oxidized. Oxidation reactions
(donating electrons) and reduction
reactions (accepting electrons)
remain coupled because every
oxidation coincides with a
reduction. In essence, cellular
oxidation-reduction constitutes the
mechanism for energy metabolism.
The stored carbohydrate, fat, and
protein molecules continually
provide hydrogen atoms in this
process. The mitochondria, the
cell’s “energy factories,” contain
carrier molecules that remove
Figure 4. In the body, the electron transport chain removes electrons from
electrons from hydrogen (oxidation)
hydrogen and ultimately delivers them to oxygen. In this oxidationreduction
and eventually pass them to oxygen
process, much of the chemical energy stored within the hydrogen atoms does not
dissipate to kinetic energy, rather, it becomes conserved in forming ATP. (reduction). Synthesis of the high-
energy phosphate ATP occurs
during oxidation-reduction reactions.
Electron Transport
Figure 4 illustrates the general scheme for hydrogen oxidation and accompanying electron transport to
oxygen. During cellular oxidation, hydrogen atoms are not merely turned loose in the cell fluid. Rather,
highly specific enzymes catalyze hydrogen's release from the nutrient substrate. The coenzyme nicotinamide
adenine dinucleotide or NAD+ accepts pairs of electrons (energy) from hydrogen. While the substrate
oxidizes and loses hydrogen (electrons), NAD+ gains a hydrogen and two electrons and reduces to NADH;
the other hydrogen appears as H+ in the cell fluid.
The riboflavin-containing coenzyme, flavin adenine dinucleotide (FAD) serves as the other important
electron acceptor in oxidizing food fragments.
The NADH and FADH2 formed in macronutrient breakdown represent energy-rich molecules because
they carry electrons with a high-energy transfer potential. The cytochromes, a series of iron-protein electron
carriers, then pass in “bucket brigade” fashion pairs of electrons carried by NADH and FADH2 on the inner
membranes of the mitochondria. The cytochromes transfer electrons to their ultimate destination, where they
reduce oxygen to form water. The NAD+ and FAD then recycle for subsequent use in energy metabolism.
Electron transport by specific carrier molecules constitutes the respiratory chain, serving as the final
common pathway where electrons extracted from hydrogen pass to oxygen. For each pair of hydrogen
atoms, two electrons flow down the chain and reduce one atom of oxygen to form water. Of the five specific
cytochromes, only the last one, cytochrome oxidase (cytochrome a3 with a strong affinity for oxygen),
discharges its electron directly to oxygen.
In the body, the electron-transport chain removes electrons from hydrogen and ultimately delivers them to
oxygen. In this oxidation-reduction process, much of the chemical energy stored within the hydrogen atom
does not dissipate to kinetic energy; rather it becomes conserved in forming ATP.
Oxidative Phosphorylation
Oxidative phosphorylation refers to how ATP becomes synthesized during the transfer of electrons
from NADH and FADH2 to molecular oxygen. This important process represents the cell’s primary means
for extracting and trapping chemical energy in the high-energy phosphates. Over 90% of ATP synthesis takes
place in the respiratory chain by oxidative reactions coupled with phosphorylation.
Think of oxidative phosphorylation as a waterfall divided into several separate cascades by the
intervention of waterwheels at different heights. The energy in NADH transfers to ADP to reform ATP at
three distinct coupling sites during electron transport (Figure 4). Oxidation of hydrogen and subsequent
phosphorylation occurs as follows:
NADH + H+ + 3ADP + 3 P + 1/2 O2 –––> NAD+ + H2O + 3 ATP
Role of Oxygen in Energy Metabolism

The continual resynthesis of ATP during coupled oxidative phosphorylation of the macronutrients
requires three prerequisites conditions.
1. Availability of the reducing agents NADH2 or FADH2
2. Presence of an oxidizing agent in the form of oxygen
3. Sufficient quantity of enzymes and metabolic machinery in the tissues to make the energy transfer
reactions “go” at the appropriate rate
Satisfying these three conditions causes hydrogen and electrons to continually shuttle down the
respiratory chain to molecular oxygen during catabolism of food substrates. In strenuous exercise,
inadequacy in oxygen delivery (condition #2) or its rate of utilization (condition #3) creates a relative
imbalance between hydrogen release and oxygen's final acceptance of them. If either of these occurs, electron
flow down the respiratory chain “backs up” and hydrogen accumulate bound to NAD + and FAD.
For aerobic metabolism, oxygen serves as the final electron acceptor in the respiratory chain and combines
with hydrogen to form water during energy metabolism. Some might argue that the term aerobic metabolism
is misleading, since oxygen does not participate directly in ATP synthesis. Oxygen's presence at the “end of
the line,” however, largely determines one’s capability for ATP production and, hence, the ability to sustain
high-intensity exercise. In this sense, use of the term aerobic seems justified.
Part 2. Energy Release From Food

The energy released in macronutrient breakdown serves one crucial purpose – to phosphorylate ADP to
reform the energy-rich compound ATP (Figure 5). Although macronutrient catabolism favors generating
phosphate-bond energy, the specific pathways of degradation differ depending on the nutrients metabolized.
Energy Release from Carbohydrate
Figure 5. Potential energy in food powers ATP resynthesis
Carbohydrate's primary function supplies energy for cellular work. Carbohydrate represents the only
macronutrient whose potential energy can generate ATP anaerobically. This becomes important in vigorous
exercise that requires rapid energy release above levels supplied by aerobic metabolic reactions.
1. During light and moderate aerobic exercise, carbohydrate supplies about one-half of the body’s energy
requirements.
2. Processing fat through the metabolic mill for energy requires some carbohydrate catabolism.
3. Aerobic breakdown of carbohydrate for energy occurs at about twice the rate as energy generated
from fatty acid breakdown. Thus, depleting glycogen reserves significantly reduces exercise power
output. In prolonged high-intensity, aerobic exercise such as marathon running, athletes often
experience nutrient-related fatigue – a state associated with muscle and liver glycogen depletion.
The complete breakdown of 1 mole of glucose (180 g) to carbon dioxide and water yields 686 kcal of
chemical free energy.
C6H12O6 + 6O2 ––––> 6CO2 + 6H2O + 689 kCal per mole
In the body, the complete breakdown of glucose liberates the same quantity of energy, with a significant
portion conserved as ATP. Synthesizing one mole of ATP from ADP and phosphate ion requires 7.3 kcal of
energy. Therefore, coupling all of the energy from glucose oxidation to phosphorylation could theoretically
form 94 moles of ATP per mole of glucose (686 kcal ÷ 7.3 kcal per mole = 94 moles). In the muscles, however,
the phosphate bonds only conserve 38% or 263 kcal of energy, with the remainder dissipated as heat. This
loss of useful energy represents the body's metabolic inefficiency for converting stored potential energy into
useful energy.
Anaerobic versus Aerobic

Glucose degradation occurs in two stages. In stage one, glucose breaks down to two molecules of
pyruvate. Energy transfers occur without oxygen (anaerobic). In stage two, pyruvate degrades further to CO 2
and H2O. Energy transfers from these reactions require electron transport and oxidative phosphorylation.
Anaerobic Energy from Glucose:

Glycolysis (Glucose Splitting)
The first stage of glucose degradation within cells
involves a series of ten chemical reactions collectively
termed glycolysis (also termed the Embden-Meyerhof
pathway for its discoverers); glycogenolysis describes these
reactions when they begin with stored glycogen. These
series of reactions occur in the watery medium of the cell
outside of the mitochondrion. In a way, glycolytic reactions
represent a more primitive form of energy transfer, well
developed in amphibians, reptiles, fish, and marine
mammals. In humans, the cells’ limited capacity for
glycolysis becomes crucial during activities that require
effort for up to 90-sec.
Figure 6 shows the glucose-to-pyruvate sequence under
anaerobic conditions in terms of the carbon atoms. The six-
Figure 6. Glycolysis. A 6-carbon glucose splits
carbon glucose splits into two 3-carbon compounds
into two, 3-carbon compounds that degrade
(pyruvate). These subsequently degrade into two molecules
into two, 3-carbon pyruvate molecules.
Glucose splitting occurs anaerobically. of pyruvate with the net release of 2 ATP (i.e., energy).
Formation of Lactic Acid

Sufficient oxygen bathes the cells during light-to-moderate of energy metabolism. The hydrogen
(electrons) stripped from the substrate and carried by NADH oxidizes within the mitochondria to form water
as they join with oxygen.
In strenuous exercise, when energy demands exceed either oxygen supply or utilization, the respiratory
chain cannot process all of the hydrogen joined to NADH. Continued release of anaerobic energy in
glycolysis depends on NAD+ availability; otherwise, the rapid rate of glycolysis stops. In anaerobic glycolysis,
NAD+ “frees-up” as pairs of “excess” non-oxidized hydrogen combine temporarily with pyruvate to form
lactic acid, catalyzed by the enzyme lactic dehydrogenase (LDH) in the reversible reaction shown in Figure 7.
The temporary storage of hydrogen with pyruvate represents a unique aspect of energy metabolism
because it provides a ready “storage bin” to temporarily hold the end products of anaerobic glycolysis. Also,
Figure 7. Lactate forms when excess hydrogen combines with pyruvate.

once lactic acid forms within muscle, it diffuses rapidly into the blood for buffering to sodium lactate and
removal from the site of energy metabolism. This allows glycolysis to continue supplying additional
anaerobic energy for ATP resynthesis. However, this avenue for extra energy remains temporary; blood
lactate and muscle lactic acid levels increase and ATP regeneration cannot keep pace with its utilization rate.
Fatigue soon sets in and exercise performance diminishes.
Even at rest, energy metabolism in red blood cells forms some lactic acid. This occurs as the red blood cells
contain no mitochondria and must derive their energy from glycolysis. Lactic acid should not be viewed as a
metabolic “waste product” as it provides a valuable source of energy that accumulates in the body during
heavy exercise. When sufficient oxygen becomes available during recovery, or when exercise pace slows,
NAD+ scavenges hydrogen attached to lactate; this hydrogen subsequently oxidizes to form ATP. Thus, blood
lactate becomes an energy source as it readily reconverts to pyruvate to undergo further catabolism.
Aerobic Energy From Glucose: The Krebs Cycle

The anaerobic reactions of glycolysis release about 10% of the energy within the original glucose; thus,
extracting the remaining energy requires additional metabolism. This occurs when pyruvate irreversibly
converts to acetyl–CoA. Acetyl–CoA enters the second stage of carbohydrate breakdown known as the Krebs
cycle (citric acid cycle). For each molecule of acetyl-CoA entering the Krebs cycle, two CO 2 molecules and 4
pairs of hydrogen atoms release. One molecule of ATP also regenerates directly from the Krebs cycle.
Figure 8. Two phases of the Citric Acid cycle. Phase 1 in the mitochondrion, Krebs cycle activity generates
hydrogen atoms. Phase 2 – significant ATP regenerates when hydrogen oxidizes via the aerobic process of
electron transport.
Oxygen does not participate directly in the Krebs cycle. The aerobic process of electron transport-oxidative
phosphorylation transfers the major portion of chemical energy in pyruvate to ADP. With adequate oxygen,
enzymes and substrate, NAD and FAD regeneration takes place allowing Krebs cycle metabolism to proceed.
Figure 8 shows the two phases of Krebs cycle activity. Phase 1 involves the introduction of pyruvate (from
glycolysis), combined with coenzyme A (a Vitamin B derivative), into the Krebs cycle with the release of
hydrogen, CO2 and ATP. Phase 2 shows significant ATP regeneration when hydrogen oxidizes via the aerobic
process of electron transport-oxidative phosphorylation (electron transport chain).
Net Energy Transfer From Glucose Catabolism

Figure 9 gives the pathways for energy transfer during glucose breakdown in muscle. Two ATP form
from in glycolysis; and 2 ATP come from acetyl-CoA degradation in Krebs cycle. The 24 released H2 atoms
(and their subsequent oxidation) are counted as follows:
 Four extramitochondrial hydrogen (2 NADH) from glycolysis yield 4 ATP (6 ATP in heart, kidney, and
liver).
 Four hydrogen (2 NADH) released as pyruvate degrades to acetyl-CoA yield 6 ATP.
 Twelve of the 16 hydrogens (6 NADH) released in the Krebs cycle yield 18 ATP.
 Four hydrogen joined to FAD (2 FADH2) in the Krebs cycle yield 4 ATP.
Figure 9. Net yield of 36 ATP from energy transfer during the complete oxidation
Figure 11
Energy Release From Fat

Stored fat represents the body’s most plentiful source of potential energy. Relative to carbohydrate and
protein, stored fat provides almost unlimited energy. The actual fuel reserves in an average young adult male
represent between 60,000 and 100,000 kcal of energy from triglyceride in fat cells (adipocytes), and about 3000
kcal from intramuscular triglyceride stored in close proximity to the mitochondria. In contrast, the
carbohydrate energy reserve would only contribute about 2000 kcal. Prior to energy release from fat, lipolysis
splits the triglyceride molecule into glycerol and three water-insoluble fatty acid molecules. The enzyme
lipase catalyzes triglyceride breakdown as follows:
Triglyceride + 3H2O ––––––> Glycerol + 3 Fatty acids
Breakdown of Glycerol and Fatty Acids

Figure 10 summarizes the pathways for the breakdown of the triglyceride molecule's glycerol and fatty
acid components.
Figure 10. Breakdown of glycerol and fatty acid fragments of a triglyceride molecule.
Glycerol
The anaerobic reactions of glycolysis accept glycerol as 3-phosphoglyceraldehyde, which then degrades to
pyruvate to form ATP by substrate-level phosphorylation. Hydrogen atoms pass to NAD +, and the Krebs
cycle oxidizes pyruvate. The complete breakdown of the single glycerol molecule in a triglyceride synthesizes
a total of 19 ATP molecules. Glycerol also provides carbon skeletons for glucose synthesis. The gluconeogenic
role of glycerol becomes prominent when glycogen reserves deplete due to dietary restriction of
carbohydrates, or in long-term exercise or heavy training.
Fatty Acids
The fatty acid molecule transforms to acetyl-CoA in the mitochondrion during beta–oxidation reactions.
This involves the successive release of 2-carbon acetyl fragments split from the fatty acid's long chain. ATP
phosphorylates the reactions, water is added, and hydrogen pass to NAD+ and FAD, and acetyl–CoA forms
when the acetyl fragment joins with coenzyme A. This acetyl unit is the same one generated from glucose
breakdown. Beta-oxidation continues until the entire fatty acid molecule degrades to acetyl–CoA so it can
directly enter the Krebs cycle. Hydrogen released during fatty acid catabolism oxidizes through the
respiratory chain. Note that fatty acid breakdown relates directly with oxygen uptake. For beta–oxidation to
proceed, oxygen must be present to join with hydrogen. Without oxygen (anaerobic conditions), hydrogen
remains joined with NAD+ and FAD bringing fat catabolism to a halt.
Total Energy Transfer From Fat Catabolism

For each 18-carbon fatty acid molecule, 147 molecules of ADP phosphorylate to ATP during beta-oxidation
and Krebs cycle metabolism. Because each triglyceride molecule contains three fatty acid molecules, 441 ATP
molecules form from the triglyceride's fatty acid components (3 x 147 ATP). Also, 19 molecules of ATP form
during glycerol breakdown, generating a total of 460 molecules of ATP for each triglyceride molecule
catabolized. This represents a considerable energy yield because only a net of 36 ATP form during a glucose
molecule's catabolism in skeletal muscle. The 40% efficiency of energy conservation for fatty acid oxidation
amounts to a value similar to glucose oxidation efficiency.

INTENSITY AND DURATION AFFECT FAT USE
Fatty acid oxidation occurs during low intensity exercise. For example, fat
combustion almost totally powers exercise at 25% of aerobic capacity.
Carbohydrate and fat contribute energy equally during moderate exercise. Fat
oxidation gradually increases as exercise extends to an hour or more and
carbohydrates become depleted. Toward the end of prolonged exercise (with
glycogen reserves low), circulating FFAs supply nearly 80% of the total energy
required.
ENERGY RELEASE FROM PROTEIN

Protein plays a contributory role as an energy substrate during endurance-type activities. The amino acids
(primarily the branched-
chain amino acids leucine,
isoleucine, valine, glutamine,
and aspartate) first must
convert to a form that readily
enters pathways for energy
release. This conversion
requires removing nitrogen
from the amino acid
molecule. In this way, the
muscle can directly use for
energy the “carbon skeleton”
by-products of donor amino
acids. Only when an amino
acid loses its nitrogen
containing amino group can
the remaining compound
(usually one of the Krebs
cycle's reactive compounds)
contribute to ATP formation.
Some amino acids are
glucogenic; they yield
intermediate products for
glucose synthesis via
gluconeogenesis. This
gluconeogenic method serves
as an important adjunct to
provide glucose during
prolonged exercise.
Figure 11 shows how
protein supplies
intermediates at three
different levels that have
energy producing
capabilities. Like fat and
Figure 11. Protein-to-energy pathways. carbohydrate, certain amino
acids are ketogenic; they
cannot synthesize to glucose, but instead when consumed in excess synthesize to fat. Amino acids that form
pyruvate provide a carbon skeleton for glucose synthesis by the body, making protein a source for glucose
when glycogen reserves run low.
The Metabolic Mill

The Krebs cycle plays a more important role than simply degrading pyruvate produced during glucose
catabolism. Fragments from other organic compounds formed from fat and protein breakdown provide
energy during the Krebs cycle.
The “metabolic mill” (Figure 12) depicts the Krebs cycle as the essential "connector" between energy from
food macronutrients energy and chemical energy of ATP. The Krebs cycle also serves as a metabolic hub to
provide intermediates to synthesize bionutrients for maintenance and growth. For example, excess
carbohydrates provide the glycerol and acetyl fragments to synthesize triglyceride. Acetyl–CoA also
functions as the starting point for synthesizing cholesterol and many hormones. In contrast, fatty acids do not
contribute to glucose synthesis because pyruvate's conversion to acetyl-CoA does not reverse (notice the one-
way arrow in Figure 12). Many of the carbon compounds generated in Krebs cycle reactions also provide the
organic starting points for synthesizing nonessential amino acids. Amino acids, particularly alanine with
carbon skeletons resembling Krebs cycle intermediates after deamination becomes synthesized to glucose.
Figure 12. The metabolic mill.

EXCESS PROTEIN ACCUMULATES FAT
Athletes and others who believe that taking protein supplements add to muscle
beware. Extra protein consumed above what the body requires ends up as body
fat. If an athlete desires to become fat, excessive protein intake achieves this end.
A protein excess does not contribute to the synthesis of muscle tissue.
Fats Burn in a Carbohydrate Flame

Interestingly, fatty acid breakdown depends in part on a continual background level of carbohydrate
breakdown. Recall that acetyl–CoA enters the Krebs cycle by combining with oxaloacetate to form citrate.
Depleting carbohydrate decreases pyruvate production during glycolysis. Diminished pyruvate further
reduces Krebs cycle intermediates, slowing Krebs cycle activity. Fatty acid degradation in the Krebs cycle
depends on sufficient oxaloacetate availability to combine with the acetyl-CoA formed during b-oxidation.
When carbohydrate level decreases, the oxaloacetate level may become inadequate. In this sense, “fats burn
in a carbohydrate flame.”
MACRONUTRIENTS IN EXCESS READILY CONVERT TO FAT

Excess energy intake from any fuel source can be counterproductive. Too much of any macronutrient
results in accumulation of body fat. Surplus dietary carbohydrate first fills the glycogen reserves. Once these
reserves fill, excess carbohydrate converts to triglycerides for storage in adipose tissue. Excess dietary calories
as fat move easily into the body’s fat deposits as does any protein excess. Excess amino acids readily convert
to fat.
LECTURE #5 WORKBOOK
1. Adenosine triphosphatase
2. Aerobic
3. Amino acid
4. Anaerobic
5. Coupled reactions
6. Enzymes
7. Free fatty acids
8. Glycerol
9. Glycolysis
10. High-energy phosphate
11. Krebs Cycle

12. Lactate
13. Metabolic mill
14. Muscle glycogen
15. PCr
16. Pyruvate
17. The metabolic mill
STUDY QUESTIONS
ATP and Phosphate Bond Energy
ATP – The Energy Currency

Complete the reaction:
ATP + H2O –––––––––>
ATP: A Limited Currency

Complete the following two equations.
ATP + H2O ––––––––>
PCr + H2O ––––––––>

Phosphocreatine (PCr): The Energy Reservoir

What main function does PCr play in energy metabolism?
Cellular Oxidation
“For every reaction involving cellular oxidation, there is a reaction involving __________________”.
Electron Transport
Briefly describe the main purpose of electron transport.
Oxidative Phosphorylation
Complete the following chemical equation:
NADH + H+ + 3ADP + 3 P + 1/2 O2 –––––––>
Role of Oxygen in Energy Metabolism

“The main role of oxygen in energy metabolism is to _______________________________________”.
Energy Release from Carbohydrate

Write the equation for the complete breakdown (hydrolysis) of one mole of glucose.
Anaerobic versus Aerobic

The two stages of carbohydrate breakdown are called ________________________ and
_________________________.
Anaerobic Energy from Glucose: Glycolysis (Glucose Splitting)

Glycolysis occurs in what part of the cell?
Formation of Lactic Acid

Write the chemical formula for lactic acid.
Aerobic Energy From Glucose: The Krebs cycle

Give the most important function of the Krebs cycle.
Net Energy Transfer From Glucose Catabolism
Give the total ATP from glucose catabolism.
Energy Release From Fat

Complete the following equation:
Triglyceride + 3H2O –––––––––>
Breakdown of Glycerol and Fatty Acids

Which substance, glycerol or fatty acid, undergoes beta oxidation?
Glycerol
How many molecules of ATP synthesize when one glycerol molecule breaks down?
Fatty Acids
Of what importance is oxygen in fatty acids catabolism?
Total Energy Transfer From Fat Catabolism

How many molecules of ATP become synthesized in the complete combustion of a neutral fat
molecule?
Energy Release From Protein

After nitrogen removal from an amino acid, what happens to the remaining “carbon skeleton” in
energy metabolism?
The Metabolic Mill

Why is the Krebs cycle so important?
Fats Burn in a Carbohydrate Flame

Explain why “fats burn in a carbohydrate flame.”
Excess Macronutrients Convert To Fat

Can protein consumed in excess of the body’s energy requirement end up as stored fat? Explain.
LECTURE #6
ENERGY TRANSFER DURING EXERCISE
Introduction
Three major factors affect differences in the magnitude of energy transfer capacity:
 Body size and body composition
 Physical fitness
 Duration and intensity of exercise
In sprint running, cycling, and swimming, energy output can increase 120 times above resting metabolism.
In contrast, during less intense but sustained marathon running, for example, energy requirements still
exceed the resting level by 20 to 30 times. This chapter explains how the body’s diverse energy systems
interact during rest and different exercise intensities.
Immediate Energy: The ATP-CP System

Performances of short duration and high intensity such as the 100-meter sprint, 25-meter swim, smashing
a tennis ball during the serve, or thrusting a heavy weight upwards require an immediate and rapid energy
supply. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) stored
within muscles almost exclusively provide this energy. The term phosphagens identifies these intramuscular
energy sources.
Each kilogram of skeletal muscle stores approximately 5 millimoles (mmol) of ATP and 15 mmol of PCr.
For a person with 30 kg of muscle mass, this amounts to between 570 and 690 mmol of phosphagens. If
physical activity activates 20 kg of muscle, then stored phosphagen energy could power a brisk walk for 1
minute, a slow run for 20 to 30 seconds, or all-out sprint running and swimming for about 6 to 8 seconds. In
the 100-meter dash, for example, the body cannot maintain maximum speed for longer than this time, and the
runner may actually slow down towards the end of the race. Thus, the quantity of intramuscular
phosphagens significantly influences the ability to generate “all-out” energy for brief durations. The enzyme
creatine kinase regulates the rate of phosphagen breakdown.
Although all movements require utilization of high-energy phosphates, many rely almost exclusively on
generating energy rapidly from this “energy system.” For example, success in wrestling, weight lifting,
routines in gymnastics, most field events such as discus, shot put, pole vault, hammer, and javelin, and
baseball and volleyball require brief but all-out, maximal effort. For longer duration ice hockey, soccer, field
hockey, lacrosse, and basketball, other energy sources continually replenish the muscles’ phosphagen stores.
For this purpose, the stored carbohydrates, fats, and proteins supply the necessary energy to recharge the
pool of high-energy phosphates.
Short-Term Energy: The Lactic Acid System

The intramuscular phosphagens must continually resynthesize rapidly for strenuous exercise to continue
beyond a brief period. In such intense exercise, intramuscular stored glycogen provides the source of energy
to phosphorylate ADP during anaerobic glycogenolysis, forming lactic acid.
When oxygen supply (or utilization) becomes inadequate to accept all hydrogen formed in glycolysis,
pyruvate converts to lactic acid (pyruvate + 2H –––––> lactic acid). This permits the continued and rapid
formation of ATP by anaerobic, substrate-level phosphorylation. Anaerobic energy for ATP resynthesis from
glycolysis can be viewed as “reserve fuel” that activates when the oxygen demand/oxygen supply ratio
exceeds 1.00. This occurs during the last phase “kick” of a one-mile race. Anaerobic ATP production also
becomes crucial during a 440-m run or 100-m swim, or in multiple-sprint sports like ice hockey, field hockey,
and soccer. These activities require rapid energy that exceeds that supplied by the stored phosphagens. If the
intensity of “all-out” exercise decreases (thereby extending exercise duration), lactic acid buildup
correspondingly decreases.
BLOOD LACTATE ACCUMULATION

Some lactic acid continually forms, even under resting conditions. However, lactic acid removal by heart
muscle and non-active skeletal muscle balances its production, yielding no net lactic acid build-up. Only
when lactic acid removal does not match production does blood lactate begin to accumulate. Aerobic training
produces cellular adaptations that allow for higher rates of lactate removal, so accumulation occurs only at
higher exercise intensities.
Figure 1 illustrates the general relationship between oxygen uptake (expressed as a percentage of
maximum) and blood lactate level during light, moderate, and strenuous exercise in endurance athletes and
untrained individuals. During light and moderate exercise in both groups, aerobic metabolism adequately
meet energy demands. Non-active tissues rapidly oxidize any lactic acid formed. This permits blood lactate to
remain fairly stable (i.e., no net blood lactate accumulates), even though oxygen uptake increases. In essence,
ATP for muscular contraction comes from energy-generating reactions requiring the oxidation of hydrogen.
Lactate begins to rise exponentially at about 55% of the healthy, untrained person’s maximal capacity for
aerobic metabolism (termed the VO2max). The usual explanation for increases in blood lactate in heavy exercise
assumes a relative tissue hypoxia (lack of oxygen). With lack of oxygen, anaerobic glycolysis partially meets
the energy requirement, but hydrogen release begins to exceed its oxidation down the respiratory chain. At
this point, lactic acid forms as the excess hydrogen produced during glycolysis pass to pyruvate. Lactic acid
formation increases at
progressively higher levels of
exercise intensity when active
muscle cannot meet the
additional energy demands
aerobically.
As Figure 1 shows, trained
individuals (dashed line) show
a similar pattern of blood lactate
accumulation, except for the
point when blood lactate
appearance sharply increases.
The point of abrupt rise in
blood lactate, known as the
“blood lactate threshold” (also
termed anaerobic threshold
and onset of blood lactate
accumulation, or OBLA),
occurs at a higher percentage
of an athlete’s aerobic capacity.
This favorable metabolic
response in the endurance
athlete could result from
genetic endowment (e.g.,
muscle fiber type distribution),
specific local muscle
Figure 1. Blood lactate concentration at different levels of exercise expressed as a adaptations with training that
percent of VO2max for endurance trained and untrained individuals. favor formation of less lactic
acid and its more rapid
removal rate, or a combination of these factors.
Research shows that endurance training significantly increases capillary density and the size and number
of mitochondria. The concentration of the various enzymes and transfer agents involved in aerobic
metabolism also increases. Such alterations certainly enhance the cell’s capacity to generate ATP aerobically,
particularly via fatty acid breakdown. These training adaptations also extend exercise intensity before the
onset of blood lactate accumulation. For example, world-class endurance athletes can perform at sustained
high exercise intensities that represent 85 to 90% of maximum capacity for aerobic metabolism.
The lactic acid formed in one part of an active muscle can be oxidized by other fibers in the same muscle
or by less active neighboring muscle tissue. Lactate uptake by less active muscle fibers helps to depress blood
lactate levels during light-to-moderate exercise and also provides an important means for glucose
conservation in prolonged work.
Lactate-Producing Capacity
Capacity to generate high levels of lactic acid during exercise enhances maximal power output for short
durations. Because tissues continually utilize lactate during exercise, blood lactate accumulation can
significantly underestimate total blood lactate production. Ability to generate a high lactic acid concentration
in maximal exercise increases with specific sprint and power training; detraining subsequently decreases this
advantage.
Well-trained “anaerobic” athletes who perform maximally for brief periods generate blood lactate levels 20
to 30% higher than untrained individuals with similar exercise. Enhanced lactate-producing capacity with
sprint-type training may result from improved motivation that often accompanies the trained state (i.e., the
trained “push” themselves harder)and an approximate 20% increase in glycolytic enzyme activity.
Blood Lactate As An Energy Source

Blood lactate serves as substrate for glucose retrieval (gluconeogenesis) and as a direct fuel source for
active muscle. Tracer studies in muscle and other tissues show that lactate produced in fast-twitch muscle
fibers can circulate to other fast-twitch or slow-twitch fibers for conversion to pyruvate. Pyruvate, in turn,
converts to acetyl-CoA for entry to the Krebs cycle for aerobic energy metabolism. Such lactate “shuttling”
between cells enables glycogenolysis in one cell to supply other cells with fuel for oxidation. This makes
muscle not only a major site of lactate production, but also a primary tissue for lactate removal via
oxidation.
Long-Term Energy: The Aerobic System

Although glycolysis releases anaerobic energy rapidly, only a relatively small total ATP yield results from
this pathway. In contrast, aerobic metabolic reactions provide for the greatest portion of energy transfer,
particularly when exercise
duration extends longer than
2 to 3 minutes.
Oxygen Uptake
During
Exercise
The curve in Figure 2
illustrates oxygen uptake
during each minute of a
relatively slow jog continued at UofM
a steady pace for 20 minutes.
The vertical Y-axis indicates
the use of oxygen by the cells
(referred to as oxygen uptake
Figure 2. Time course of oxygen uptake during continuous jogging at a relatively
slow pace. The dots along the curve represent measured values of oxygen uptake.
or oxygen consumption); the horizontal X-axis displays exercise time. The abbreviation VO 2 indicates oxygen

LIMITED DURATION OF STEADY RATE
Theoretically, exercise could continue indefinitely if performed at a steady-
rate of aerobic metabolism, if the person desired. However, factors other
than motivation place a limit on the duration of steady-rate work. These
include loss of body fluids in sweat and depletion of essential nutrients,
especially blood glucose and glycogen stored in liver and active muscle.
uptake, where the V denotes the volume consumed; the dot placed above the V expresses oxygen uptake as a
per minute value. Oxygen uptake during any minute can easily be determined by locating time on the X-axis
and its corresponding point for oxygen uptake on the Y-axis. For example, after running four minutes,
oxygen uptake equals approximately 1.6 mL•kg-1•min-1.
From the graph, oxygen uptake rises rapidly during the first minutes of exercise and reaches a relative
plateau between minutes three and six. Oxygen uptake then remains relatively stable throughout the
remainder of exercise. The flat portion or plateau of the oxygen uptake curve represents the steady-rate of
aerobic metabolism – a balance between energy required by working muscles and the rate of aerobic ATP
production. Oxygen consuming reactions supply the energy for exercise during steady-rate; any lactic acid
produced either oxidizes or reconverts to glucose in the liver, kidneys, and skeletal muscle. No accumulation
of blood lactate occurs under these steady-rate metabolic conditions.
Many Levels of Steady-rate

Certain steady-rate exercise levels for the endurance athlete could exhaust the untrained. For some, lying
in bed, working around the house, and playing an occasional round of golf represent the activity spectrum
for which adequate oxygen maintains a steady-rate. A champion marathon runner, on the other hand, can run
26.2 miles in slightly more than 2 hours and still be in steady-rate! This sub-5-minute-per-mile pace represents
a magnificent physiologic-
metabolic accomplishment to
maintain the required level of
aerobic metabolism. Two of
these crucial functional
capacities consist of: (1)
delivering adequate oxygen to
active muscles, and (2)
processing oxygen for aerobic
ATP production.
Oxygen Deficit
The upward trending curve of
oxygen uptake shown in
Figure 2 and 3 does not
increase instantaneously to a
steady-rate at the start of
Figure 3. Oxygen uptake and deficit for trained and untrained individuals
during submaximum cycle ergometer exercise. Both individuals reach the
same steady-rate VO2 but the trained person reaches it at a faster rate,
reducing the oxygen deficit.
exercise. Instead, it remains considerably below the steady-rate level in the first minute of exercise, even
though the exercise energy requirement remains essentially unchanged throughout the activity period. The
temporary “lag” in oxygen uptake occurs because ATP provides the muscle’s immediate energy requirement
without the need for oxygen. Oxygen becomes important in subsequent energy transfer reactions to serve as
an electron acceptor to combine with the hydrogen produced during:
 Glycolysis
 Beta- oxidation of fatty acids
 Krebs cycle reactions
Thus, a deficit always exists in the oxygen uptake response to a new, higher steady-rate level, regardless of
activity or exercise intensity.
The oxygen deficit quantitatively represents the difference between the total oxygen actually consumed
during exercise and the amount that would have been consumed had a steady-rate, aerobic metabolism
occurred immediately when exercise began. Energy provided during the deficit phase of exercise represents a
predominance of anaerobic energy transfer. Stated in metabolic terms, oxygen deficit represents the quantity
of energy produced from stored intramuscular phosphagens plus energy contributed from rapid glycolytic
reactions that yield phosphate-bond energy until oxygen uptake and energy demands reach the steady rate.
Oxygen Deficit in Trained and Untrained

Figure 3 shows the oxygen uptake response to submaximum cycle ergometer exercise for a trained and
untrained person. Similar values for steady-rate oxygen uptake during light and moderate exercise generally
occur in trained and untrained individuals. The trained person, however, reaches the steady-rate quicker;
hence, this person has a smaller oxygen deficit for the same exercise duration compared to the untrained
person. This means a greater total oxygen consumed during exercise for the trained person, with a
proportionately smaller anaerobic component of energy transfer. A likely explanation for the differences in
oxygen deficit between trained and untrained individuals relates to a more highly developed aerobic
bioenergetic capacity of the trained person. An augmented aerobic capacity results from either improved
central cardiovascular function or training-induced local muscular adaptations known to increase a muscle’s
capacity to generate ATP aerobically. These adaptations would cause earlier aerobic ATP production in
exercise with less lactic acid formation for the trained person.
Maximal Oxygen Uptake (VO2max)

Figure 4 depicts the curve for oxygen uptake during a series of constant-speed runs up six hills, each
progressively steeper than the next. The laboratory simulates these “hills” by increasing the elevation of a
treadmill, raising the height of a step bench, or providing greater resistance to pedaling a bicycle ergometer.
Each successive hill (equivalent to an increase in exercise intensity, or load) requires greater energy output,
and thus an additional demand for aerobic metabolism. Increases in oxygen uptake relate linearly and in
direct proportion to exercise intensity during the climb up the first several hills. Although the runner
maintains speed up the last two hills, oxygen uptake does not increase the same magnitude as with prior
hills. No increase in oxygen uptake occurs during the run up the last hill. The maximal oxygen uptake or
simply VO2max describes the region where oxygen uptake plateaus and shows no further increase (or increases
only slightly) despite additional increase in exercise intensity. The VO2max holds great physiological
significance because of its dependence on the functional capacity and integration of the systems required for
oxygen supply, transport, delivery, and utilization.
The VO2max provides a good indication of an individual’s capacity for aerobically resynthesizing ATP.
Exercise performed above VO2max can only take place by energy transfer predominantly from anaerobic
glycolysis with lactic acid formation. Under such conditions, performance deteriorates and the individual
cannot continue at that intensity. The large build up of lactic acid, due to the additional anaerobic muscular
effort, disrupts the already high
rate of energy transfer for the
aerobic resynthesis of ATP. To
borrow an analogy from
business economics: supply
(aerobic resynthesis of ATP)
fails to meet demand (energy
required for muscular effort).
An aerobic energy supply-
demand imbalance affects
production (lactic acid
accumulates) and compromises
exercise performance.
Figure 4. Attainment of maximal oxygen uptake while running up hills of increasing
slope. VO2max occurs in the region where a further increase in exercise intensity does The Energy
not produce an additional increase in oxygen uptake.
Spectrum of
Exercise
Figure 5 depicts the relative contributions of anaerobic and aerobic energy sources during various
durations of maximal exercise. The data represent estimates from experiments of all-out treadmill running
and bicycling, they can relate to other activities by drawing the appropriate time relationships. For example, a
100-m sprint run equates to any all-out activity lasting about 10 s, while an 800-m run lasts approximately 2
minutes. All-out exercise for one minute includes the 400-m dash in track, the 100-m swim, and multiple full-
court presses during a basketball game.
Intensity and Duration Determine the Blend

The body's energy transfer systems should be viewed along a continuum in terms of
exercise bioenergetics. Anaerobic sources supply most of the energy for fast
movements, or during increased resistance to movement at a given speed.
Also, when movement begins at either fast or slow speed (from performing a
front handspring to starting a marathon run), the intramuscular
phosphagens provide immediate anaerobic energy for the
required muscle action.
At the short-duration extreme of maximum effort, the intramuscular
phosphagens ATP and PCr supply the
major energy for the entire exercise. The
ATP-PCr and lactic acid systems provide about one-half of the energy
required for “best-effort“ exercise lasting 2 minutes, whereas aerobic
reactions provide the remainder. For top performance in all-out, 2-
minute exercise, a person must possess a well-developed
capacity for both aerobic and anaerobic metabolism. Intense
exercise of intermediate Figure 5. Relative contribution of aerobic and anaerobic energy metabolism during
duration performed for 5 to 10 minutes, like middle-
maximal physical effort of various durations; 2 min requires about 50% of the
energy from both aerobic and anaerobic processes. At worldclass 4min mile pace,
aerobic metabolism supplies approximately 65% of the energy, with the remaining
from anaerobic processes.
distance running and swimming or stop-and-go sports like basketball and soccer, produces a greater demand
for aerobic energy transfer. Longer duration marathon running, distance swimming and cycling, recreational
jogging, cross-country skiing, and hiking and backpacking require a continual energy supply derived
aerobically without reliance on lactic acid formation.
Intensity and duration determine which energy system and metabolic mixture predominate during
exercise. The aerobic system predominates in low intensity exercise with fat serving as the primary fuel
source. The liver markedly increases its release of glucose to active muscle as exercise progresses from low to
high intensity. Simultaneously, glycogen stored within muscle serves as the predominant carbohydrate
energy source during the early stages of exercise and when exercise intensity increases. During high-intensity
aerobic exercise, the advantage of selective dependence on carbohydrate metabolism lies in its two times
more rapid energy transfer capacity compared to fat and protein fuels.
Compared to fat, carbohydrate also generates about 6% greater energy per unit oxygen consumed. As
exercise continues and muscle glycogen depletes, progressively more fat (intramuscular triglycerides and
circulating FFA) enters the metabolic mixture for ATP production. In maximal anaerobic effort (reactions of
glycolysis), carbohydrate becomes the sole contributor to ATP production.
A sound approach to exercise training analyzes an activity for its specific energy components and then
establishes a training regimen to improve those systems that assure optimal physiologic and metabolic
adaptations. An improved capacity for energy transfer usually translates into improved exercise performance.
Excess Post-Exercise Oxygen Consumption: The So-

Called “Oxygen Debt”
Bodily processes do not immediately return to resting levels after exercise ceases. In light exercise (e.g.,
golf, archery, bowling), recovery to a resting condition takes place rapidly and is often unnoticed. With
particularly intense physical activity (running full speed for 800 m or trying to swim 200 m as fast as
possible), however, it takes considerable time for the body to return to resting levels. The difference in
recovery from light and strenuous exercise relates largely to the specific metabolic and physiologic processes
in each form of exercise.
A.V. Hill (1886-1977), the British Nobel physiologist (see Lecture 2), referred to oxygen uptake during
recovery as the “oxygen debt.” Contemporary theory no longer uses this term. Instead, recovery oxygen
uptake or excess post-exercise oxygen consumption (EPOC) defines the excess oxygen uptake above the
resting level in recovery. Regardless of the term used, the meaning refers to the total oxygen consumed
following exercise in excess of a pre-exercise baseline level.
Figure 6 shows that light exercise produces
a rapid attainment of steady-rate and a small
oxygen deficit. Rapid recovery ensues from
such exercise with an accompanying small
EPOC. In moderate to heavy aerobic exercise
would take longer to reach steady-rate and the
oxygen deficit would become larger compared
to light exercise. Oxygen uptake in recovery
from more strenuous exercise returns more
slowly to the pre-exercise resting level. There Figure 6. Oxygen uptake during exercise and recovery from
light steadyrate exercise.
occurs an initial rapid decline in recovery oxygen
uptake (similar to recovery from light exercise) followed by a more gradual decline to baseline.
Metabolic Dynamics of Recovery Oxygen Uptake

Current understanding of the specific chemical dynamics in exhaustive exercise does not permit a precise
biochemical partitioning of EPOC, especially in terms of lactic acid.
No doubt exists that the elevated aerobic metabolism in recovery contributes to restoring the body’s
processes to pre-exercise conditions. Oxygen uptake following light and moderate exercise replenishes high-
energy phosphates depleted in the preceding exercise. In recovery from strenuous exercise, some oxygen
resynthesizes a portion of lactic acid to glycogen. However, a significant portion of recovery oxygen uptake
supports physiologic functions actually taking place during recovery. The considerably larger recovery
oxygen uptake compared to oxygen deficit with high-intensity, exhaustive exercise results from factors such
as elevated body temperature. Core temperature frequently increases by about 3ºC (5.4ºF) during vigorous
exercise, and can remain elevated for several hours into recovery. This thermogenic “boost” directly
stimulates metabolism and increase EPOC.
In essence, all of the physiologic systems activated to meet the demands of muscular activity increase their
own need for oxygen during recovery. The recovery oxygen uptake reflects:
 Anaerobic metabolism of previous exercise
 Respiratory, circulatory, hormonal, ionic, and thermal adjustments during recovery as a consequence

CAUSES OF EXCESS POST EXERCISE OXYGEN
CONSUMPTION (EPOC) WITH HEAVY EXERCISE
 Resynthesis of ATP and PCr
 Rsynthesize blood lactate to glycogen
 Oxidize blood lactate in energy metabolism
 Restore oxygen to blood, tissue fluids and myoglobin
 Thermogenic effects of elevated core temperature
 Thermogenic effects of hormones (catecholamines)
 Increase in pulmonary and circulatory dynamics
of prior exercise
Active Versus Passive Recovery

Procedures for speeding recovery from exercise can be categorized as active or passive. Active recovery
(often called “cooling-down” or “tapering-off”) involves submaximum aerobic exercise performed
immediately after the exercise. Many believe that continued movement prevents muscle cramps, stiffness,
and facilitates the recovery process. In contrast, in passive recovery a person usually lies down assuming that
complete inactivity reduces the resting energy requirements and “frees” oxygen for the recovery process.
Modifications of active and passive recovery have included the use of cold showers, massages, specific body
positions, ice application, and ingesting cold fluids. Research findings have shown ambiguous results for
many of these recovery procedures.
Optimal Recovery From Steady-rate Exercise

Most people can perform exercise below 55 to 60% of VO2max in steady-rate with little blood lactate
accumulation. Recovery from such exercise resynthesizes high-energy phosphates, replenishes oxygen in the
blood, body fluids, and muscle myoglobin, and has a small energy cost to sustain circulation and ventilation.
Passive procedures produce the most rapid recovery in such cases because exercise would only serve to
elevate total metabolism and delay recovery.
Optimal Recovery from Non Steady-rate Exercise

Lactic acid formation exceeds its rate of removal and blood lactate accumulates when exercise intensity
exceeds maximum steady-rate. As work intensity increases, lactate levels rise sharply and the exerciser soon
becomes exhausted. Although the precise mechanisms of fatigue during intense anaerobic exercise are not
fully understood, the blood lactate level does provide an objective indication of the relative strenuousness of
exercise and reflects the adequacy of the recovery process.
Active aerobic exercise in recovery accelerates lactic acid removal. The optimal level of exercise in recovery
ranges between 30 and 45% of VO2max for bicycle exercise, and 55 to 60% of VO2max when recovery involves
treadmill running. The variation between these two forms of exercise probably results from the more
localized nature of bicycling (i.e., more intense effort per unit muscle mass), which produces a lower lactate

KEEP MOVING IN RECOVERY FROM HEAVY EXERCISE
Active recovery facilitates lactate removal because of increased perfusion of blood
through “lactate-using” organs like the liver and heart. In addition, increased blood
flow through the muscles in active recovery certainly enhances lactate removal
because muscle tissue oxidizes this substrate during Krebs cycle metabolism.
threshold compared to running.

LECTURE #6 STUDY GUIDE

1. Criteria for VO2max
2. EPOC
3. Ergometer
4. Fast-twitch fibers
5. Immediate energy system
6. Lactic Acid
7. Long–term energy system
8. Maximal oxygen uptake
9. Oxygen debt
10. Oxygen uptake
11. Short–term energy system

12. Slow–twitch fibers
13. Steady-rate
STUDY QUESTIONS
Immediate Energy: The ATP-CP System

Indicate the quantity of ATP and PCr stored within the body’s muscles.
ATP
PCr
Indicate the duration of a brisk walk, a slow run, and an all-out sprint that the intramuscular high-
energy phosphates powers.
Brisk walk
Slow run
All-out sprint
Short-Term Energy: The Lactic Acid System

List three activities powered primarily by the lactic acid energy system.
1. 3.
2.
Blood Lactate Accumulation

Give a reasonable explanation why blood lactate accumulates during exercise.
Lactate-Producing Capacity
How much more blood lactate can a sprint/power trained athlete accumulate compared to an
untrained counterpart?
Oxygen Uptake During Exercise
Draw and label the curve for oxygen uptake during 10 minutes of moderate running exercise.
Indicate the area of oxygen deficit and the area of steady-rate.
Oxygen uptake, L•min 1
Time, min
Express oxygen uptake in relation to body mass (mL•kg-1•min-1)for an individual who weighs 85
kg and consumes 2.0 L•min-1 of oxygen during jogging.
Many Levels of Steady-rate

What two metabolic-physiologic factors determine a person’s ability to perform exercise at a
steady-rate?
1.
2.
Oxygen deficit
Define the oxygen deficit
Oxygen Deficit in Training and Untrained

Do trained or untrained or untrained reach steadyrate faster?
Maximal Oxygen Uptake (VO2max)

Draw and label the oxygen uptake curve during exercise of progressively increasing work intensity
(every 3 min) to exhaustion. Indicate the VO2max.
Exercise Intensity
The Energy Spectrum of Exercise

What two factors determine which energy system and metabolic mixture are used during exercise.
1.
2.
Excess Post-Exercise Oxygen Consumption: The So-Called “Oxygen Debt”

Draw and label the oxygen uptake curves during recovery from light, steady-rate exercise and
exhaustive exercise. Include the fast the slow component of the recovery where applicable.
Rest Exercise Recovery
Time
Metabolic Dynamics of Recovery Oxygen Uptake
Give two factors that reflect the recovery oxygen uptake
1.
2.
Optimal Recovery From Steady-rate Exercise

What procedures optimize recovery from steady-rate exercise?
LECTURE #7
EVALUATING ENERGY-GENERATING CAPACITIES
Introduction
In this lecture, I will discuss the capacity of the various energy transfer systems discussed previously, with
special reference to measurement, specificity, and individual differences.
We all possess the capability for anaerobic and aerobic energy metabolism, although the capacity for
each form of energy transfer varies considerably among individuals. These differences among individuals
underlie the concept of individual differences in metabolic capacity for exercise. A person’s capacity for energy
transfer (and for many other physiologic functions) does not exist as some general factor for all types of
exercise, but depends largely on the exercise mode used for training and evaluation. A high maximum
oxygen uptake in running, for example, does not necessarily assure a similar aerobic power when activating
different muscle groups as in swimming and rowing. This disparity represents an example of specificity of
metabolic capacity. On the other hand, some individuals with high aerobic power in one form of exercise also
possess an above average aerobic power in other diverse activities. This illustrates the generality of metabolic
capacity. For the most part, more specificity exists than generality in metabolic and physiologic function.
Lecture Objectives
 Explain specificity and generality as they apply to exercise.
 Describe procedures to administer two practical “field tests” to evaluate power output capacity of the
high-energy intramuscular phosphates (immediate energy system).
 Describe a commonly used test to evaluate the power output capacity of glycolysis (short-term energy
system).
 Define maximal oxygen uptake (VO2max), including the physiological significance of this aerobic fitness
measure.
 Describe a graded exercise test.
 List criteria that indicate when a person reaches a “true” VO2max during a graded exercise test.
 Explain how each of the following affect maximal oxygen uptake: (1) mode of exercise, (2) heredity, (3)
state of training, (4) gender, (5) body composition, and (6) age.
Overview of Energy Transfer Capacity During Exercise

The immediate and short-term energy systems mainly power all-out exercise for up to 2-minutes duration.
Both systems operate anaerobically because their transfer of chemical energy does not require oxygen (refer
to lecture 6.) Generally, fast movements or resistance to movement at a given speed place great reliance on
anaerobic energy transfer. Figure 1 shows the relative involvement of the anaerobic and aerobic energy
transfer systems for different durations of all-out exercise.
At the initiation of either
high- or low-speed movements,
the intramuscular phosphagens,
ATP and PCr, provide
immediate and nonaerobic
energy for muscle action. After
the first few seconds of
movement, the glycolytic
energy system provides an
increasingly greater proportion
of the total energy. For exercise
to continue, although at a lower
intensity, a progressively
greater demand becomes placed
on the aerobic metabolic
pathways of ATP resynthesis.
Some activities require the
capacity of more than one
energy transfer system, whereas
other activities rely
predominately on a single
Figure 1. Three energy systems and their percentage contribution (Yaxis) to
system. However, all activities total energy output during allout exercise of different durations (Xaxis).
activate each energy system to
some degree, depending on exercise intensity and duration. Of course, the greater demand for anaerobic
energy transfer occurs for higher intensity, shorter duration activities.
Anaerobic Energy: The Immediate and Short-Term Energy

Systems
Evaluation of the Immediate Energy System

Performance tests that rely on maximal activation of the intramuscular ATP-PCr energy reserves have
been developed as “field tests” to evaluate the immediate energy transfer system. These maximal effort
performances, generally referred to as power tests, evaluate the time-rate of doing work (i.e., work
P = F x D
T
accomplished per unit time). The following formula computes power output:
where, F equals force generated, D equals distance through which the force moves, and T equals exercise
duration.
Watts represents a common expression of power
One watt equals 0.73756 ft-lb•sec–1 or 6.12 kg-m•min–1
STAIR-SPRINTING POWER TESTS

Researchers have measured short-term power by sprinting up a flight of stairs. Figure 2 shows a subject
running up a staircase as fast as possible taking three steps at a time. The external work performed equals the
total vertical distance the body rises up the stairs; for six stairs this distance usually equals about 1.05 meters.
Figure 2. Stairsprinting power test. The subject begins at point A and runs as fast as
possible up a flight of stairs, taking 3 steps at a time. Electric switch mats placed on the
steps record the time to cover the distance between stair 3 and 9 to the nearest 0.01 s.
Power output equals the product of the subject’s mass (F) and vertical distance covered
(D), divided by the time (T).
The power output for a 65-kg woman who traverses six steps in 0.52 seconds computes as follows:
F = 65 kg; D = 1.05 m; T = 0.52 s
Power = [65 kg x 1.05 m] ÷ 52 s
Power = 131.3 kg-m•s-1 (1287 watts)
Because body mass greatly influences the power-output score in stair sprinting, a heavier person
necessarily generates greater power at the same speed as a lighter person who covers the same vertical
distance. Because of the influence of body mass, use caution in interpreting differences in stair-sprinting
power scores and making inferences about individual differences in ATP-PCr energy capacity. The test may
be better suited for evaluating individuals of similar body mass, or the same people before and after a specific
training regimen.

INTERCHANGEABLE EXPRESSIONS FOR ENERGY AND
WORK
1 foot-pound (ft-lb) = 0.13825 kilogram-meters (kg-m)
1 kg-m = 7.233 ft-lb = 9.8066 joules
1 kilocalorie (kcal) = 3.0874 ft-lb = 426.85 kg-m = 4.186 kilojoules (kJ)
1 Joule (J) = 1 Newton-meter (Nm)
1 kilojoule (kJ) = 1000 J = 0.23889 kcal
Jumping-Power Tests
For years, physical fitness test batteries have included jumping tests such as the jump-and-reach test or a
standing broad jump. The jump-and-reach test score equals the difference between a person’s standing reach
and the maximum jump-and-touch height. For the broad jump, the score represents the horizontal distance
covered in a leap from a semicrouched position. Although both tests purport to measure leg power, they
probably fail to achieve this goal. For one thing, with jump tests, power generated in propelling the body
from the crouched position occurs only in the time the feet contact the floor's surface. This brief period cannot
sufficiently evaluate a person’s ATP and PCr power capacity.
OTHER POWER TESTS

A 6 to 8-second performance involving all-out exercise measures the person’s capacity for immediate
power from the intramuscular high-energy phosphates (refer to Figure 1). Examples of other such tests
include sprint running or cycling, shuttle runs and more localized movements such as arm cranking or
simulated stair climbing, rowing, or skiing. In the popular Quebec 10-second test of leg cycling power, the
subject performs two all-out 10-second rides at a frictional resistance equal to 0.09 kg per kg of body mass,
with 10- minutes rest between exercise bouts. Exercise begins by pedaling as fast as possible as the friction
load is applied and continues all-out for 10 seconds. Performance represents the average of the two tests
reported in peak joules per kg of body weight, and total joules per kg of body weight.
Power tests may be used to show changes in an athlete’s performance with specific training. Such tests
also serve as an excellent means for self-testing and motivation, and provide the actual movement-specific
exercise for training the immediate energy system. Many football teams, for example, routinely use the 40-
yard dash as a criterion to evaluate a player’s speed. Although many types of “speed” need to be evaluated in
football, the 40-yard scores may provide useful information for player evaluation. It should be emphasized,
however, that research needs to establish how 40-yard speed in a straight line relates to overall football ability
for players at similar positions. A run test of shorter duration (up to 20 yd), or one with frequent changes in
direction, may be an equal or more suitable performance measure.
Several physiologic and biochemical measures, in addition to exercise performance, can estimate the
energy-generating capacity of the immediate energy system. These include:
 Size of the intramuscular ATP-PCr pool
 ATP and PCr depletion rates from all-out exercise of short duration
 Magnitude of the oxygen deficit calculated from the oxygen uptake curve
 Magnitude of the alactic (fast component) portion of recovery oxygen uptake
Evaluation of the Short-Term Energy System

As displayed in Figure 1, the anaerobic reactions of glycolysis (short-term energy system) generate
increasingly greater energy for ATP resynthesis when all-out exercise continues longer than a few seconds.
This does not mean that aerobic metabolism remains unimportant at this stage of exercise, or that the oxygen-
consuming reactions have not been “switched-on.” To the contrary, Figure 2 reveals an increase occurs in
aerobic energy contribution very early in exercise. However, the energy requirement in all-out exercise
significantly exceeds energy generated by hydrogen's oxidation in the respiratory chain. This means that the
anaerobic reactions of glycolysis predominate, with large quantities of lactic acid accumulating within the
active muscle and ultimately appearing in the blood.
Unlike tests for maximal oxygen uptake, no specific criteria exist to indicate that a person has reached a
maximal anaerobic effort. In fact, one's level of self-motivation, including external factors in the test
environment, likely influences the test score. Researchers most commonly use the level of blood lactate to
indicate the degree of activation of the short-term energy system.
Performance Tests of Glycolytic Power

Activities that require substantial activation of the short-term energy system demand maximal work for
up to three minutes. All-out runs and cycling exercise have usually been used, although weight lifting
(repetitive lifting of a certain percentage of maximum) and shuttle and agility runs have also been used.
Because age, sex, skill, motivation, and body size affect maximal physical performance, difficulty exists
selecting a suitable criterion test for developing normative standards for glycolytic energy capacity. A test
that maximally uses only the leg muscles cannot adequately assess short-term anaerobic capacity for upper-
body exercise such as rowing or swimming. Within the framework of exercise specificity, the performance
test must be similar to the activity or sport for which the energy capacity is being evaluated. In most cases, the
actual activity serves as the test.
Figure 3 presents the relative contribution of each metabolic pathway during three different duration all-
out cycle ergometer tests. The results are shown as a percent of the total work output. Note the progressive
change in the percentage contribution of each of the energy systems to the total work output as duration of
effort increases.
Figure 3. Contribution of each of the energy systems to the total work accomplished in three
tests of shortduration.
10 sec 30 sec 90 sec

Shortduration tests
Blood Lactate Levels

Blood lactate levels remain relatively low during steady-rate exercise up to about 55% of the VO 2max.
Thereafter, blood lactate begins to accumulate, with a precipitous increase noted in the region of the VO 2max.
Glycogen Depletion
Because the short-term energy system largely depends on glycogen stored in the specific muscles activated
by exercise, these muscles' pattern of glycogen depletion provides an indication of the contribution of
glycolysis to exercise.
Figure 4 shows that the rate

of glycogen depletion in the
quadriceps femoris muscle
during bicycle exercise closely
parallels exercise intensity.
With steady-rate exercise at
about 30% of VO2max, a
considerable reserve of muscle
glycogen remains, even after
cycling for 180 minutes.
Because relatively light
exercise relies mainly on a low
level of aerobic metabolism,
large quantities of fatty acids
provide energy with only
moderate use of stored
glycogen. The most rapid and
pronounced glycogen
depletion occurs at the two
heaviest workloads. This
makes sense from a metabolic
standpoint because glycogen
provides the only stored
nutrient for anaerobic ATP
resynthesis. Thus, glycogen
has high priority in the
“metabolic mill” during
Figure 4. Glycogen depletion from the vastus lateralis portion of the quadriceps femoris muscle strenuous exercise.
in bicycle exercise of different intensities and durations. Exercise at 31% of VO2max (the lightest
Changes in total muscle
workload) caused some depletion of muscle glycogen, but the most rapid and largest depletion
occurred with exercise that ranged from 83% to 150% of VO2max. glycogen as illustrated in
Figure 4 may not give a
precise indication of the degree of glycogen breakdown in specific muscle fibers, however. Depending on
exercise intensity, glycogen depletion occurs selectively in either fast- or slow-twitch fibers. For example,
during all-out one-minute sprints on a bicycle ergometer, activation of the fast-twitch fibers provides the
predominant power for the exercise. Glycogen content in these fibers becomes almost totally depleted
because of the sprint's anaerobic nature. In contrast, slow-twitch fibers become glycogen-depleted early
during moderate to heavy prolonged aerobic exercise. Glycogen utilization (and depletion) mainly in specific
muscle type fibers makes it difficult to evaluate the degree of glycolytic activation from changes in a muscle’s
total glycogen content before and after exercise.
Anaerobic Energy Transfer Capacity

Differences in training level, capacity to buffer acid metabolites produced in heavy exercise, and
motivation contribute to individual differences in capacity to generate short-term anaerobic energy.
Effects of Training
Short-term supermaximal exercise on a bicycle ergometer in trained subjects always produces higher
levels of blood and muscle lactic acid, and greater muscle glycogen depletion. For all subjects, better
performances are usually associated with higher blood lactate levels. These results support the belief that
training for brief, all-out exercise enhances the glycolytic system's capacity to generate energy. In sprint and
middle-distance activities, individual differences in anaerobic capacity account for much of the variation in
exercise performance.
Buffering of Acid Metabolites

Lactic acid accumulates when anaerobic energy transfer predominates. This causes an increase in the
muscle's acidity, negatively affecting the intracellular environment. The deleterious intracellular alterations
during anaerobic exercise have caused speculation that anaerobic training might enhance short-term energy
capacity by increasing the body’s buffering reserve to enable greater lactic acid production through more
effective buffering. However, only a small increase in alkaline reserve has been noted in athletes compared to
sedentary individuals. Thus, the
general consensus is that trained
people have similar buffering
capability as untrained
individuals.
Motivation
Individuals with greater
“pain tolerance,” “toughness,” or
ability to “push” beyond the
discomforts of fatiguing exercise
definitely accomplish more
anaerobic work. These people
usually generate greater levels of
blood lactate and glycogen
depletion; they also score higher
on tests of short-term energy
capacity. Although difficult to
categorize and quantify,
motivation plays a key role in
superior performance at all levels
of competition.
Aerobic Energy:
The Long-
Term Energy
System
The data in Figure 5 illustrate
that persons who engage in
Figure 5. Maximal oxygen uptake of male and female Olympiccaliber athletes in
different sport categories compared to healthy sedentary subjects.
sports that require sustained, high-intensity exercise (i.e., endurance) generally possess a large aerobic energy
transfer capacity. Men and women who compete in distance running, swimming, bicycling, and cross-
country skiing generally record the highest maximal oxygen uptakes. These athletes have almost twice the
aerobic capacity as sedentary individuals. This does not mean that only VO2max determines endurance exercise
capacity. Other factors, especially those at the muscle level such as capillary density, enzymes, and fiber type,
strongly influence the capacity to sustain a high percentage of VO2max. However, the VO2max does provide
useful information about the capacity of the long-term energy system. Attainment of VO 2max requires
integration of ventilatory, cardiovascular, and neuromuscular systems; this gives significant physiologic
“meaning” to this metabolic measure. For these reasons, VO2max represents a fundamental measure in exercise
physiology and often serves as the standard against which to compare performance estimates of aerobic
capacity and endurance fitness.
Measurement of Maximal Oxygen Uptake

Tests for VO2max use exercise tasks that activate large muscle groups with sufficient intensity and duration
to engage maximal aerobic energy transfer. Exercise includes treadmill walking or running, bench stepping,
or cycling. VO2max has also been measured during free, tethered, and flume swimming and swim-bench
ergometry, and simulated rowing, skiing, stair climbing, as well as ice skating and arm-crank exercise.
Considerable research effort has been directed toward (1) development and standardization of tests for
VO2max, and (2) establishment of norms related to age, sex, state of training, and body composition.
Criteria for VO2max

A leveling-off, or peaking-over, in oxygen uptake during increasing exercise intensity signifies attainment
of maximum capacity for aerobic metabolism (i.e., a “true” VO2max). When this generally accepted criterion is
not met, or local muscle fatigue in the arms or legs rather than central circulatory dynamics limits test
performance, the term “peak oxygen uptake” (VO 2peak) usually describes the highest oxygen uptake value
during the test.
Tests of Aerobic Power

Numerous tests have been devised and standardized to measure VO2max. These test performances should
be independent of muscle strength, speed, body size, and skill, with the exception of specialized swimming,
rowing, and ice skating tests.
The VO2max test may require a continuous 3- to 5-minute “supermaximal” effort, but it usually consists of
increments in exercise intensity (referred to as a graded exercise test or GXT) until the subject stops. Some
researchers have imprecisely termed this end point “exhaustion,” but it should be kept in mind that the
subject terminates the test (for whatever reason). A variety of psychological or motivational factors can
influence this decision, and it may not reflect true physiologic exhaustion. It can take considerable urging and
prodding to get subjects to the point of acceptable criteria for VO2max, particularly individuals unaccustomed
to producing maximal exercise. Children and adults encounter particular difficulty if they have had little
prior experience performing strenuous exercise. Practical experience has shown that attaining a plateau in
oxygen uptake during the VO2max test requires high motivation and a relatively large anaerobic component.
Factors That Affect Maximal Oxygen Uptake

Of the many factors influencing VO2max, the most important include mode of exercise and the person’s
heredity, training state, sex, body composition, and age.
Mode of Exercise
Variations in VO2max during different modes of exercise reflect the quantity of muscle mass activated
during the performance. In experiments that determined VO2max on the same subjects during exercise,
treadmill exercise produced the highest values. Bench stepping, however, has generated VO 2max scores
identical to treadmill values and significantly higher than values on a bicycle ergometer. With arm-crank
exercise, aerobic capacity reaches only about 70% of one’s treadmill VO2max.
The treadmill represents the laboratory apparatus of choice for determining VO 2max in healthy subjects.
The treadmill provides easy quantification and regulation of exercise intensity. Compared with other forms of
exercise, subjects achieve one or more of the criteria for establishing VO2max more easily on the treadmill.
Bench stepping or bicycle exercise is suitable alternatives under non-laboratory “field” conditions.
Heredity
A question frequently raised concerns the relative contribution of natural endowment to physiologic
function and exercise performance. For example, to what extent does heredity determine extremely high
aerobic capacities of the endurance athletes? Do these exceptionally high levels of functional capacity reflect
more than the training effect? Although the answer remains incomplete, some researchers have focused on
the question of how genetic variability accounts for differences between individuals in physiologic and
metabolic capacity.
Studies were made of 15 pairs of identical twins (with the same heredity since they came from the same
fertilized egg) and 15 pairs of fraternal twins (who do not differ from ordinary siblings because they result
from separate fertilization of two eggs) raised in the same city by parents with similar socioeconomic
backgrounds. The researchers concluded that heredity alone accounted for up to 93% of the observed
differences in aerobic capacity as measured by the VO2max. In addition, genetic determination accounted for
81% of the capacity of the short-term glycolytic energy system and 86% of maximum heart rate. Subsequent
investigations of larger groups of brothers, fraternal twins, and identical twins indicate a significant but much
smaller effect of inherited factors on aerobic capacity and endurance performance.
Estimates of the genetic effect equal about 20–30% for VO2max, 50% for maximum heart rate, and 70% for
physical working capacity. Similar muscle fiber composition occurs for identical twins, whereas wide
variation in fiber type exists among fraternal twins and brothers. Future research may determine the upper
limit of genetic determination, but currently available data show that inherited factors contribute significantly
to both functional capacity and exercise performance. A large genotype-dependency also exists for the
potential for improving maximal aerobic and anaerobic power, and the adaptations of most muscle enzymes
to training. In other words, members of the same twin-pair generally show the same response to exercise
training. Genetic makeup plays such a prominent role in determining training response that it is nearly
impossible to predict a specific individual’s response to a given training stimulus.
Training State
VO2max scores must be evaluated relative to the person’s state of training at the time of measurement.
Improvements in aerobic capacity with training generally range between 6 and 20%, although increases have
been reported as high as 50% above pretraining levels.
Gender
VO2max values (mL•kg-1•min-1) for women typically average 15 to 30% below scores for men. Even among
trained athletes, this difference ranges between 15 and 20%. Such differences increase considerably when
expressing the VO2max as an absolute value (L•min–1) rather than relative to body mass (mL•kg-1•min-1).
Between world-class male and female cross-country skiers, for example, a 43% lower VO 2max value for women
(6.54 vs. 3.75 L•min–1) decreased to 15% (83.8 v 71.2 mL•kg-1•min-1) using the athletes' body mass in the ratio
expression of VO2max.
Sex difference in VO2max has generally been attributed to differences in body composition and hemoglobin
content. Untrained young adult women generally possess about 25% body fat, whereas the corresponding
value for men averages 15%. Although trained athletes have a lower percentage of fat, trained women still
possess significantly more body fat than male counterparts. Thus, the male generally generates more total
aerobic energy simply because he possesses a relatively large muscle mass and less fat than the female.
Probably due to their higher level of testosterone, men show a 10 to 14% greater concentration of
hemoglobin. This difference in the blood's oxygen-carrying capacity potentially enables males to circulate
more oxygen during exercise and gives them a slight edge in aerobic capacity.
Although lower body fat and higher hemoglobin provide the male with some advantage in aerobic power,
we must look for other factors to fully explain the disparity between the sexes. Differences in normal physical
activity level between an “average” male and “average” female provide a possible explanation. Perhaps
considerably less opportunities exist for women to become as physically active as men due to social structure
and constraints. In fact, even among prepubertal children, boys become more active in daily life than their
female counterparts.
Age
Changes in VO2max relate to chronological age. Although limitations exist in drawing inferences form cross-
sectional studies of different people at different ages,
the available data provide insight into the possible
effects of aging on physiologic function. Figure 6
shows the VO2max as a function of age. Note the
dramatic increases during the growth years.
Longitudinal studies (measuring the same people
over a prolonged period) of children’s aerobic
capacity show that absolute VO2max increases from
about 1.0 L•min-1 at age 6 years to 3.2 L•min-1 at age
16 years. VO2max in girls peaks at about age 14 and
declines thereafter. At age 14, the differences in
VO2max between boys and girls approximate 25%,
with the spread reaching 50% by age 16. Note also
Figure 6. General trend for maximal oxygen uptake with age
the decline in VO2max with increasing age. Beyond and level of activity in males and females.
age 25, VO2max declines steadily at about 1% per year,
so that by age 55 it averages 27% below values reported for 20 year olds.
One’s habitual level of physical activity through middle age determines changes in aerobic capacity to a
greater extent than chronological age.
Body Composition
Differences in body mass explain roughly 70% of the differences in VO2max scores among individuals.
Thus, meaningful comparisons of exercise performance or the absolute value (L•min -1) for VO2max become
difficult among individuals who differ in body size or body composition. This has led to the common practice
of expressing oxygen uptake in terms of these components – either related to body surface area (BSA), body
mass, fat-free body mass (FFM), or limb volume.

1. Anaerobic capacity
2. Anaerobic power
3. Average power
4. Glycogen depletion
5. Graded exercise test
6. Joule
7. Jumping power tests
8. Peak VO2max
9. Power
10. Relative VO2max
11. Stair sprinting power test

12. “True” VO2max
13. VO2max
14. VO2max Criteria
15. Watt
16. Wingate test
STUDY QUESTIONS
Overview of Energy Transfer Capacity During Exercise

Identify the energy system that primarily supports each of the following activities:
Standing vertical jump and reach
Four hundred meter run
Three mile run
Power = ______________ x _______________ ÷ _______________.
Anaerobic Energy: The Immediate and Short-Term Energy Systems

Evaluation of the Immediate Energy System
What type of tests typically measures the immediate anaerobic energy system?
Stair-Sprinting Power Tests

Compute the power output for a person who weighs 55 kg and traverses nine steps in 0.75 seconds
(vertical rise each step equals 0.175 meters).
Jumping-Power Tests
Give one factor that might limit power jumping test scores as measures of the power output
capacity of intramuscular high-energy phosphates.
Other Power Tests

List two tests (other than stair-sprinting) to estimate power output capacity of the immediate
energy system.
1.
2.
Evaluation of the Short-Term Energy System

What type of test best estimates the power output capacity of the short-term energy system?
Performance Tests of Glycolytic Power

List two tests to measure short-term energy transfer capacity.
1.
2.
List three factors that affect anaerobic power performance.

1. 3.
2.
Other Anaerobic Tests

Name one other exercise performance test to measure anaerobic power and capacity.
Glycogen Depletion
List two factors that determine muscle glycogen depletion in different muscle fiber types within the
same muscle.
1.
2.
Buffering of Acid Metabolites

Do athletes have an enhanced buffering capacity compared to non-athletes?
Motivation
What relationship would you expect between “pain tolerance” and one’s capacity for anaerobic
exercise? Explain.
Aerobic Energy: The Long-Term Energy System

List three categories of athletes that typically exhibit high values for VO 2max?
1. 3.
2.
Measurement of Maximal Oxygen Uptake
Criteria for VO2max
Describe the “gold standard” to indicate attainment of true VO2max.
Tests of Aerobic Power

List two general criteria for a good test of VO2max.
1.
2.
Factors That Affect Maximal Oxygen Uptake

List six factors that influence VO2max.
1. 4.
2. 5.
3. 6.
Mode of Exercise
Indicate the most common piece of exercise equipment to determine VO 2max.
Heredity
What is the estimated magnitude of heredity in determining VO2max?
Training State
Give the general range for VO2max improvement with training?
Sex
Give one reasons for sex-related differences in VO2max.
Age
After age 30 y what happens to VO2max?
Body Composition
How does body size influence VO2max?
What is the “best” way to express VO2max? Explain.
PRACTICE QUIZ
1. Power Output: b. DxT/F

a. FxD/T c. work / time
d. force x work 7. Estimates of genetic effects on VO2max:

e. none of the above a. no effect
2. A Watt: b. 5%
a. measure of oxygen uptake c. 20-30%
b. measure of glycolysis d. 60%
c. measure of power e. none of the above
d. measure of distance 8. VO2max decreases about ___% in aging:
e. none of the above a. 1% per year
3. Jumping tests measure: b. 10% per year
a. aerobic power c. 15% per year
b. OBLA d. 25% per year
c. EPOC e. none of the above
d. localized energy depletion 9. Body composition can explain about ___of
e. none of the above the differences in VO2max:
a. 10%
b. 30%
4. Trained athletes compared to untrained: c. 50%
a. have greater buffering capacity d. 70%
b. have lower buffering capacity e. none of the above
c. have the same buffering capacity 10. Performance tests of anaerobic power
would include:
d. have reduced buffering after
training a. long distance runs
e. none of the above b. flexibility tests
5. Among the following athletes who has the c. stair-sprinting power test
highest VO2max: d. walking tests
a. fencers e. none of the above
b. speed skaters
c. swimmers
d. cross-country skiers
e. weight lifters
6. Women compared to men:

a. have lower VO2max
b. have higher VO2max
c. have about the same VO2max
d. higher buffering capacities
e. none of he above
LECTURE #8
PHYSIOLOGIC SUPPORT SYSTEMS AND EXERCISE
Introduction
Most sport, recreational, and occupational activities require a moderately intense yet sustained energy
release. The aerobic breakdown of carbohydrates, fats, and proteins generates this energy for ADP
phosphorylation to ATP. Without a steady rate between oxidative phosphorylation and the energy
requirements of physical activity, an anaerobic-aerobic energy imbalance develops, lactic acid accumulates,
tissue acidity increases, and fatigue quickly ensues. Two factors limit an individual’s ability to sustain a high
level of exercise intensity without undue fatigue:
 Capacity for oxygen delivery
 Capacity of specific muscle cells to generate ATP aerobically
Understanding the role of the ventilatory, circulatory, muscular, and endocrine systems during exercise
enables us to appreciate the broad range of individual differences in exercise capacity. Knowing the energy
requirements of exercise and the corresponding physiologic adjustments necessary to meet these
requirements provides a sound basis to formulate an effective physical fitness program and evaluate one's
physiologic and fitness status before and during such a program.
Part 1. Pulmonary System and Exercise

Pulmonary Structure and Function
If oxygen supply depended only on diffusion through the skin, it would be impossible to support the
basal energy requirement, let alone the 3- to 5-liter oxygen uptake each minute to sustain a world class 5-
minute per mile marathon pace. The remarkably effective ventilatory system meets the body’s needs for gas
exchange.
The ventilatory system, depicted in Figure 1, regulates the gaseous state of our “external” environment for
aerating fluids of the “internal” environment during rest and exercise. The major functions of the ventilatory
system include:
 Supply oxygen for metabolic needs
 Eliminate carbon dioxide produced in metabolism
 Regulate hydrogen ion concentration to maintain acid-base balance
Anatomy of Ventilation
The "term pulmonary
ventilation" describes how
ambient air moves into and
exchanges with air in the
lungs. About 1 foot (0.3 m)
represents the distance
between the ambient air just
outside the nose and mouth
and the blood flowing
through the lungs. Air
entering the nose and mouth
flows into the conductive
portion of the ventilatory
system. Here it adjusts to
body temperature, and
becomes filtered and almost
completely humidified as it
moves through the trachea.
The trachea is a short one-inch
diameter tube that extends
from the and divides into two
tubes of smaller diameter
called bronchi. The bronchi
Figure 1. Overview of the ventilatory system showing the respiratory passages, serve as primary conduits
alveoli, and gas exchange function in an alveolus. within the right and left lungs.
They further subdivide into numerous bronchioles that conduct inspired air through a tortuous, narrow
route until it eventually mixes with the air in the alveoli, the terminal branches of the respiratory tract.
Lungs
The lungs provide the surface between blood and the external environment. Lung volume varies between
4 and 6 liters (amount of air in a basketball) and provides an exceptionally large moist surface. For example,
the lungs of an average-sized person weigh about 1 kg, yet if spread out as in Figure 2, they would cover a
surface of 60 to 80 m2. This equals about 35 times the surface of the person, and would cover almost one-half a
tennis court! This represents a considerable interface for aeration of blood because during any one second of
maximal exercise, no more than 1 pint of blood flows in the lung tissue’s fine network of blood vessels.
Alveoli
Lung tissue contains more than 300 million alveoli each. These
elastic, thin-walled, membranous sacs provide the vital surface for gas
exchange between the lungs and blood. Alveolar tissue has the largest
blood supply of any organ in the body. In fact, the lung receives the
entire output of blood from the heart (cardiac output). Millions of thin-
walled capillaries and alveoli lie side by side, with air moving on one
side and blood on the other. The capillaries form a dense mesh that
covers almost the entire outside of each alveolus. This web becomes so
dense that blood flows as a sheet over each alveolus. Once blood
reaches the pulmonary capillaries, only a single cell barrier, the
respiratory membrane, separates blood from air in the alveolus. This
thin tissue-blood barrier permits rapid gas diffusion between the blood
and alveolar air.
During rest, approximately 250 mL of oxygen leaves the alveoli each
minute and enter the blood, and about 200 mL of carbon dioxide diffuse
in the reverse direction into the alveoli. When trained endurance
athletes perform heavy exercise, about 20 times the resting oxygen
uptake transfers across the respiratory membrane. The primary
Figure 2. The lungs provide an function of pulmonary ventilation during rest and exercise is to
exceptional surface for gas exchange. maintain a fairly constant, favorable concentration of oxygen and
carbon dioxide in the alveolar chambers. This ensures effective
gaseous exchange before the blood leaves the lungs for its transit throughout the body.
Mechanics of Ventilation
The lungs do not merely suspend in the chest cavity. Rather, the difference in pressure within the lungs
and the lung-chest wall interface causes the lungs to adhere to the chest wall interior and literally follow its
every movement. Any change in thoracic cavity volume thus produces a corresponding change in lung
volume. Because lung tissue does not contain voluntary muscle, the lungs depend on accessory means to
alter their volume. The action of voluntary skeletal muscle during inspiration and expiration alters thoracic
dimensions, which brings about changes in lung volume.
Inspiration
The diaphragm, a large, dome-shaped sheet of muscle makes an airtight separation between the
abdominal and thoracic cavities. During inspiration, the diaphragm muscle contracts, flattens out, and moves
downward up to 10 cm toward the abdominal cavity. This enlarges the chest cavity and makes it more
elongated. The air in the lungs then expands reducing its pressure (referred to as intrapulmonic pressure) to
about 5 mm Hg below atmospheric pressure.
Inspiration concludes when thoracic cavity expansion ceases and intrapulmonic pressure increases to
equal atmospheric pressure.
Expiration
Expiration, a predominantly a passive process, occurs as air moves out of the lungs. It results from the
recoil of stretched lung tissue and relaxation of the inspiratory muscles. This makes the sternum and ribs
swing down, while the diaphragm moves back toward the thoracic cavity. These movements decrease the
volume of the chest cavity, compressing alveolar gas and move it out through the respiratory tract into the
atmosphere. During ventilation in moderate to heavy exercise, the internal intercostal muscles and abdominal
muscles act powerfully on the ribs and abdominal cavity. This triggers a more rapid and greater depth of
exhalation.
Respiratory muscle actions change thoracic dimensions to create a pressure differential between the inside
and outside of the lung to drive airflow along the respiratory tract. Greater involvement of the pulmonary
musculature (as occurs during progressively heavier exercise), causes larger pressure differences and
concomitant increases in air movement.
Lung Volumes and Capacities

Figure 3 depicts the various lung volume measures that reflect one’s ability to increase the depth of
breathing. The figure also shows average values for men and women while breathing from a calibrated
recording spirometer that measures oxygen uptake by the closed-circuit method. Two types of measurements,
static and dynamic, provide
information about lung function
dimensions and capacities.
Static lung function measures
evaluate the dimensional
component for air movement
within the pulmonary tract, and
impose no time limitation on the
subject. In contrast, dynamic
lung functions evaluate the
power component of pulmonary
performance during different
phases of the ventilatory
excursion.
Static Lung
Volumes
During measurement of
static lung function the
spirometer bell falls and rises
with each inhalation and
exhalation to provide a record
of the ventilatory volume and
Figure. 3. Static measures of lung volume and capacity.
breathing rate. Tidal volume (TV) describes air moved during either the inspiratory or expiratory phase of
each breathing cycle. For healthy men and women, TV under resting conditions usually ranges between 0.4
and 1.0 liters of air per breath.
After recording several representative TVs, the subject breathes in normally and then inspires maximally.
This additional volume of about 2.5 to 3.5 liters above the inspired tidal air represents the reserve for
inhalation, termed the inspiratory reserve volume (IRV). The normal breathing pattern begins once again
following the IRV. After a normal exhalation, the subject continues to exhale and forces as much air as
possible from the lungs. This additional volume, the expiratory reserve volume (ERV), ranges between 1.0
and 1.5 liters for an average-sized man (and 10 to 20% lower for a woman). During exercise, TV increases
considerably because of encroachment on IRV and ERV, particularly the IRV.
Forced vital capacity (FVC) represents the total air volume moved in one breath from full inspiration to
maximum expiration, or vice versa, with no time limitation. Although values for FVC can vary considerably
with body size and body position during the measurement, average values usually equal 4 to 5 liters in
healthy young men and 3 to 4 liters in healthy young women. FVCs of 6 to 7 liters are not uncommon for tall
individuals, and values of 7.6 liters have been reported for a professional football player and 8.1 liters for an
Olympic gold medalist in cross-country skiing. Large lung volumes of some athletes probably reflect genetic
influences because static lung volumes do not change appreciably with exercise training.
Dynamic Lung Volumes

Dynamic measures of pulmonary ventilation depend on two factors:
 Volume of air moved per breath (tidal volume)
 Speed of air movement (ventilatory rate)
Airflow speed depends on the pulmonary airways' resistance to the smooth flow of air and resistance
offered by the chest and lung tissue to changes in shape during breathing.
Forced Expiratory Volume-To-Forced Vital Capacity Ratio

Normal values for vital capacity can occur in severe lung disease if no limit exists on the time to expel air.
For this reason, a dynamic lung function measure such as the percentage of the FVC expelled in one second
(FEV1.0) is more useful for diagnostic purposes. Forced expiratory volume-to-forced vital capacity ratio
(FEV1.0/FVC) reflects expiratory power and overall resistance to air movement in the lungs. Normally, the
FEV1.0/FVC averages about 85%. With severe pulmonary (obstructive) lung disease (e.g., emphysema and/or
bronchial asthma), the FEV1.0/FVC becomes greatly reduced, often reaching less than 40% of vital capacity.
The clinical demarcation for airway obstruction equals the point at which less than 70% of the FVC can be
expelled in one second.
Maximum Voluntary Ventilation

Another dynamic test of ventilatory capacity requires rapid, deep breathing for 15 seconds. Extrapolation
of this 15-second volume to the volume breathed had the subject continued for one minute represents the
maximum voluntary ventilation (MVV). For healthy, college-aged men, the MVV usually ranges between 140
and 180 liters. The average for women equal 80 to 120 liters. Male members of the United States Nordic Ski
Team averaged 192 liters per minute, with an individual high MVV of 239 liters per minute. Patients with
obstructive lung disease achieve only about 40% of the MVV predicted normal for their age and body size.
Specific pulmonary therapy benefits patients because training the breathing musculature increases the
strength and endurance of the respiratory muscles (and enhances MVV).
Pulmonary Ventilation
Minute Ventilation
During quiet breathing at rest, an adults" breathing rate averages 12 breaths per minute (about 1 breath
every 5 s), whereas tidal volume averages about 0.5 liter of air per breath. Under these conditions, the volume
of air breathed each minute (minute ventilation) equals 6 liters.
Minute ventilation (VE) = Breathing rate x Tidal volume
6.0 L•min–1 = 12 x 0.5 L
An increase in depth or rate of breathing or both significantly increases minute ventilation. During
maximal exercise, the breathing rate of healthy young adults usually increases to 35 to 45 breaths per minute,
although elite athletes can achieve 60 to 70 breaths per minute. In addition, tidal volume commonly increases
to 2.0 liters and larger during heavy exercise, causing exercise minute ventilation in adults to easily reach 100
liters or about 17 times the resting value. In well-trained male endurance athletes, ventilation may increase to
160 liters per minute during maximal exercise. In fact, several studies of elite endurance athletes report
ventilation volumes of 200 liters per minute. Even with these large minute ventilations, the tidal volume
rarely exceeds 55 to 65% of vital capacity.
Alveolar Ventilation
Alveolar ventilation refers to the portion of minute ventilation that mixes with the air in the alveolar
chambers. A portion of each breath inspired does not enter the alveoli, and thus does not engage in gaseous
exchange with the blood. This air that fills the nose, mouth, trachea, and other nondiffusible conducting
portions of the respiratory tract constitutes the anatomical dead space. In healthy people, this volume
averages 150 to 200 mL, or about 30% of the resting tidal volume.
Because of dead-space volume, approximately 350 mL of the 500 mL of ambient air inspired in each tidal
volume at rest mixes with existing alveolar air. This does not mean that only 350 mL of air enters and leaves
the alveoli with each breathe. To the contrary, if tidal volume equals 500 mL, then 500 mL of air enters the
alveoli but only 350 mL represents fresh air (or about one-seventh of the total air in the alveoli). Such a
relatively small, seemingly inefficient alveolar ventilation prevents drastic changes in the composition of
alveolar air; this ensures a consistency in arterial blood gases throughout the entire breathing cycle.
Table 1 shows that minute ventilation does not always reflect actual alveolar ventilation. In the first
example of shallow breathing, tidal volume decreases to 150 mL, yet a 6-L minute ventilation results when
breathing rate increases to 40 breaths per minute. The same 6-L minute volume results by decreasing
breathing rate to 12 breaths per minute and increasing tidal volume to 500 mL. Doubling tidal volume and
halving the ventilatory rate, as in the example of deep breathing, again produces a 6-L minute ventilation.
Table 1. Relationship among tidal volume, breathing rate, and minute and alveolar minute ventilation.
Each ventilatory adjustment drastically affects alveolar ventilation. In the example of shallow breathing,
Gas pressure represents the force exerted by the gas molecules against the
surfaces they encounter.
dead-space air represents the entire air volume moved (no alveolar ventilation has taken place.)
Depth Versus Rate

Increases in the rate and depth of breathing maintain alveolar ventilation during increasing exercise
intensities. In moderate exercise, well-trained endurance athletes achieve adequate alveolar ventilation by
increasing tidal volume and only minimally increasing breathing rate. With deeper breathing, alveolar
ventilation can increase from 70% of the minute ventilation at rest to over 85% of the total exercise ventilation.
Ventilatory adjustments during exercise occur unconsciously; each individual develops a “style” of
breathing by blending breathing rate and tidal volume so alveolar ventilation matches alveolar perfusion.
Conscious attempts to modify breathing during general physical activities such as running usually fail and do
not benefit exercise performance. In fact, conscious manipulation of breathing detracts from the exquisitely
regulated ventilatory adjustments to exercise. At rest and exercise, each individual should breathe in the
manner that seems most natural.
Gas Exchange
Our oxygen supply depends on the oxygen concentration in ambient air and its pressure. Ambient
(atmospheric) air composition remains relatively constant at 20.93% for oxygen, 79.04% for nitrogen (includes
small quantities of inert gases that behave physiologically like nitrogen), 0.03% for carbon dioxide, and
usually small quantities of water vapor. The gas molecules move at great speeds and exert a pressure against
any surface they contact. At sea level, the pressure of air's gas molecules raises a column of mercury to an

RESPIRED GASES: CONCENTRATION AND PARTIAL
PRESSURES
Gas concentration should not be confused with gas pressure.
Gas concentration reflects the amount of gas in a given volume – determined by
the gas' partial pressure x solubility [Gas concentration = partial pressure x
solubility]
average height of 760 mm (29.9 in.). This barometric reading varies somewhat with changing weather
conditions and decreases predictably at increased altitude.
Partial Pressure = Percent concentration x Total pressure of gas mixture
Ambient Air
Table 2. Percentages, partial pressures, and volumes of gases in 1
liter of dry ambient air at sea level.
Gas Percentage Partial Pressure Volume of
(at 760 mmHg) Gas (mL•L-1)
Oxygen 20.93 159 209.3
Carbon dioxide 0.03 0.02 0.4

Nitrogen 79.04 600 790.3
Table 2 presents the volume, percentage, and partial pressures of gases in dry, ambient air at sea level. The
partial pressure of oxygen equals 20.93% of the total 760 mm Hg pressure exerted by air, or 159 mmHg
(0.2093 x 760 mm Hg); the random movement of the minute quantity of carbon dioxide exerts a pressure of
only 0.2 mm Hg (0.0003 x 760 mmHg), while nitrogen molecules exert a pressure that raises the mercury in a
manometer about 600 mm (0.7904 x 760 mmHg). The letter P before the gas symbol denotes partial pressure.
For sea level ambient air: PO2 = 159 mmHg; PCO2 = 0.2 mmHg; PN2 = 600 mmHg.
Tracheal Air
Air entering the nose and mouth passes down the respiratory tract; it becomes completely saturated with
water vapor, that slightly dilutes the inspired air mixture. At body temperature, for example, the pressure of
water molecules in humidified air equals 47 mm Hg; this leaves 713 mmHg (760 - 47) as the total pressure
exerted by the inspired dry air molecules at sea level. Consequently, the effective Po 2 in tracheal air decreases
by about 10 mmHg from its ambient value of 159 mm Hg to 149 mmHg (0.2093 x [760 - 47 mmHg]).
Humidification has little effect on the inspired PCO2 because of carbon dioxide's almost negligible
concentration in inspired air.
Alveolar Air
Alveolar air composition differs considerably from the incoming breath of moist ambient air because
carbon dioxide continually enters the alveoli from the blood, whereas oxygen leaves the lungs for transport
throughout the body. Table 3 shows that alveolar air contains approximately 14.5% oxygen, 5.5% carbon
dioxide, and 80.0% nitrogen.
Table 3. Percentages, partial pressures, and volumes of gases in 1
liter of dry alveolar air at sea level.
Gas Percentage Partial Pressure Volume of
(at 760-47 mmHg) Gas (mL•L-1)
Oxygen 14.5 103 145
Carbon dioxide 5.5 39 55
Nitrogen 80.0 571 800
Water 47
After subtracting vapor pressure in moist alveolar gas, the average alveolar Po 2 equals 103 mmHg (0.145 x
[760 - 47 mmHg]) and 39 mmHg (0.055 x [760 - 47 mmHg]) for PCO2. These values represent the average
pressures exerted by oxygen and carbon dioxide molecules against the alveolar side of the respiratory
membrane. They do not exist as physiologic constants, but vary slightly with the phase of the ventilatory
cycle and adequacy of ventilation in various lung segments.
Gas Exchange in the Body

The exchange of gases between the lungs and blood, and their movement at the tissue level, takes place
entirely passively by diffusion.
Gas Exchange in Lungs

The first step in oxygen transport involves oxygen transfer from oxygen alveoli into the blood. The
alveolar Po2 equals 100 mmHg, which is less than the Po2 of ambient air. Three main reasons for the dilution
of oxygen in inspired air include:
 Water vapor saturates relatively dry inspired air
 Oxygen is continually removed from alveolar air
 Carbon dioxide is continually added to alveolar air
The pressure of oxygen molecules in alveolar air averages about 60 mm Hg higher than the Po 2 in venous blood
entering the pulmonary capillaries. Consequently, oxygen diffuses through the alveolar membrane into the
blood. Carbon dioxide exists under slightly greater pressure in returning venous blood than in the alveoli
causing diffusion of carbon dioxide from the blood into the lungs. Although only a small pressure gradient of
6 mm Hg exists for carbon dioxide diffusion compared with oxygen, adequate carbon dioxide transfer occurs
rapidly because of carbon dioxide's high solubility. Nitrogen, an inert gas in metabolism, remains essentially
unchanged in alveolar-capillary gas.
Gas Exchange in the Tissues

In the tissues, where energy metabolism consumes oxygen at a rate almost equal to carbon dioxide
production, gas pressures can differ considerably from arterial blood. At rest, the average Po 2 in the muscle's
extracellular fluid rarely drops below 40 mmHg, while cellular PCO2 averages about 46 mmHg. In contrast,
heavy exercise can reduce the pressure of oxygen molecules in muscle tissue to 3 mmHg, whereas the
pressure of carbon dioxide approaches 90 mmHg. The pressure differential between gases in plasma and
tissues establishes the gradients for diffusion – oxygen leaves capillary blood and diffuses toward
metabolizing cells, while carbon dioxide flows from the cell to the blood. Blood then enters the veins and
returns to the heart for delivery to the lungs. Diffusion rapidly begins once again as venous blood enters the
lung's dense capillary network.
Oxygen and Carbon Dioxide Transport

Oxygen Transport in the Blood
The blood transports oxygen in two ways:
1. In physical solution – dissolved in the fluid portion of the blood.
2. Combined with hemoglobin – in loose combination with the iron-protein hemoglobin molecule in the
red blood cell
Oxygen Transport in Physical Solution

Oxygen does not dissolve readily in fluids. At an alveolar Po2 of 100 mm Hg, only about 0.3 mL of gaseous
oxygen dissolves in the plasma of each 100 mL of blood (3 mL of oxygen per liter of blood). Because the
average adult’s total blood volume equals about 5 liters, 15 mL of oxygen dissolve for transport in the fluid
portion of the blood (3 mL per L x 5 = 15 mL). This amount of oxygen could sustain life for only about four
seconds. Viewed from a different perspective, the body would need to circulate 80 liters of blood each minute
just to supply the resting oxygen requirements if oxygen were transported only in physical solution. This
represents a blood flow two times higher than the maximum ever recorded for an exercising human!
Oxygen Combined With Hemoglobin (Hb)

The blood of many animal species contains a metallic compound to augment its oxygen-carrying capacity.
In humans, the iron-containing protein pigment hemoglobin constitutes the main component of the body’s 25
trillion red blood cells. Hemoglobin increases the blood’s oxygen-carrying capacity 65 to 70 times above that
normally dissolved in plasma. Thus, for each liter of blood, hemoglobin temporarily “captures” about 197 mL
of oxygen. Each of the four iron atoms in a hemoglobin molecule loosely binds one molecule of oxygen to
form oxyhemoglobin in the reversible oxygenation reaction:
Hb + 4 O2 ––––––––> Hb4O8
This reaction requires no enzymes. The partial pressure of oxygen in solution solely determines the
oxygenation of hemoglobin to oxyhemoglobin.
Oxygen-Carrying Capacity of Hemoglobin

In men, each 100 mL of blood contains approximately 15 to 16 g of hemoglobin. The value averages 5 to
10% less for women, or about 14 g per 100 mL of blood. Sex difference in hemoglobin concentration
contributes to the lower aerobic capacity of women, even after adjusting for differences in body mass and fat.
Each gram of hemoglobin can combine loosely with 1.34 mL of oxygen. Thus, oxygen-carrying capacity
can be calculated by knowing blood’s hemoglobin concentration as follows:
Blood’s oxygen capacity = Hb (g•100 mL-1 blood) x Oxygen capacity of Hb (1.34 mL)
For example, if the blood’s hemoglobin concentration equals 15, then approximately 20 mL of oxygen (15 g
per 100 mL x 1.34 mL = 20.1) would be carried with the hemoglobin in each 100 mL of blood if hemoglobin
achieved full oxygen saturation (i.e., if all Hb existed as Hb408).
Po2 and Hemoglobin Saturation

Thus far, the discussion of
blood’s oxygen-carrying capacity
assumes that hemoglobin achieves
full saturation with oxygen when
exposed to alveolar gas.
Figure 4 shows the relationship
between percent hemoglobin
saturation (left vertical axis) at
various Po2s under normal resting
physiologic conditions (arterial pH
7.4, 37°C) and the effects of changes
in pH (Figure 6B) and temperature
(Figure 6C) on hemoglobin’s
affinity for oxygen. Percent
saturation of hemoglobin computes
as follows:
Percent saturation = (Total O2
combined with Hb (Oxygen
carrying capacity of Hb) x 100
Figure 4. Oxyhemoglobin dissociation curve under physiologic conditions at rest
(arterial pH 7.4, tissue temperature 37°C). The right vertical axis shows the
quantity of oxygen combined with Hb in each 100 mL of blood. The horizontal
red line indicates Hb’s percent saturation at sea level alveolar PO2. The dashed
line shows percent saturation at a PO2 of 40 mm Hg (tissue and venous blood).
This curve, termed the "oxyhemoglobin dissociation curve", quantifies the amount of oxygen carried in
each 100 mL of normal blood in relation to plasma Po2 (right axis). For example, at a Po2 of 90 mm Hg the
normal complement of hemoglobin in 100 mL of blood is about 19 mL of oxygen; at 40 mm Hg the oxygen
quantity falls to 15 mL, and 6.5 mL at a Po2 of 20 mm Hg.
The Bohr Effect

Figures 5B and 5C show that increases in acidity (H+ concentration and CO2) or temperature cause the
oxyhemoglobin dissociation curve to shift downward to the right (to enhance unloading of oxygen),
particularly in the Po2 range of 20 to 50 mm Hg. This phenomenon, known as the Bohr effect (named after its
discoverer physiologist Christian Bohr), results from alterations in hemoglobin’s molecular structure.
Bohr Effect becomes
important in vigorous
exercise, as increased
metabolic heat and
acidity in tissues
augments oxygen
release. For example, at
a Po2 of 20 mm Hg and
normal body
temperature (37°C),
%O2 saturation of
hemoglobin equals
35%. At the same Po2,
with body temperature
increased to 43°C (like
at the end of a
marathon run),
hemoglobin’s
saturation decreases to
about 23%. Thus, more
oxygen unloads from
hemoglobin for use in
cellular metabolism.
Similar effects take
place with increased
acidity.
Figure 6B, Oxyhemoglobin dissociation curve. Effects of
changes in pH ([H+]) on hemoglobin’s affinity for oxygen. 6C,
Effects of changes in temperature on hemoglobin’s affinity.
Part 2. Circulation System and Exercise

Introduction
The Greek physician Galen (Lecture 2) theorized about blood flow in the body. He believed blood flowed
like the tides of the sea, surging and abating into arteries, then away from the heart and back again. In Galen’s
view, fluid carried with it “humors”, good and evil that determined one’s well-being. If a person became ill,
the standard practice required bloodletting to drain off the diseased humors and restore health. This theory
prevailed until the seventeenth century when physician William Harvey (Lecture 2) proposed a different
scenario. Experimenting with frogs, cats, and dogs, Harvey demonstrated the existence of valves in the heart
that provided for one-way movement of fluid, a finding incompatible with Galen’s “ebb-and-flow” view
because it suggested a circular flow of blood through the body. In a set of ingenious experiments, Harvey
measured the volume of the heart chambers and counted the number of times the heart contracted in one
hour. He concluded that if the heart emptied only one-half its volume with each beat, the body’s total blood
volume would be pumped in minutes. These finding led Harvey to hypothesize that blood moved
(circulated) within a closed system in a circular pattern throughout the body. Harvey, of course, was correct;
we now know that the heart pumps the entire blood volume, approximately five liters, in one minute.
Harvey’s experiments changed medical science forever, although it would take nearly two hundred more
years for his ideas to play important roles in physiology and medicine.
From Harvey’s early experiments of the sophisticated research at the dawn of the twenty first century, we
now know that the highly efficient ventilatory system complements a rapid transport and delivery system
comprised of blood, the heart, and more than 60,000 miles of blood vessels that integrate the body as a unit.
The circulatory system serves five important functions during physical activity:
1. Delivers oxygen to active tissues
2. Aerates blood returned to the lungs
3. Transports heat, a by-product of cellular metabolism, from the body's core to the skin
4. Delivers fuel nutrients to active tissues
5. Transports hormones, the body’s chemical messengers
Components of the Cardiovascular System

The cardiovascular system consists of an interconnected, continuous vascular circuit containing a pump
(heart), a high-pressure distribution system (arteries), exchange vessels (capillaries), and a low-pressure
collection and return system (veins). Figure 6 presents a schematic view of this system.
Figure 6. Schematic view of the cardiovascular system consisting of the heart and
the pulmonary and systemic vascular circuits.
Heart
The heart provides the force to propel blood throughout the vascular circuit. This four-chambered organ, a
fist-sized pump, beats at rest an average of 70 times a minute, 100,800 times a day, and 36.8 million times a
year. Even for a person of average fitness, maximum output of blood from this remarkable organ exceeds
fluid output from a household faucet turned wide open!
Functionally, the heart consists of two separate pumps: one pump (left heart pump) receives blood from
the body and pumps it to the lungs for aeration (pulmonary circulation and the other pump (right heart
pump) accept oxygenated blood from the lungs and pump it throughout the body (systemic circulation).
The hollow chambers of the heart’s right side (right heart) perform two important functions:
1. Receive blood returning from all parts of the body
2. Pump blood to the lungs via the pulmonary circulation for aeration
The left side of the heart (left heart) also performs two important functions:
1. Receive oxygenated blood from the lungs
2. Pump blood into the thick-walled, muscular aorta for distribution throughout the body in the
systemic circulation
A thick, solid muscular wall (septum) separates the left and right sides of the heart. The atrioventricular
(AV) valves situated within the heart direct the one-way flow of blood from the right atrium to the right
ventricle (tricuspid valve) and from the left atrium to the left ventricle (mitral or bicuspid valve). The
semilunar valves located in the arterial wall just outside the heart prevent blood from flowing back into the
heart between ventricular contractions.
The relatively thin-walled, sac-like atrial chambers serve as primer pumps to receive and store blood
returning from the lungs and body during ventricular contraction. About 70% of the blood that returns to the
atria flows directly into the ventricles before the atria contract. Simultaneous contraction of both atria forces
remaining blood into their respective ventricles directly below. Almost immediately after atrial contraction,
the ventricles contract and force blood into their specific arterial systems.
Arteries
The arteries provide the high-pressure tubing that conducts oxygen-rich blood to tissues. Arteries are
composed of layers of connective tissue and smooth muscle. Because of their thickness, no gaseous exchange
takes place between arterial blood and surrounding tissues. Blood pumped from the left ventricle into the
highly muscular yet elastic aorta circulates throughout the body via arterioles, or smaller arterial branches.
Arteriole walls contain circular layers of smooth muscle that either constrict or relax to regulate peripheral
blood flow. This redistribution function becomes particularly important during exercise because blood
diverts to working muscles from areas that temporarily compromise their blood supply.
Capillaries
The arterioles continue to branch and form smaller and less muscular vessels called metarterioles. These
tiny vessels end in capillaries, a network of microscopic blood vessels so thin they provide only enough room
for blood cells to squeeze through in single file. Capillaries generally contain about 5% of the total blood
volume at any time. Gases, nutrients, and waste products rapidly transfer across the thin, porous, capillary
walls. A ring of smooth muscle (precapillary sphincter) encircles the capillary at its origin to control the
vessel’s internal diameter. This sphincter provides a local means for regulating capillary blood flow within a
specific tissue in response to metabolic requirements that change rapidly and dramatically in exercise.
Veins
The vascular system maintains continuity of blood flow as capillaries feed deoxygenated blood at almost a
trickle into small veins called venules. Blood flow then increases slightly because the venous system cross-
sectional area is less than for capillaries. The lower body’s smaller veins eventually empty into the largest
vein, the inferior vena cava, that travels through the abdominal and chest cavities toward the heart. Venous
blood draining the head, neck, and shoulder regions empties into the superior vena cava and moves
downward to join the inferior vena cava at heart level. The mixture of blood from the upper and lower body
then enters the right atrium and descends into the right ventricle for delivery through the pulmonary artery
to the lungs. Gas exchange takes place in the lungs’ alveolar-capillary network; here, the pulmonary veins
return oxygenated blood to the left heart, where the journey through the body resumes.
VENOUS RETURN
A unique characteristic of veins solves a potential problem related to the low pressure of venous blood.
Because of low venous blood pressure, muscular contractions or minor pressure changes within the chest
cavity during breathing compress the veins. Alternate venous compression and relaxation, combined with the
one-way action of valves, provides a “milking” effect similar to the action of the heart. Venous compression
imparts considerable energy for blood flow, whereas “diastole” (relaxation) allows vessels to refill as blood
moves toward the heart. Without valves, blood would stagnate or pool (as it sometimes does) in veins of the
extremities, and people would faint every time they stood up because of reduced blood flow to the brain.
A SIGNIFICANT BLOOD RESERVOIR

The veins do not merely function as passive conduits. At rest, the venous system normally contains about
65% of the total blood volume; hence, the veins serve as capacitance vessels, or blood reservoirs. A slight
increase in tension (tone) by the vein’s smooth muscle layer alters the diameter of the venous tree. A
generalized increase in venous tone rapidly redistributes blood from peripheral veins toward the central
blood volume returning to the heart. In this manner, the venous system plays an important role as an active
blood reservoir to either retard or enhance blood flow to the systemic circulation.
VARICOSE VEINS
Sometimes valves within a vein become defective and fail to maintain one-way blood flow. This condition
of varicose veins usually occurs in superficial veins of the lower extremities from the force of gravity that
retards blood flow in an upright posture. As blood accumulates, these veins become excessively distended
and painful, often impairing circulation from surrounding areas. In severe cases, the venous wall becomes
inflamed and degenerates – a condition called phlebitis, which often requires surgical removal of the vessel.
Individuals with varicose veins should avoid excessive straining exercises like heavy resistance training.
Venous Pooling
The fact that people faint when forced to maintain an upright posture without movement (e.g., standing at
attention for a prolonged period) demonstrates the importance of muscle contractions to venous return. Also,
changing from a lying to a standing position affects the dynamics of venous return and triggers physiologic
responses. Heart rate and blood pressure stabilize during bed rest. If a person suddenly rises and remains
erect, an uninterrupted column of blood exists from heart level to the toes, creating a hydrostatic force of 80 to
100 mm Hg. Swelling (edema) occurs from pooling of blood in the lower extremities and creates “back
pressure” that forces fluid from the capillary bed into surrounding tissues. Concurrently, impaired venous
return decreases blood pressure; at the same time, heart rate accelerates, and venous tone increases to counter
the hypotensive condition. Maintaining an upright position without movement leads to dizziness and
eventual fainting from insufficient cerebral blood supply. Resuming a horizontal or head-down position
restores circulation and consciousness.
The Active Cool-Down

The existence of venous pooling justifies continued slow jogging or walking after strenuous exercise. A
“cooling down” with rhythmic exercise facilitates blood flow through the vascular circuit (including the
heart) during recovery. An “active recovery” also aids in lactic acid removal from the blood. The pressurized
suits worn by test pilots and special support stockings also aid in retarding hydrostatic shifts of blood to
veins of the lower extremities in the upright position. A similar supportive effect occurs in upright exercise in
a swimming pool because the water’s external support facilitates venous return.
Blood Pressure
A surge of blood enters the
aorta with each contraction of the
left ventricle, distending the
vessel and creating pressure
within it. The stretch and
subsequent recoil of the aortic
wall propagates as a wave
through the entire arterial system.
The pressure wave appears in the
following areas: as a pulse in the
superficial radial artery on the Figure. 7. Pulse rate taken at (A) temporal, (B) carotid, and (C) radial arteries.
thumb side of the wrist, in the
temporal artery (on the side of the head at the temple), and/or at the carotid artery along the side of the
trachea (Figure 7).
In
Blood pressure classification
Systolic (mmHg)Diastolic (mmHg)Category<130<85Normal1301398589High normal1401599099(Stage 1)
hypertension160179100109Moderate (Stage 2) hypertension180209110119Severe (Stage 3)
hypertension>210120Very severe (Stage 4) hypertension
healthy persons, pulse rate equals heart rate. The highest pressure generated by left ventricular contraction
(systole) to move blood through a healthy, resilient vascular system at rest usually reaches 120 mm Hg. As the
heart relaxes (diastole) and aortic valves close, the natural elastic recoil of the aorta and other arteries provide
a continuous head of pressure to move blood to the periphery until the next surge from ventricular systole.
During the cardiac cycle’s diastole, arterial blood pressure decreases to 70-80 mm Hg. Arteries “hardened” by
mineral and fatty deposits within their walls, or with excessive peripheral resistance to blood flow from
kidney malfunction or nervous strain, induce systolic pressures as high as 300 mm Hg and diastolic pressures
above 120 mmHg.
Rest
Resting High blood pressure (resting-hypertension) imposes a chronic strain on normal cardiovascular
function. If left untreated, severe hypertension leads to heart failure; the heart muscle weakens, unable to
maintain its normal pumping ability. Degenerating, brittle vessels can obstruct blood flow, or can burst,
cutting off vital blood flow to brain tissue causing a stroke.

DETERMINANTS OF BLOOD PRESSURE
Arterial blood pressure reflects arterial blood flow per minute (cardiac output) and
peripheral vascular resistance to that flow in the following relationships:
Total peripheral resistance (TPR) = Blood Pressure (BP) ÷ Cardiac Output (CO)
Blood Pressure = Cardiac Output x Total Peripheral Resistance
During Rhythmic Exercise
During rhythmic muscular activities like brisk walking, hiking, jogging, swimming, and bicycling, dilation
of the active muscles’ blood vessels increases the vascular area for blood flow. The alternate, rhythmic
contraction and relaxation of skeletal muscles provides significant force to propel blood through the vessels
and return it to the heart. Increased blood flow during moderate exercise causes systolic pressure to rapidly
rise in the first few minutes and level off, usually between 140 and 160 mm Hg; diastolic pressure remains
relatively unchanged.

BLOOD PRESSURE AND RACE
African Americans have twice the incidence of high blood pressure as Caucasians and
nearly seven times the rate of severe hypertension. The fact that African Americans in the
United States have a much greater incidence of hypertension than blacks in Africa
compounds the issue of race and hypertension. Researchers now focus on the possible
causative role of diet, stress, cigarette smoking, and other lifestyle and environmental
factors that trigger this chronic blood pressure response in genetically susceptible blacks.
During Resistance Exercise
Straining-type exercises (e.g., heavy resistance exercise, shoveling wet snow) produce acute, dramatic
blood pressure increases because sustained muscular force compresses peripheral arterioles, significantly
increasing resistance to blood flow. The heart’s additional workload from acute elevations in blood pressure
increases risk for individuals with existing hypertension or coronary heart disease. In such cases, rhythmic
forms of moderate physical activity provide health benefits..
BODY INVERSION
Inversion devices that allow a person to hang upside-down have been used for years to increase
relaxation, facilitate a strength-training response, and relieve lower back pain. However, no one has yet
demonstrated with careful research that inverting the body provides any practical medical or physiologic
benefits. On the negative side, the maneuver can trigger a significant rise in blood pressure at the start and
throughout the inversion period. This raises concern about possible consequences of inversion for people
with hypertension, and the wisdom of performing exercises in the upside-down position. A brief period of
inversion also doubles pressure within the eye in healthy adults. Clearly, individuals with eye disorders
should refrain from inversion.
IN RECOVERY
Following a bout of sustained light- to moderate-intensity exercise, systolic blood pressure temporarily
decreases below pre-exercise levels for up to 12 hrs in normal and hypertensive subjects. Pooling of blood in
the visceral organs and lower limbs during recovery reduces central blood volume, which contributes to a
lower blood pressure. The hypotensive recovery response further supports the use of exercise as important
nonpharmacologic hypertension therapy. A potentially effective approach spreads several bouts of moderate
physical activity throughout the day.

Cardiac Output In Trained And Untrained
Subjects at Rest and During Maximal Exercise
Cardiac
= Heart rate x Stroke Volume
Output
Untrained
Rest 5000 mL = 70 b•min1 x 71 mL•b1
Maximal Ex. 22,000 mL = 195 b•min1 x 113 mL•b1
Endurance Trained
Rest 5000 mL = 50 b•min1 x 100 mL•b1
Maximal Ex. 35,000 mL = 195 b•min1 x 179 mL•b1
Cardiovascular Dynamics During Exercise
Cardiac Output
Cardiac output provides the primary indicator of the circulatory system’s functional capacity to meet the
demands of physical activity. As with any pump, the rate of pumping (heart rate) and quantity of blood
ejected with each stroke (stroke volume) determine the heart’s output:
Cardiac output (CO) = Heart rate (HR) x Stroke volume (SV)
Resting Cardiac Output

UNTRAINED PERSONS
Each minute, the left ventricle ejects the entire 5-liter (5000 mL) blood volume of an average-sized adult
male. This value remains similar for most individuals, but stroke volume and heart rate vary considerably
depending on cardiovascular fitness status. A heart rate of about 70 beats per minute generally sustains the
average adult’s 5-liter resting cardiac output. Substituting this heart rate value in the cardiac output equation
(cardiac output = stroke volume x heart rate; stroke volume = cardiac output ÷ heart rate), yields a calculated
stroke volume of 71 mL per beat.
ENDURANCE ATHLETES
Resting heart rate for an endurance athlete generally averages about 50 beats per minute. Because the
athlete’s resting cardiac output also averages 5 liters per minute, blood circulates with a proportionately
larger stroke volume of 100 mL per beat (5000 mL ÷ 50). Stroke volumes for women usually average 25%
below values for men of equivalent training status. The smaller body size of the average woman chiefly
accounts for this “sex difference.”
The underlying mechanisms for the heart rate and stroke volume differences between trained and
untrained individuals remain unclear. Two factors probably interact as aerobic fitness improves:
1. Increased vagal tone slows the heart allowing more time for ventricular filling
2. Enlarged ventricular volume and a more powerful myocardium combine to eject a larger volume of
blood with each systole
Exercise Cardiac Output

Blood flow from the heart increases in direct proportion to exercise intensity. From rest to steady-rate
exercise, cardiac output increases rapidly, followed by a more gradual increase until it plateaus so blood flow
matches exercise metabolic requirements.
In sedentary, college-aged men, cardiac output in strenuous exercise increases about four times resting to
an average maximum of 22 L per minute. HRmax for these young adults averages about 195 bpm. Thus, stroke
volume averages 113 mL of blood per beat during maximal exercise (22,000 mL/195). In contrast, world-class
endurance athletes generate max cardiac outputs of 35 L•min-1, with similar or slightly lower HRmax than the
untrained. Thus, difference between maximum cardiac output relates to differences in stroke volume.
Exercise Stroke Volume

Stroke volume increases linearly to about 50% VO2max and
Sedentary
then levels off until termination of exercise. For some subjects,
stroke volume decreases slightly at higher exercise intensities.
Trained Physiologists agree that stroke volume and oxygen uptake
increase linearly to about 50% VO2max.
Heart Rate During Exercise

Graded Exercise
Figure 8 shows the relationship between heart rate and
oxygen uptake during exercise of increasing intensity to
maximum for endurance athletes (triangles) and sedentary
college students (circles). Similar lines relate heart rate and
Figure 8. Heart rate in relation to oxygen uptake oxygen uptake for both groups throughout the major portion of
during upright exercise in endurance athletes. the exercise range. Heart rate for the untrained person
The triangles are for athletes and the circles are
accelerates rapidly with increasing oxygen uptake; a much
for sedentary college students.
smaller heart rate increase occurs for athlete. Consequently,
trained persons achieve a higher level of exercise oxygen uptake at a particular submaximal heart rate than a
sedentary person.
Figure 9. Relative distribution of cardiac output during rest (A) and strenuous endurance exercise (B). Numbers in parenthesis =
percent of total cardiac output. Despite its large mass, muscle receives about the same amount of blood as the much smaller kidneys
at rest. In strenuous exercise, however, 85% of cardiac output diverts to active muscle.
Submaximum Exercise
Heart rate increases rapidly and levels off within several minutes during submaximum steady-rate
exercise. A subsequent increase in exercise intensity causes heart rate to rise to a new plateau as the body
attempts to match the cardiovascular response to metabolic demands. Each increment in exercise intensity
requires progressively more time to achieve heart rate stabilization.
Cardiac Output Distribution

Blood flow to specific tissues generally increases in proportion to their metabolic activity.
Rest
Figure 9 (A) shows the approximate distribution of a 5-liter cardiac output at rest. More than one-fourth of
the cardiac output flows to the liver; one-fifth to muscle tissue; and the brain, kidneys, and digestive tract also
require relatively large amounts of blood.
During Exercise
Figure 9 (B) illustrates the distribution to various tissues during intense aerobic exercise. Although
regional blood flow varies considerably depending on environmental conditions, level of fatigue, and the
mode of exercise, active muscles receive a disproportionately large portion of the cardiac output. Each 100 g
of muscle receives 4 to 7 mL of blood per minute during rest. Muscle blood flow increases steadily during
exercise to reach a maximum of between 50-75 mL per 100 g of tissue.

1. Alveolar ventilation
2. Alveoli
3. Ambient air
4. Anatomical dead space
5. Arteriovenous oxygen difference
6. Bohr effect
7. Dyspnea
8. Emphysema
9. FEV1.0 / FVC
10. Forced vital capacity
11. Hemoglobin
12. Hyperventilation
13. Minute ventilation
14. Oxyhemoglobin
15. Oxyhemoglobin dissociation curve
16. Partial pressure of gas
17. Percent saturation
18. Po2
19. Pulmonary ventilation
20. Ventilatory system
21. Arteries
22. Bradycardia
23. Cardiac output

24. Diastolic blood pressure
25. ECG
26. Hypertension
27. Stroke volume
28. Systole
29. Veins
STUDY QUESTIONS
Pulmonary Structure and Function

List three functions of the ventilatory system.
1. 3.
2.
Anatomy of Ventilation
Place the following terms in the order of airflow movement during the inspiratory cycle:
bronchioles, trachea, alveoli, and bronchi.
1. 3.
2. 4.
Lungs
Give the surface area dimension of the lungs?
Alveoli
What is the primary function of the alveoli?
Mechanics of Ventilation
What causes the changes in lung volume during inspiration and expiration?
Inspiration
List three muscles involved in inspiration.
1. 3.
2.
Expiration
List three factors that cause expiration of air from lungs.
1. 2.
3.
Static Lung Volumes

Name three static lung volumes
1.
2.
3.
Dynamic Lung Volumes

What two factors determine dynamic lung volumes?
1.
2.
Forced Expiratory Volume-to-Forced Vital Capacity Ratio.

Forced expiratory volume provides an indication of what two components of lung function?
1.
2.
Maximum Voluntary Ventilation

Discuss whether or not the MVV exceeds the ventilation volume observed during maximal exercise.
Pulmonary Ventilation
Minute Ventilation
Minute Ventilation = ___________________ x ____________________
Alveolar Ventilation
What is the best way to increase alveolar minute ventilation, increasing depth or rate of breathing?
Depth Versus Rate

Discuss the contributions of breathing rate and tidal volume to the increased ventilation during
heavy exercise.
Gas Exchange
Ambient Air
Compute the partial pressures of O2, CO2, and N2 of ambient air at sea level (barometric pressure =
760 mm Hg).
Po2 = ___________________ x ___________________
Pco2 = __________________ x ___________________
Pn2 = ___________________ x ___________________

Alveolar Air
Give the average percent of O2, CO2 and N2 in alveolar air at sea level.
O2 =
CO2 =
N2 =
Gas Exchange in the Body

What is the average partial pressure of O2 and CO2 in the alveoli at rest? How does heavy exercise
affect these values?
O2 CO2
Rest
Heavy Exercise
Gas Exchange In the Lungs

List three reasons that account for the dilution of oxygen in inspired air compared to ambient air.
1. 3.
2.
Gas Exchange in the Tissues

Give the average partial pressures of O2 and CO2 in tissues at rest. How does heavy exercise affect
these values?
Oxygen and Carbon Dioxide Transport

Oxygen Transport in the Blood
List two ways for oxygen to transport in the blood.
1.
2.
Oxygen Transport in Physical Solution

For every 100 mL of blood how much oxygen is dissolved?
Oxygen Combined With Hemoglobin (Hb)

Write the formula for the oxygenation of hemoglobin to oxyhemoglobin:
Oxygen-Carrying Capacity of Hemoglobin

List the average hemoglobin values (g per 100 mL blood) for men and women.
Men
Women
Each gram of hemoglobin loosely combines with _______ mL of oxygen.
Po2 and Hemoglobin Saturation

Give the formula for calculating percent saturation of hemoglobin.
The Bohr Effect

List three factors that cause the oxyhemoglobin dissociation curve shift downward and to the right
to facilitate oxygen release.
1. 3.
2.
Components of the Cardiovascular System

List four important functions of the circulatory system.
1. 3.
2. 4.
Heart
What type of muscle makes up the myocardium?
Arteries
What is the main function of the arteries and arterioles?
Capillaries
How long does it take a blood cell to pass through a typical capillary?
Veins
Venous Return
What do veins have that arteries do not have?
A Significant Blood Reservoir

About how blood do the veins contain during rest?
Venous Pooling
Describe venous pooling.
The Active Cool-Down

Why is it always beneficial to actively cool down after exercise compared to lying down in
recovery?
Blood Pressure
Rest
Identify three good places on the body to feel the pulse wave as blood passes through the arterial
system?
1. 3.
2.
During Rhythmic Exercise

Give a typical blood pressure during rhythmic muscular exercise.
During Resistance Exercise

Why shouldn't hypertensive individuals engage in heavy resistance training?
Body Inversion
Discuss whether or not hypertensive individuals should perform body inversion exercises.
In Recovery
Why is aerobic exercise sometimes recommended as a therapy modality for hypertensive
individuals?
Cardiovascular Dynamics During Exercise

Cardiac Output
Write the equation for cardiac output.
Resting Cardiac Output

Untrained Persons
List a typical cardiac output for an untrained man and women?
Man
Women
Endurance Athletes
List a typical cardiac output for an endurance trained man and women?
Man
Women
Exercise Cardiac Output

Give a typical maximum cardiac output for a sedentary person.
Heart Rate During Exercise

Calculate your maximum heart rate.
Cardiac Output Distribution

In the following table show the relative distribution (%) of the cardiac output during rest and
exercise to the skeletal muscles, digestive tract, liver, and kidneys.
Rest Exercise
Muscles
Digestive tract
Liver
Kidneys
PRACTICE QUIZ
1. There are about ______ alveoli per lung: c. volume inspired or expired per breadth
a. 100 million d. same as residual volume
b. 300 million e. none of the above
c. 800 million 4. FVC:
d. 1 billion a. maximum volume expired after
e. none of the above maximum inspiration
2. Inspiration: b. volume in lungs after tidal expiration
a. passive procedure c. same as residual volume
b. active procedure d. decreases due to training
c. does not require energy e. none of the above
d. initiates with heart beat

e. none of the above
5. Partial pressure:
a. gas concentration x solubility
b. gas concentration x % in air
3. Tidal volume: c. gas pressure x volume
a. volume in lungs after tidal expiration d. %concentration x total pressure
b. volume in lungs after inspiration e. none of he above

6. Oxygen combined with hemoglobin:
a. Hb4O8 b. cardiac output x stroke volume

b. HbCO2 c. stroke volume x blood pressure
c. only in venous blood d. heart rate x stroke volume
d. 1.34 mL e. none of the above
e. none of he above 9. True or false: In healthy people, pulse rate
7. Bohr effect: equals heart rate:
a. effects of temperature and pressure on a. T

HbO2 curve b. F
b. effects of oxygen on Hb saturation 10. A normal resting cardiac output:
c. effects of Hb on oxygen curve a. 5000 mL
d. occurs in venous blood only b. 10000 mL
e. none of the above c. 200 mL
8. Blood pressure =: d. 195 beats per minute
a. cardiac output x total peripheral e. none of the above
resistance
LECTURE #9
TRAINING THE ENERGY SYSTEMS
Introduction
Figure 1 illustrates exercise classified in terms of duration and predominant energy pathways. It is difficult
to place certain activities into only one category. For example, as a person increases aerobic fitness, an activity
previously classified as anaerobic
may reclassify as aerobic. In
many cases, all three energy-
transfer systems operate at
different times. Their
contributions to the energy
continuum directly relate to the
duration and intensity (power
output) of the specific activity.
Brief power activities lasting
up to 6-sec rely exclusively on
“immediate” energy generated
from breakdown of stored
intramuscular high-energy
phosphates, ATP and PCr. As all-
out exercise progresses to 1 min
duration and power output
decreases, the major portion of
energy still generates through
anaerobic pathways. These
metabolic reactions involve the
short-term energy system of
glycolysis with subsequent
lactate accumulation. As exercise
intensity diminishes and
duration extends to 2-4 minutes
aerobic ATP production becomes
Figure 1. Classification of physical activity on the basis of duration of allout exercise more important. Prolonged
and the corresponding predominant intracellular energy pathway. exercise progresses on a “pay-
as-you-go” basis, with aerobic
metabolism generating 99% of the energy requirement. The basic approach to physiologic conditioning
applies similarly to men and women within a broad age range: both respond similarly.
Objectives
 Discuss and provide examples of exercise training principles of overload, specificity, individual
differences, and reversibility.
 Outline metabolic adaptations from anaerobic exercise training.
 Describe influences of (1) initial fitness level, (2) genetics, (3) training frequency, (4) training duration,
and (5) training intensity on the response to aerobic training.
 Discuss the rationale for using heart rate to establish exercise intensity for aerobic training.
 Discuss the term “training-sensitive zone.”
 Describe the most common cause of the overtraining syndrome.
Physiological Training Principles

Stimulating functional adaptations that improve performance in specific tasks represents the major
objective of exercise training. These adaptations require adherence to carefully planned programs, with
attention focused on factors such as frequency and length of workouts, type of training, speed, intensity,
duration, and repetition of the activity, rest intervals, and appropriate competition. Application of these
factors varies depending on the performance and fitness goals. However, several principles of physiologic
conditioning remain common to improving performance in the diverse physical activity classifications
illustrated in Figure 1.
Overload Principle
The regular application of a specific exercise overload enhances physiologic function to bring about a
training response. Exercising at intensities higher than normal induces a variety of highly specific adaptations
that enable the body to function more efficiently. Achieving the appropriate overload for each person requires
manipulating combinations of training frequency, intensity, and duration, with specific attention paid to
exercise mode.
The concept of individualized and progressive overload applies to athletes, sedentary people, the
disabled, and even cardiac patients. An increasing number in this latter group have applied appropriate
exercise rehabilitation to walk, jog, and eventually run marathons! Achieving significant health-related
benefits of regular exercise (e.g., metabolic parameters, lipid profile, blood pressure) requires a focus on
accumulation of total exercise and a considerably lower exercise intensity than necessary to improve
cardiovascular fitness.
Specificity Principle
Exercise training specificity refers to adaptations in metabolic and physiologic functions that depend
upon the type of overload imposed. The acronym “SAID” – specific adaptations to imposed demands,
describes this principle. A specific anaerobic exercise stress (e.g., strength-power training) induces specific
strength-power adaptations, while specific endurance exercise stress elicits specific aerobic system
adaptations — with only a limited interchange of benefits derived between strength-power and aerobic
training. However, the specificity principle extends beyond this broad demarcation. For example, “aerobic
training” does not represent a singular entity requiring only cardiovascular overload. Aerobic training
utilizing the specific muscles in the desired performance most effectively improves aerobic fitness for
activities like swimming, bicycling, running, or upper-body exercise. Some evidence even suggests a
temporal specificity in training response such that indicators of training improvement reach there highest
when measurements take place at the time of day training regularly occurred. Furthermore, the most effective
evaluation of sport-specific performance results when the laboratory measurement most closely simulates the
actual sport activity and/or activates the muscle mass required by the sport. Simply stated, specific exercise
elicits specific adaptations creating specific training effects (SAID).
Individual Differences Principle

Many factors contribute to individual variation in the training response. For example, a person’s relative
fitness level at the start of training exerts an influence. Even for a relatively homogenous group who starts
exercise training together, one cannot expect different people who start exercise training together all
individuals to reach the same “state” of fitness (or performance) after 10 or 12 weeks. Consequently, a coach
should not insist that all athletes on the same team (or even in the same event) train the same way or at the
same relative or absolute exercise intensity. It also is unrealistic to expect all individuals to respond to a given
training stimulus in precisely the same manner.
Reversibility Principle
Loss of physiologic and performance adaptations (detraining) occurs rapidly when a person terminates
participation in regular exercise. Only 1 or 2 weeks of detraining significantly reduces both metabolic and
exercise capacity, with many training improvements totally lost within 8 weeks. One research group provides
particularly interesting findings. In five subjects confined to bed for 20 consecutive days, VO 2max decreased by
25% (1% per day). This decrease accompanied a similar decrement in maximal stroke volume and cardiac
output. Additionally, the number of capillaries within trained muscle decreases between 14 and 25% within 3
weeks after training ceased. For elderly subjects, 4 months of detraining results in the complete loss of
adaptations in the cardiovascular system.
Even among highly trained athletes, the beneficial effects of many years of prior exercise training remain
transient and reversible. For this reason, most athletes begin a reconditioning program several months prior
to the start of the competitive season, or maintain some moderate level of off-season, sport-specific exercise to
blunt the decline in physiologic functions during deconditioning.
Physiologic Consequences of Training

The following section present a listing of the diverse adaptations in response to anaerobic and aerobic
exercise training outlined in Table 1.
Table 1. Typical Metabolic and Physiologic Values for Health, Trained
and Untrained Men.
Variable Untrained Trained Percent Diff
Glycogen, mM 85.0 120 41
# mitochondria, mMol 0.59 1.20 103
Mitochondrial volume,%muscle 2.15 8.0 272
Resting ATP, mM 3.0 6.0 100
Resting creatine, mM 10.7 14.5 35
Aerobic Enzymes, SDH 5-10 15-20 133
Max stroke volume mL/b 120 180 50
Resting HR, b/min 70 40 -43
Max Cardiac output, L/min 20 30-40 75
Max Heart rate, b/min 190 180 -5
Max a-v O2diff, mL/dL 14.5 16.0 10
VO2max, mL/kg/min 30-40 65-80 107
Anaerobic System Changes With Training

Consistent with the concept of training specificity, activities that demand a high level of anaerobic
metabolism bring about specific changes in the immediate and short-term energy systems, without a
concomitant increase in aerobic functions. The changes that occur with sprint-power training include:
 Increased levels of anaerobic substrates. As determined from muscle biopsies taken before and after
resistance training, significant increases in the trained muscle’s resting levels of ATP, PCr, free creatine,
and glycogen accompanied a 28% improvement in muscular strength.
 Increased quantity and activity of key enzymes that control anaerobic-phase glucose catabolism. These
changes do not reach the magnitude observed for oxidative enzymes with aerobic training. The most
dramatic increases in anaerobic enzyme function and fiber size occur in the fast-twitch muscle fibers.
 Increased capacity to generate high levels of blood lactate during all-out exercise. An enhanced lactate-
producing capacity probably results from: (1) increased levels of glycogen and glycolytic enzymes, and
(2) improved motivation and “pain” tolerance to fatiguing exercise.
Aerobic System Changes With Training

Table 2 illustrates that aerobic overload training induces significant adaptations in a variety of functional
capacities related to oxygen transport and utilization. With an adequate training stimulus, the majority of
these responses occur independent of gender and age. Many of the training-induced aerobic adaptations also
occur in coronary heart disease patients undergoing high-intensity aerobic training.
Table 2. Physiologic factors that affect aerobic conditioning.
Ventilation-Aeration Active Muscle Central Blood Peripheral Blood

Metabolism Flow Flow
 Minute ventilation  Enzymes and  Cardiac output  Flow to nonactive

 Ventilation:perfusion oxidative potential (heart rate, stroke regions
ratio  Energy stores and volume)  Arterial vascular
 Oxygen diffusion substrate availability  Arterial blood reactivity
capacity  Myoglobin pressure  Muscle blood flow
 Hb-O2 affinity concentration  Oxygen transport  Muscle capillary
 Mitochondria size capacity density
 Arterial oxygen
saturation and number  Muscle vascular
 Active muscle mass conductance
 Muscle fiber type  Oxygen extraction
 Venous compliance
and reactivity
Aerobic Metabolic Adaptations

Aerobic training significantly improves the capacity for respiratory control in skeletal muscle.
Metabolic Machinery
The primary effect of endurance training produces an increase in muscle mitochondrial capacity. The
results of many different experiments indicate that mitochondria do not increase in specific activity per se,
rather, trained skeletal muscle contains larger and more numerous mitochondria but its activity remains the
same as less active muscle fibers. The exact training stimuli (intensity, time, recovery, etc.) resulting in more
mitochondria remains a central focus of current research.
Fat Metabolism
Endurance training increases an individual’s capacity to mobilize, deliver, and oxidize fatty acids for
energy during submaximal exercise. Enhanced fat catabolism with aerobic training becomes particularly
apparent at the same absolute submaximal exercise workload whether under fed or fasted conditions.
Impressive increases also occur in the trained muscle’s capacity to utilize intramuscular triglycerides as the
primary source for fatty acid oxidation. A more lively, training-induced lipolysis (fat use) results from:
 Greater blood flow within trained muscle
 Enhanced quantity of fat-mobilizing and fat-metabolizing enzymes
 Enhanced muscle mitochondrial respiratory capacity (see above)
 Blunted catecholamine release for the same absolute power output after training
Carbohydrate Metabolism
Reduced total carbohydrate utilization in submaximal exercise with endurance training results from the
combined effects of (1) decreased muscle glycogen utilization, and (2) reduced production (decreased hepatic
glycogenolysis and gluconeogenesis) and utilization of plasma-borne glucose. Fatty acid oxidation combined
with a reduced level of carbohydrate metabolism contributes to blood glucose homeostasis and improved
endurance capacity following aerobic training. Training-enhanced hepatic gluconeogenic capacity further
provides resistance to hypoglycemia during prolonged exercise.
Muscle Fiber Type and Size

Aerobic training elicits metabolic adaptations in each type of muscle fiber. The basic fiber type probably
does not “change” to any great extent, but, rather, all fibers maximize their already-existing aerobic potential.
Selective hypertrophy occurs in the different muscle fiber types in response to specific overload training.
Highly trained endurance athletes have larger slow-twitch fibers than fast-twitch fibers in the same muscle.
Conversely, the fast-twitch fibers of athletes trained in anaerobic-power activities occupy a much greater
portion of the muscle’s cross-sectional area.
Cardiovascular Adaptations
Table 3 summarizes the most important adaptations in cardiovascular function with aerobic exercise
training that increase the delivery of oxygen to active muscle. Because of the intimate linkage of the
cardiovascular and pulmonary systems to aerobic processes, endurance training produces significant
dimensional and functional cardiovascular adaptations.
Table 3. Adaptations in cardiovascular function with aerobic exercise training that

increases oxygen delivery to active muscles.
• Increase plasma volume • Increase ejection fraction
• Increase red blood cell mass • Increase maximum stroke volume
• Increase total blood volume • Increase maximum cardiac output
• Increase ventricular compliance • Optimize peripheral blood flow
• Increase internal ventricular dimensions • Increase blood flow to active muscle
• Increase venous return • Increase end diastolic volume
• Increase myocardial contractility • Increase effectiveness of cardiac output •
Decrease heart rate (12-15 b/min) distribution
The most important of the above changes resulting from training include:
 Decreased exercise heart rate at a given load
 Increased resting stroke volume resulting from enhanced left ventricular function
 Increased exercise stroke volume including maximum stroke volume
 Increased maximum cardiac output

 Increased maximum oxygen extraction
 Enhanced blood flow redistribution
 Increased blood flow to the heart
 Decreased blood pressure

PSYCHOLOGICAL BENEFITS
Significant potential benefits on psychological state emerge from regular exercise
(either aerobic or resistance training), regardless of age. Adaptations include a
reduction in state anxiety and blood pressure, decreased level of mild to moderate
depression, reduction in neuroticism, and improved mood, self-esteem, self-concept,
and general perception of personal worth, often to an extent equal to that achieved
with other therapeutic interventions including pharmacologic therapy.
Factors That Affect the Aerobic Training Response
Four factors significantly influence the aerobic training response:
1. Initial level of aerobic fitness 3. Training frequency
2. Training intensity 4. Training duration
Initial Level of Aerobic Fitness

The magnitude of the training response depends upon one’s initial fitness level. Someone who rates low at
the start has considerable room for improvement. If capacity already rates high, the magnitude of
improvement usually remains relatively small. Studies of sedentary, middle-aged men with heart disease
showed that VO2max improved by 50%, while similar training in normally active, healthy adults elicited a 10 to
15% improvement. Of course, a 5% improvement in aerobic capacity represents as crucial a change for elite
athlete as a 40% increase for the sedentary person. As a general guideline, aerobic fitness improvements
generally range between 5 to 25% with systematic programs of endurance training. A portion of this
improvement occurs within the first week of training.102
Training Intensity
Training-induced physiologic adaptations depend primarily on the intensity of overload. There are at least
seven different expressions of exercise intensity:
1. As energy expended per unit time (e.g., 9 kcal•min-1 or 37.8 kJ•min-1).
2. As absolute exercise level or power output (e.g., cycle at 900kg-m•min-1 or 147 W).
3. As relative metabolic level expressed as percentage of VO2max (e.g., 85% VO2max).
4. As exercise below, at, or above the lactate threshold (e.g., 4 mmol lactate).
5. As exercise heart rate or percentage of maximum heart rate (e.g., 180 b•min -1 or 80% HRmax).
6. As multiples of resting metabolic rate (e.g., 6 METs).
7. As rating of perceived exertion (e.g., RPE = 14).

An example of absolute training intensity involves having all individuals exercise at the same power
output or energy expenditure (e.g., 9.0 kcal•min-1) over a 30-minute exercise session. When everyone
exercises at the same exercise intensity, however, the task may pose a considerable stress for one person yet
fall short of the training threshold for another more fit person. For this reason, the relative stress on a person’s
physiologic systems is usually used. Consequently, the assigned exercise intensity usually relates to some
break point for steady-rate exercise (e.g., lactate threshold, OBLA) or some percentage of maximum
physiologic capacity (e.g., VO2max, HRmax, or maximum exercise capacity. The general practice establishes
aerobic training intensity via direct measurement (or estimation) of VO2max (or HRmax), followed by assigning
an exercise level that corresponds to some percentage of these maximums.
Although establishing training intensity from measures of oxygen consumption provides a high degree of
accuracy, its use requires sophisticated equipment and thus becomes impractical for the general population.
An effective alternative uses heart rate to classify exercise for relative intensity when establishing the training
protocol. Use of exercise heart rate becomes possible because %VO2max and %HRmax relate in a predictable way
regardless of gender, fitness level, or age. <tbl21.7>Table 21.7 presents selected values for %VO 2max and
corresponding %HRmax obtained from several sources. The error in estimating %VO2max from %HRmax, or vice
versa, equals about ±8%. Thus, one need only monitor heart rate to estimate the relative exercise stress or
%VO2max, within the given error range. The relationship between %HRmax and %VO2max remains essentially the
same for arm or leg exercises among healthy subjects, normal weight and obese groups, cardiac patients, and
people with spinal cord injuries. Importantly, however, arm (upper-body) exercise produces significantly
lower HRmax compared to leg exercises.
Train at a Percentage of HRmax

As a general rule, aerobic capacity improves if exercise intensity regularly increases heart rate to at least 55
to 70% of maximum. During lower-body exercise like cycling, walking, or running, this heart rate increase
equals about 45 to 55% of the VO2max, or, for college-aged men and women a heart rate of 120 to 140 b•min-1.
An alternative and equally effective method for establishing the training threshold, termed the Karvonen
method has subjects exercise at a heart rate equal to 60% of the difference between resting and maximum.
With the Karvonon method heart rate computes as follows:
HRthreshold = HRrest + 0.60 (HRmax – HRrest)
This approach to determining heart rate training threshold gives a somewhat higher value compared to
computing the threshold heart rate simply as 70% HRmax.
Clearly, positive training adaptations do not require strenuous levels of exercise. An exercise heart rate of
70% maximum represents “moderate” exercise with little or no discomfort for most healthy people. This
training level, frequently referred to as “conversational exercise,” reaches sufficient intensity to stimulate a
training effect, yet does not produce a level of discomfort that limits a person from talking during the
workout. This conversational exercise level indicates a lack of heavy breathing associated with lactic acidosis
induced hyperpnea, a level of exercise where individuals can no longer talk and exercise comfortably. A
previously sedentary person need not exercise above this heart rate to improve physiologic capacity.
The “Training-Sensitive Zone”

One can determine maximum
exercise heart rate immediately
after several minutes of all-out
effort in a specific form of exercise.
This exercise intensity requires
considerable motivation and stress
—a requirement certainly
inadvisable for adults without
medical clearance, particularly
individuals predisposed to
coronary heart disease.
Consequently, people should
consider themselves “average” and
use the age-predicted maximum
heart rates presented in Figure 2.
Although individuals of a
specific age possess varying HRmax
values, the inaccuracy resulting
from individual variation (±10
b•min-1 standard deviation for any
age-predicted HRmax) has little Figure 2. Maximum heart rates and the training sensitivity zone for use in
influence in establishing effective aerobic training of men and women of different ages.
training for healthy people.
Maximum heart rate computes as 220 minus the person’s age in years, with values independent of race or
gender in children and adults.
HRmax + 220 – age, y
Although this formula represents a convenient “rule of thumb,” it does not determine a specific person’s
maximum heart rate. Within normal variation, the maximum heart rate of 95% (±2 standard deviations) of 40-
year-old men and women ranges between 160 and 200 b•min-1. Figure 2 also depicts the “training-sensitive
zone” in relation to age. Conditioning the aerobic systems occurs as long as exercise heart rate remains within
this zone.
A 40-year-old woman or man desiring to train at moderate intensity but still achieve the threshold level
would select a training heart rate equal to 70% of age-predicted HRmax, or a target exercise heart rate of 126
b•min-1 (0.70 x 180). Then, using progressive increments of light to moderate exercise, the person achieves a
walking, jogging, or cycling intensity that produces this heart rate. To increase training to 85% of maximum,
exercise intensity must increase to produce a heart rate of 153 b•min-1 (0.85 x 180).
Is Strenuous Training More Effective?

Generally, the higher the training intensity above threshold, the greater the training improvement,
particularly for VO2max. Although there exists a minimal “threshold” intensity below which a training effect
does not occur, there may also exist a “ceiling” above which no further gains accrue. More fit men and
women generally require higher threshold levels to stimulate a training response than less fit counterparts.
The ceiling for training intensity remains unknown, although 85% VO2max (corresponding to 90% HRmax)
probably represents an upper limit. Importantly, however, regardless of the exercise level selected, more does
not necessarily produce greater results. Excessive intensity of physical training and abrupt increases in
training volume increase the risk for injury to bones, joints, and muscles.
Is Less Intense Training Effective?

The often cited recommendation of 70% HRmax as a training threshold for aerobic improvement represents
a general guideline for effective, yet comfortable exercise. The actual lower limit may depend on the
participant’s initial exercise capacity and current state of training. In addition, older and less fit, and
sedentary, overweight men and women show training thresholds closer to 60% HRmax, which corresponds to
about 45% VO2max. Twenty to 30 minutes of continuous exercise at the 70% HRmax level stimulates a training
effect; exercise at the lower intensity of 60% for 45
minutes also proves beneficial. Generally, a longer
exercise duration offsets a lower exercise intensity.
Train at a Perception of Effort

In addition to oxygen consumption, heart rate, and
blood lactate as indicators of exercise intensity, one also
can use the rating of perceived exertion (RPE). Using
this psycho-physiological approach, the exerciser rates
on a numerical scale (Borg scale, after the researcher
who developed this system) perceived feelings in
relation to the exertion level.
Monitoring and adjusting RPE during exercise
represents a relatively easy and effective means for
prescribing exercise based on an individual’s perception
of effort that coincides nicely with objective measures of
physiologic/metabolic strain (%HRmax, %V02max, blood
lactate concentration). Exercise levels corresponding to
higher levels of energy expenditure and physiologic
strain produce higher RPE ratings. For example, an RPE
of 13 or 14 (exercise that feels “somewhat hard;” Figure
4) coincides with about 70% HRmax during cycle Figure 3. Borg perceived exertion scale.
ergometer and treadmill exercise; an RPE between 11
and 12 corresponds to exercise at the lactate threshold for trained and untrained individuals. The RPE
establishes an exercise prescription for exercise intensities corresponding to blood lactate concentrations of 2.5
mM (RPE - 15) and 4.0 mM (RPE - 18) during a 30 min treadmill run where subjects self regulated exercise
intensity. Individuals learn quickly to exercise at a specific RPE.
Training Duration
A threshold duration per workout has not been identified for optimal aerobic improvement. This
threshold probably depends on the interaction of many factors including total work accomplished (duration
or training volume), exercise intensity, training frequency, and initial fitness level. Whereas 3- to 5 minute
daily exercise periods produce training effects in some poorly conditioned people, 20- to 30-minute exercise
sessions achieve more optimal results (within practicality for time) if intensity reaches at least 70% HR max.
With higher-intensity training, significant improvements occur with only a 10-minute workout. Conversely, it
requires at least 60 minutes of continuous exercise to produce a training effect when exercise intensity falls
below 70% HRmax.
As for training volume, more does not necessarily produce greater results. In a study of collegiate
swimmers, for example, one group trained for 1.5 hours daily while another group performed two 1.5-hour
exercise sessions each day. Despite one group exercising at twice the daily exercise volume, no differences in
swimming power, endurance, or performance time improvements emerged between groups.
Training Frequency
Does 2 or 5 day-a-week training produce differing effects if exercise duration and intensity remain
constant for each training session?
Improvements in VO2max over time Unfortunately, the precise answer remains
elusive. Some investigators report that
4.4 training frequency significantly influences
4.2 cardiovascular improvements while others
4
maintain that this factor contributes
VO2max (L/min
3.8
considerably less than either exercises
intensity or duration. Studies using interval
3.6
training showed that training 2 days per
3.4
week produced VO2max changes similar in
3.2
magnitude to those when training 5 days per
3
0 1 2 3 4 5 6 7 8 9 10
week. In other studies that held total exercise
Training Duration (weeks) volume constant, no differences emerged in
VO2max improvements between training
Figure 4. Absolute and percentage improvement in VO2max. frequencies of 2 versus 4, or 3 versus 5 days
per week. As in the case with training
duration, more frequent training becomes beneficial when training at a lower intensity.
While the extra time invested to increase training frequency may not prove profitable for improving
physiologic function, the extra quantity of exercise (e.g., 3- vs. 6-day per week training) often represents a
considerable caloric expenditure. To affect meaningful weight loss through exercise, each exercise session
should last at least 60 minutes at a sufficient intensity to expend 300 kcal or more. Training only one day per
week generally does not produce meaningful changes in anaerobic or aerobic capacity, body composition, or
weight loss.
Typical aerobic exercise training programs take place 3 days per week with a rest day usually spaced
between workout days. One could reasonably question whether training on consecutive days would produce
equally effective results? In an experiment concerned with this exact question, nearly identical improvements
in VO2max occurred regardless of sequencing of the 3-day-per-week training schedule. This finding suggests
that the stimulus for aerobic training links closely to exercise intensity and total work accomplished and not
to the sequencing of training days.
Exercise Mode
Holding exercise intensity, duration, and frequency constant produces a similar training response,
regardless of training mode—as long as the exercise involves relatively large muscle groups. Bicycling,
walking, running, rowing, swimming, in-line skating, rope skipping, bench stepping, stair climbing, and
simulated arm-leg climbing all provide excellent overload for the aerobic system. Of course, based on the
specificity concept, the magnitude of training improvement varies considerably depending on the mode of
testing. Individuals trained on a bicycle show greater improvements when tested on the bicycle than on the
treadmill.195 Likewise, individuals who train by swimming or arm cranking show the greatest improvements
when measured during upper-body exercise.
How Long Before Improvements Occur?

The answer to the above question depends on the specific biologic systems affected by training. Aerobic
fitness adaptations occur rapidly, with significant improvements noted within several weeks.
Figure 4 shows improvements in VO2max for subjects who trained 6 days per week for 10 weeks. Training
consisted of stationary cycling for 30 minutes 3 days per week combined with running for up to 40 minutes
alternate days. The continuous week-to-week change in aerobic capacity indicates that training improvements
in previously sedentary people occur rapidly and progress in relatively steady fashion. Of course, adaptive
responses to training eventually level off as subjects approach their “genetically predisposed” maximums.
The exact time for this leveling off remains unknown, particularly for those undergoing high-intensity
training.
Trainability and Genes

While a vigorous exercise-training program enhances a person’s level of fitness regardless of genetic
background, the limits for developing fitness capacity link closely to genetic endowment. For two individuals
undertaking the same exercise program, one person might show 10 times more improvement than the other.
Research in genetics indicates a genotype dependency for much of our sensitivity in responding to maximal
aerobic and anaerobic power training, including the adaptations of most muscle enzymes. In other words,
both members of an identical twins pair generally show a similar magnitude in training response. If one twin
showed high responsiveness to training, a high likelihood existed that the other twin would also behave as a
responder; similarly, the brother of a nonresponder to exercise training generally showed little improvement.
Presence of the muscle-specific creatine kinase gene provides one example of the possible contribution of
genetic makeup to individual differences in the responsiveness of VO2max to endurance training. Genetic
makeup plays such a predominant role in training responsiveness that it is almost impossible to predict a
specific individual’s response to a given training stimulus.
Maintenance of Aerobic Fitness Gains

An important question concerns the optimal frequency, duration, and intensity of exercise required to
maintain aerobic improvements with training. In one study, healthy young adults increased VO 2max 25% with
10 weeks of interval training by bicycling and running 40 minutes, 6 days a week. They then joined one of two
groups that continued to exercise an additional 15 weeks at the same intensity and duration but at a reduced
frequency of either 4 or 2 days a week. Both groups maintained their gains in aerobic capacity despite as
much as a two-thirds reduction in training frequency.
A similar study evaluated the effect of reduced training duration on the maintenance of improved aerobic
fitness. Upon completion of the same protocol outlined above for the initial 10 weeks of training, the subjects
continued to maintain intensity and frequency of training for an additional 15 weeks, but reduced training
duration from the original 40-minute sessions to either 26- or 13-minutes per day. They maintained almost all
VO2max and performance increases despite a two-thirds reduction in training duration. However, if intensity
of training decreased and frequency and duration remained constant, even a one-third-exercise intensity
reduction caused a significant decline in VO2max.
It appears that aerobic capacity improvement involves somewhat different training requirements than its
maintenance. With intensity held constant, the frequency and duration of exercise required to maintain a
certain level of aerobic fitness remains considerably less than that required for its improvement. A small drop
off in exercise intensity, on the other hand, reduces VO2max. This indicates that exercise intensity plays a
principal role in maintaining the increase in aerobic power achieved through training.
Fitness components other than VO2max more readily suffer adverse effects of reduced exercise training
volume. Well-trained endurance athletes who normally trained 6 to 10 hours a week reduced weekly training
to one 35-minute session showed no decrease in VO2max over a 4-week period. However, their endurance
capacity at 75% VO2max significantly decreased, which related to reduced pre-exercise glycogen stores and a
diminished level of fat oxidation during exercise. Such findings indicate that single measure like VO 2max
cannot adequately evaluate all factors that affect training and detraining adaptations.
Methods of Training
Each year, performance improvements occur in almost all athletic competitions. These advances generally
relate to increased opportunities for participation: individuals with “natural endowment” more likely become
exposed to particular sports. Also, improved nutrition and health care, better equipment, and more
systematic and scientific approaches to athletic training contribute to superior performance.
In the following sections I present general guidelines for anaerobic and aerobic training, with particular
emphasis on three general training classifications: (1) interval training, (2) continuous training, and (3) fartlek
training.
Anaerobic Training
Figure 1 demonstrated that the capacity to perform all-out exercise for up to 60 seconds duration largely
depends on ATP generated by the immediate and short-term anaerobic energy systems.
The Intramuscular High-Energy Phosphates

Sports such as football, weightlifting, and other brief, sprint-power activities rely almost exclusively on
energy derived from ATP and PCr that comprise the muscles’ high-energy phosphates. Engaging specific
muscles in repeated maximum bursts of effort for 5- to 10-second duration overloads this phosphagen pool.
Because the intramuscular high-energy phosphates supply energy for brief, intense exercise, only small
amounts of lactate accumulate and recovery progresses rapidly (alactic recovery oxygen consumption). Thus,
exercise can begin again after about a 30-second rest period. The use of brief, all-out exercise interspersed
with recovery represents a specific application of interval training to anaerobic conditioning.
The activities selected in training to enhance ATP-PCr energy transfer capacity must engage the specific
muscles at the movement speed and power output for which the athlete desires improved anaerobic power.
Not only does this enhance the metabolic capacity of the specifically trained muscle fibers, but it also
facilitates recruitment and modulation of firing sequence of the appropriate motor units activated in the
actual movement.
Lactate–Generating Capacity
As duration of all-out effort extends beyond 10-seconds duration, dependence on anaerobic energy from
the intramuscular high-energy phosphates decreases with a proportionate increase in the magnitude of
anaerobic energy from glycolysis. To improve energy transfer capacity by the short-term lactic acid energy
system, training must overload this aspect of energy metabolism.
Anaerobic training requires extreme physiological and psychological demands and considerable
motivation. Repeated bouts of up to 1-minute maximum exercise stopped 30 seconds before subjective
feelings of exhaustion cause blood lactate to increase to near-maximum levels. The individual repeats each
exercise bout after 3 to 5 minutes of recovery. Repetition of exercise causes a “lactate stacking,” which results
in a higher blood lactate level than achieved with just one bout of all-out effort to exhaustion. Of course, as
with all training, one must exercise the specific muscle groups that require enhanced anaerobic capacity. A
backstroke swimmer trains by swimming the backstroke, a cyclist should bicycle, and basketball, hockey, or
soccer players rapidly perform various movements and direction changes similar to those required by the
demands of their sport.
Recovery requires considerable time when exercise involves a significant anaerobic component. For this
reason, anaerobic power training should occur at the end of the conditioning session. Otherwise, fatigue
might carry over and perhaps hinder one’s ability to perform subsequent aerobic training.
Aerobic Training
Figure 5 indicates two important
factors in formulating an aerobic
training program: Training must
provide a sufficient cardiovascular
overload to stimulate increases in
stroke volume and cardiac output. The
central circulatory overload must
result from exercising the sport-
specific muscle groups to enhance
their local circulation and “metabolic
machinery.” In essence, proper
endurance training overloads all
components of oxygen transport and
utilization. This consideration
embodies the specificity principle as
applied to aerobic training. Simply
stated, runners should run, cyclists
should bicycle, rowers should row,
and swimmers should swim.
Relatively brief bouts of repeated
exercise (interval training), as well as
continuous, long-duration efforts
(continuous training), enhance aerobic
capacity, provided exercise reaches sufficient Figure 5. The two major goals of aerobic training: Goal #1 –
intensity to overload the aerobic system. Interval develop the capacity of the central circulation to deliver
training, continuous training, and fartlek oxygen; Goal #2 – Enhance the capacity of the active
musculature to supply and process oxygen.
training represent three common methods to
improve aerobic fitness.
Interval Training
With correct spacing of exercise and rest, one can perform extraordinary amounts of high-intensity
exercise, normally not possible if the exercise progressed continuously. The repeated exercise bouts (with rest
periods or relief intervals) vary from a few seconds to several minutes or longer depending on the desired
training outcome. The interval training prescription evolves from the following considerations:
 Intensity of exercise interval
 Duration of exercise interval
 Length of recovery interval

 Number of repetitions of the exercise-recovery cycle
Consider the following example of the ability to perform a considerable volume of high-intensity exercise
during an interval-training workout. Few people can maintain a 4-minute-mile pace for longer than 1 minute,
let alone complete a mile within 4 minutes. Suppose we limited running intervals to only 10 seconds,
followed by 30 seconds of recovery. This scenario makes it reasonably easy to maintain these exercise-rest
intervals and complete the mile in 4 minutes of actual running. Although this does not parallel a world-class
performance, the example does indicates that a person can accomplish a significant quantity of normally
exhausting exercise given proper spacing of rest and exercise intervals.
Rationale for Interval Training

Interval training has a sound basis in physiology and energy metabolism. In the example of a continuous
run at a 4-minute-mile pace, a large portion of energy derives from anaerobic glycolysis. Within a minute or
two, the lactate level rises precipitously and the runner fatigues. During interval training, on the other hand,
repeated 10-second exercise bouts permit completion of intense exercise without appreciable lactate buildup
because the intramuscular high-energy phosphates provide the primary exercise energy source. Minimal
fatigue results during the predominantly “alactic” exercise interval and recovery progresses rapidly. The
exercise interval can then begin after only a brief rest.
The two factors are used in formulating an interval training programs include
 Exercise interval
 Relief interval
Continuous Training
Continuous or long slow distance (LSD) training involves steady-paced, prolonged exercise at either
moderate or high aerobic intensity, usually between 60 to 80% VO2max. The exact pace can vary, but it must at
least meet a threshold intensity to ensure aerobic physiologic adaptations. Continuous training for an hour or
longer has become popular among joggers and other fitness enthusiasts including competitive endurance
athletes such as triathletes and cross-country skiers. For example, some elite distance runners train twice a
day and run between 100 and 150 miles each week while preparing for competition. In one report, a man
training for the 52.5 mile ultramarathon ran twice daily, 20 miles in the morning and 13 miles in the evening;
he interspersed these runs with occasional 30- to 60-mile non-stop runs at a 7- to 8-minute per mile pace.
Within this schedule, he ran more than 800 miles each month and totaled 9600 miles for the year! The precise
benefits of such considerable training remain unknown.
Because of its submaximum nature, continuous exercise training progresses for a considerable time in
relative comfort. This contrasts with the potential hazards of high-intensity interval training for coronary-
prone individuals and the high level of motivation required for such strenuous exercise. Continuous training
ideally suits those beginning an exercise program or wishing to accumulate a large caloric expenditure for
weight loss. When applied in athletic training, continuous training actually represents “over-distance”
training, with most athletes training two to five times the actual distances of competitive events.
An advantage of continuous training for endurance athletes permits exercising at nearly the same
intensity as actual competition. Because specific motor unit recruitment depends on exercise intensity,
continuous training may best apply to endurance athlete in terms of adaptations at the cellular level. This
contrasts to interval training that often places disproportionate stress on the fast-twitch motor units, not the
slow-twitch units predominantly recruited in endurance competition.
Fartlek Training
Fartlek, a Swedish word means “speed play,” represents a training method introduced to the United
States in the 1940s. This relatively “unscientific” blending of interval and continuous training has particular
application to exercise out-of-doors over natural terrain. The system utilizes alternate running at fast and
slow speeds over both a level and hilly course.
In contrast to the precise exercise interval training prescription, fartlek training does not require systematic
manipulation of the exercise and relief intervals. Instead, the performer determines the training schema based
on “how it feels” at the time, in a way similar to gauging exercise intensity based on one’s rating of perceived
exertion. If used properly, this method can overload one or all of the energy systems. Although lacking the
systematic and quantified approaches of interval and continuous training, fartlek training provides an ideal
means for general conditioning and off-season training. It also maintains a certain “freedom” and variety in
workouts.
Insufficient evidence prevents proclaiming superiority of any specific training method for improving
aerobic capacity. Each form of training produces success. One can probably use the various methods
interchangeably, particularly to modify training and achieve a more psychologically pleasing exercise
program.
Overtraining: Too Much of a Good Thing

With significant increases in heavy and prolonged exercise training over the past 15 years, particularly in
high-volume endurance sports, as many as 10 to 20% of athletes experience the syndrome of overtraining or
“staleness.” As a result of a complex interaction of biological and psychological influences, the athlete fails to
endure and adapt to training, normal exercise performance deteriorates, and the individual encounters
increasing difficulty fully recovering from a workout. This takes on crucial importance for elite athletes where
performance decrements of from 1 to 3% might cause a gold medallist to fail to qualify for competition.
Two clinical forms of overtraining have been described:
1. The less common sympathetic form, characterized by increased sympathetic activity during rest.
Generally typified by hyper-excitability, restlessness, and impaired exercise performance. This form of
overtraining may reflect the result of excessive psychological/ emotional stress that accompanies the
interaction among training, competition, and responsibilities of normal living.
2. The more common parasympathetic form, characterized by predominance of vagal activity during rest
and exercise. More properly termed “overreaching” in the early stages (within as few as 10 days), the
syndrome is qualitatively similar in symptoms to the full-blown parasympathetic overtraining
syndrome but of shorter duration. Overreaching generally results from excessive and protracted
overload with inadequate recovery and rest. Initially, maintenance of exercise performance requires
greater effort, which eventually leads to performance deterioration in training and competition. Short-
term rest intervention of a few days up to several weeks usually brings about full recovery. Untreated
overreaching eventually leads to the overtraining syndrome.
Parasympathetic overtraining syndrome represents more than just short-term inability to train as hard as
usual or a slight dip in competition-level performance. Rather, it involves chronic fatigue experienced during
exercise workouts and subsequent recovery periods. Associated symptoms include sustained poor exercise
performance, altered sleep patterns and appetite, frequent infections, persistent high fatigue ratings, altered
immune and reproductive function, acute and chronic alterations in systemic inflammatory responses, mood
disturbances (anger, depression, anxiety), and a general malaise and loss of interest in high-level training.
Injuries occur more frequently in the overtrained state. The syndrome may also result from complex
interactions and subsequent effects of acute and chronic alterations in systemic inflammatory responses.

THE OVERTRAINING SYNDROME: SYMPTOMS OF STALENESS
• Unexplained and persistently poor performance and high fatigue ratings
• Prolonged recovery from typical training sessions or competitive events
• Disturbed mood states characterized by general fatigue, apathy, depression,
irritability, and loss of competitive drive
• Persistent feelings of muscle soreness and stiffness in muscles and joints
• Elevated resting pulse, painful muscles, and increases susceptibility to upper
respiratory infections (altered immune function) and gastrointestinal disturbances
• Insomnia
• Loss of appetite, weight loss, and inability to maintain proper body weight for
competition
• Overuse injuries
Significant effects of overtraining include: (1) functional impairments in the hypothalamo-pituitary-

gonadal and adrenal axis, and sympathetic neuroendocrine system as reflected by depressed urinary
excretion of norepinephrine, and (2) exercise-induced increase in adrenocorticotropic hormone and growth
hormone and depressed values of cortisol and insulin. In some ways the syndrome reflects the body’s attempt
to enforce upon the athlete an appropriate recuperative period from the sustained levels of arousal caused by
prolonged heavy training and competition. No simple, reliable method exists to diagnose overtraining in its
earliest stages, although deterioration in physical performance and alterations in mood state rather than
immune function changes provide the best indications. Conditions that cause some athletes to thrive in
training initiate overtraining in other athletes. Generally, when symptoms emerge they persist unless the
athlete rests, with complete recovery requiring weeks or even months. Currently, no reliable method exists to
determine the point of complete recovery from the overtraining syndrome.

1. Age-predicted maximum heart rate
2. Anaerobic energy system
3. Continuous training
4. Fartlek training
5. Health-related fitness
6. HR threshold = HRrest + 0.60 (HRmax - HRrest)
7. Individual differences principle
8. Interval training
9. LSD training
10. Overload principle
11. Overtraining syndrome

12. Rating of perceived exertion (RPE)
13. Reversibility principle
14. SAID principle
15. Training-sensitive zone
STUDY QUESTIONS
Physiological Training Principles

List three sports requiring high levels of aerobic energy transfer and three sports requiring high
levels of anaerobic energy transfer.
Aerobic Anaerobic
1.
2.
3.
Overload Principle
List four variables manipulated to achieve exercise overload.
1. 3.
2. 4.
Specificity Principle
Briefly describe training specificity.
Individual Differences Principle

Give one example why the principle of individual differences is important in formulating an
exercise program.
Reversibility Principle
Describe the reversibility principle in 10 words or less (Hint: Use it or……….)
Anaerobic System Changes With Training

List three physiologic changes that occur with sprint- and power-type training.
1. 3.
2.
Aerobic System Changes With Training

List six specific physiologic factors that affect aerobic conditioning.
1. 4.
2. 5.
3. 6.
Metabolic Machinery
List five metabolic adaptations that enhance aerobic training.
1. 4.
2 5.
Fat Metabolism
Give two reasons for increased lipolysis with aerobic training.
1.
2.
Carbohydrate Metabolism
List two reasons for enhanced carbohydrate breakdown with aerobic training.
1.
2.
Muscle Fiber Type and Size

Which muscle fiber shows the greatest hypertrophy with aerobic training?
List five variables that change with aerobic training and give the direction of change (+ or -)
1. 4.
2. 5.
3.
Factors That Affect the Aerobic Training Response

List four factors that influence the response to aerobic conditioning.
1. 3.
2. 4.
Initial Level of Aerobic Fitness

How much can VO2max be expected to improve during a 12-week aerobic training program?
Training Intensity
List five ways to express the exercise intensity.

1. 4.
2. 5.
3.
Train at a Percentage of HRmax

Calculate your percent VO2max training level from your age, and your ability to train at 80% of your
HRmax.
Is Strenuous Training More Effective?

What is generally considered the “ceiling” training intensity for percent HRmax and percent VO2max.
% Heart rate
% VO2max
The “Training-Sensitive Zone”

Calculate the predicted HRmax for the following individuals:
22 year old male
32 year old female
80 year old male
Train at a Perception of Effort.

Describe the procedure to determine training intensity based on how you “feel” during exercise?
Training Duration
Is there an optimal training duration per session?
Training Frequency
Give the minimum training frequency to induce a training effect.
Exercise Mode
Give the optimum training mode to induce a training effect.
Trainability and Genes

Explain differences between “responders” and “nonresponders” in terms of trainability.
Maintenance of Aerobic Fitness Gains

Is the requirement for maintenance of aerobic fitness the same as the requirement for its
improvement?
Methods of Training
Describe three differences between aerobic and anaerobic training.
1. 3.
2.
Anaerobic Training
List two activities that can be used for anaerobic training.
1. 2.
Aerobic Training
Interval Training
What two factors formulate the interval training exercise prescription?
1.
2.
Continuous Training
Define “continuous training” and indicate the group best suited for this training method.
Definition
Group best suited
Fartlek Training
What does Fartlek mean?
Overtraining: Too Much of a Good Thing

Describe three symptoms of overtraining.
1. 3.
2.
PRACTICE QUIZ
1. Brief power activities lasting up to 6 sec c. decreases muscle fiber number

rely on: d. changes fast to slow muscle fibers
a. ATP and PCr e. none of the above
b. glycolysis 4. The most important factor affecting aerobic
c. aerobic metabolism training response:
d. lactic acid production a. initial level of fitness
e. none of the above b. training intensity
c. training duration
2. SAID: d. training mode
a. relates to overload principle e. none of the above
b. relates to choosing exercise modes 5. Training intensity:
c. relates to specificity principle of a. can be measured in only 1 way
training b. can be measured in many ways
d. relates to reversibility principle of c. no minimum level necessary to
training initiate a training response
e. none of the above d. never set below 80% of maximum
3. Exercise training: capacity
a. increases muscle fiber number e. none of he above
b. increases muscle fiber density 6. Training sensitive zone:
a. refers to minimum and maximum c. same as interval training

heart rate to illicit a training response d. originated in Spain
b. refers to maximum running speed to e. none of the above
illicit a training response
9. True or False: LSD training stands for
c. refers to minimum running speed to “long slow distance training”.
illicit a training response
a. True
d. the same for all 18 y olds
b. False
e. none of he above
10. With training maximum cardiac output:
7. :A type of overtraining:
a. decreases
a. sympathetic
b. increases
b. neurogenic
c. stays the same
c. familiar
d. increases for males and stays the same
d. athletic for females
e. none of the above e. none of the above
8. Fartlek training:
a. same as LSD training
b. same as continuous training
LECTURE #10
PHYSICAL ACTIVITY, HEALTH AND AGING
Introduction
Aside from the positive effects of exercise in maintaining physiologic function, regular physical activity
protects against the ravages of this nation’s greatest killer, coronary heart disease (CHD). Individuals in
physically active occupations have a two- to threefold lower risk of heart attack than individuals in sedentary
jobs. Furthermore, chances of surviving a heart attack increase substantially for those with a physically
demanding job or lifestyle. Physical activity also favorably modifies important CHD risk factors. Regular
aerobic exercise lowers elevated blood pressure, reduces excess body fat, and improves the blood lipid
profile. The blood clotting mechanism can normalize with exercise training, which reduces the chances of a
blood clot forming on the roughened surface of a coronary artery. Regular exercise may also improve
myocardial blood flow. This adaptation could retard the progression of heart disease, or at least maintain
adequate blood supply to the heart muscle to compensate for coronary arteries narrowed by fatty deposits
within their walls.
Objectives
 Describe the physical activity level of typical American men and women.
 Outline the major findings of the Surgeon General’s Report on physical activity.
 Answer the question: “How safe is exercise?”
 List important age-related changes in: (a) muscular strength, (b) joint flexibility, (c) nervous system
function, (d) cardiovascular function, (e) pulmonary function, and (f) body composition.
 Describe research that shows that regular physical activity protects against disease and may even extend
life.
 List major risk factors for coronary heart disease, and describe how regular exercise affects each.
 List factors that affect blood cholesterol level.
 Explain how regular physical activity reduces the risk of coronary heart disease.
The Graying of America

Elderly persons make up the fastest growing segment of American society. Thirty years ago, age 65
represented the onset of old age. Now gerontologists mark 85 as the demarcation of “oldest-old” and age 75
as the “young old.” Currently, nearly 12% of all Americans (about 35 million) exceed age 65 and by the year
2030, 70 million Americans will exceed age 85. Some demographers project that one-half of the girls and one-
third of the boys born in developed countries near the end of the 20th century actually will live in three
centuries. In the short term, disease prevention, health care, and more effective treatment of age-related
diseases like heart disease and osteoporosis continue the advances in longevity. Far fewer people now die
from infectious childhood diseases, so those with the genetic potential actualize their proclivity for longevity.
Centenarians currently represent proportionately the fastest growing age group in the United States.
Numbers range between 30,000 and 50,000, up from the estimate of 15,000 in 1980 and almost none at
beginning of the 20th century. No longer viewed as a quirk of nature, 1 in 10,000 Americans live to the age of
100. Demographers project that by the middle of the next century more than 800,000 Americans will exceed
age 100, with many of these men and women remaining in relatively good health. Old-age mortality actually
appears on the decline in that the death rate (number of people per 100 in a specific age group) levels off in
the 90-year-old age category (approximately 11 per 100) and decreases to 8 per 100 after age 100! On a
disturbing front, the Centers for Disease Control and Prevention reports that nearly one in ten Americans
over age 70 needs help with daily activities such as bathing and four in ten use assistive devices such as
walkers or hearing aides. In addition, about one-half of men and two-thirds of women older than age 70 have
arthritis; one-third of all Americans in this age group also have high blood pressure and 11% have diabetes.
Of all seniors, women over age 85 are the most likely to need everyday help, with 23% requiring assistance
with at least one basic activity (e.g., dressing or going to the toilet).
The New Gerontology

Genes exert strong influence over life span, patterns of aging, and susceptibility to disease. Yet scientists
know little why humans live five times longer than cats, cats five times longer than mice, mice outlive fruit
flies by a factor of 25, or why the onset of different diseases (e.g., Alzheimer’s disease) often differ by many
years in identical twins.
The contribution of genetics to the unprecedented increase in human life expectancy remains unanswered.
In the early 1900s, for example, 4% of the U.S. population exceeded 65 years of age. By 1998, that percentage
increased to 13%. A citizen’s average life expectancy has increased from 47 years in 1900 to 76 years today,
and should reach 83 years by the year 2050. Sixty-three percent of today’s 65-year-olds will achieve their 85th
birthday, and 24% will celebrate age 95. Researchers now believe that the average child born today may
readily live healthfully to age 95 or 100, with the limit of human life span currently estimated at 130 years.
Improved overall health accompanies extended life span. The prevalence of chronic disorders (e.g.,
arthritis, dementia, hypertension, stroke, and emphysema) continues to decline. Eighty-nine percent of
Americans age 65 to 74 years reports no disability; even after 85 years of age, 4% remain fully functional. A
decline in the population of elders living in nursing homes (6.3% in 1982 to 5.2% in 1998) accompanies the
upgraded functional status of the elderly. Concurrently, a “new gerontology” expands the focus on aging
from preoccupation with disease and frailty to a more positive, notion of “successful aging.”
The Concept of “Healthspan” and “Successful Aging”

The aging process, including the development of physical frailty towards the last decade of life,
traditionally has been viewed as physiologically inevitable. The typical “aging syndrome” includes a
constellation of chronological age-related and/or lifestyle-dependent deleterious changes in blood pressure,

bone mass, body composition and body fat distribution, insulin sensitivity, and homocysteine levels that
convey increased health risk, dysfunction, or actual disease. This traditional view has changed dramatically; it
now seems evident that chronological aging does not conform to a grim stereotype of unalterable decline and
loss of body structure and functional capacity. As more people reach that “ripe old age,” the concept of
successful aging encompasses more than just the avoidance or delay of disease. Successful aging entails
maintenance and even enhancement of physical and cognitive functions. It requires full engagement in life,
including productive activities and interpersonal relations.
To a large extent, lifestyle changes that include sound nutrition and diverse forms of exercise substantially
blunt the decline in function and increased disease risk with aging. The lack of muscle strength often limits an
increasing number of the healthy elderly’s chances to live a full, independent, and productive life into the
ninth and tenth decade. In a study of 100 frail nursing home residents (average age 87 years), resistance
training for only 45 minutes, three times weekly for ten weeks doubled muscular strength and improved gait
and stair climbing. Such findings demonstrate the substantial responsiveness of the healthy human body at
any age to regular exercise.
Many gerontologists maintain that research on aging must focus not simply on increasing lifespan but
rather improving “healthspan,” the total number of years a person remains in excellent health. Researchers
now view much of the physiologic deterioration previously considered as “normal aging” as dependent on
lifestyle and environmental influences subject to significant modification with proper diet and exercise. For
those achieving older age, poor muscular strength, cardiovascular function, and joint range of motion as well
as sleep disturbances link directly to functional limitations regardless of disease status.
Physical Activity Epidemiology

Epidemiology involves quantifying factors that influence the occurrence of illness to ultimately better
understand, modify, and/or control a disease pattern in the general population. The specific field of physical
activity epidemiology applies the general research strategies of epidemiology to study the association of
physical activity as a health-related behavior with disease and other outcomes. 38
TERMINOLOGY
Physical activity epidemiology applies specific definitions to characterize behavioral patterns and
outcomes of the groups under investigation. Examples of relevant terminology include:
 Physical activity: Body movement produced by muscle action that increases energy expenditure.
 Exercise: Planned, structured, repetitive, and purposeful physical activity.
 Physical fitness: Attributes related to one’s ability to perform physical activity.
 Health: Physical, mental, and social well being, not simply the absence of disease.
 Health-related physical fitness: Components of physical fitness associated with some aspect of good
health and/or disease prevention include cardiovascular fitness, abdominal muscular strength and
endurance, optimal body composition, flexibility of the lower back and hamstrings.
 Longevity: Length of life.
Within this framework, physical activity becomes a generic term and exercise comprises the major
component. Similarly, the definition of health focuses on the broad spectrum of well being that ranges from
the complete absence of health (death) to the highest levels of physiological function. Such definitions often
challenge our ability to objectively measure and quantify. However, they do provide the broad frame of
reference to study the role of physical activity and exercise in health and disease.
Surgeon General’s Report On Physical Activity and

Health
The Surgeon General of the United States acknowledged the importance of physical activity in 1996 in a
wide-ranging report summarizing the benefits of physical activity in disease prevention. The conclusions and
recommendations of this hallmark report apply to all individuals interested in health improvement. In
essence, the Surgeon General proposed a national agenda that urges the nation to adopt and maintain a
physically active lifestyle to combat the increasing number of physical ailments associated with the country’s
generally low level of energy expenditure. Hopefully, this document will generate as great an impact as the
1964 Surgeon General’s Report on the hazards of smoking.
The Report focuses on three objectives:
1. Summarize existing literature relating regular physical activity to disease prevention
2. Evaluate current status of physical activity in the population
3. Stimulate increased physical activity among Americans of all ages.
Concerning benefits of regular physical activity, the Report concludes
1. Almost everyone derives overall health benefits from participation in regular physical activity
2. Significant health and quality of life benefits emerge with only moderate, daily physical activity (e.g.,
30 minutes brisk walking or raking leaves, 15 minutes running, or 45 minutes playing volleyball)
People who maintain a regular regimen of vigorous activity of longer duration obtain the greatest health-
related benefits
Regular physical activity reduces general premature mortality risk, and specific risks of coronary heart
disease, hypertension, osteoporosis, colon cancer, and adult-onset diabetes. It also enhances overall mental
well being, and contributes to optimal neuromuscular-skeletal functioning.
For Your Information

Physical Activity Levels of Adults and Children in the USA
Adults
•• 15% of adults engage in regular vigorous physical •• 22%of adults engage regularly in light-to-
activity during leisure time (3/wk for at least 20 moderate physical activity during leisure time
min) (5/wk for at least 30 min)
•• More than 60% of American adults do not engage •• Physical inactivity occurs more among women
regularly in physical activity; 25% lead sedentary than men, blacks and Hispanics than whites,
lives older than younger adults, and less affluent than
wealthier persons
•• Walking, gardening, and yard work represent the •• Participation in fitness activities declines with
most popular leisure-time activities for adults age. A large number of older citizens have such
poor functional capacity that they cannot raise
from a chair or bed, walk to the bathroom, or
climb stairs without assistance
Children and Teenagers
•• Nearly one-half between ages 12 and 21 yrs do •• 25% engage in light to moderate physical
not vigorously exercise on a regular basis; a sharp activity nearly every day (e.g., walk or bicycle)
decline in physical activity occurs during
adolescence
•• 14% report no recent physical activity (more •• More males participate in vigorous physical
prevalent among females, particularly black) activity, strengthening activities, and walking or
bicycling than females
•• Participation in all types of physical activity •• Daily attendance in school physical education
declines strikingly as age and school grade programs declined from 42% in early 1990 to
increase only 25% in 1996
•• 19% of high school students report being
physically active for at least 20 min in daily
physical education classes
SAFETY OF EXERCISING
People have questioned the safety of exercise because of several well-publicized reports of sudden death
during physical activity. Actually, sudden death rates during exercise have declined over the past 20 years
despite an overall increase in exercise participation. In one report of cardiovascular episodes over a five-year
period, 2935 exercisers recorded 374,798 exercise hours that included 2,726,272 km (1.7 million miles) of
running and walking. No deaths occurred during this time (with only two nonfatal cardiovascular
complications). Certainly, a small increased risk of a cardiovascular episode during exercise exists compared
to resting. However, the total reduction in heart disease risk from regular physical activity (compared with
remaining sedentary) far outweighs any slight increase in risk during the actual exercise.
Perhaps not surprisingly, musculoskeletal injury represents the most prevalent exercise complications. For
351 participants and 60 instructors at six aerobic dance facilities, 327 medical complaints were reported
during nearly 30,000 hours of activity. Eighty-four of the injuries caused disability (2.8 per 1000 person-hours
of participation), and only 2.1% of the injuries required medical attention. The greatest orthopedic injury
potential for jogging and running activities exists among individuals who exercise for extended durations:
more is certainly not better.
Aging and Bodily Function

Figure 1 shows that various bodily functions generally improve rapidly during childhood to reach a
maximum between age 20 and 30
years; thereafter, a general decline
in functional capacity occurs with
advancing age. Although a similar
age trend exists for the physically
active, physiologic function
averages about 25% higher
compared with the sedentary at
each age category (an active 50-
year old man or woman often
maintains the functional level of a
30-year-old). Although all
physiological measures
eventually decline with age, not
all decrease at the same rate.
Figure 1. Generalized curve to illustrate agerelated changes in physiologic
function. All comparisons made against the 100% value achieved by the 20 to 30
yearold sedentary person.
Considerable variation exists from person-to-person, and from biologic system-to-biologic system within the
same person.
Nerve conduction velocity, for example, declines only 10 to 15% from 30 to 80 years of age, whereas
resting cardiac index (ratio of cardiac output to surface area) and joint flexibility decline 20 to 30%; maximum
breathing capacity at age 80 averages 40% of values for a 30-year-old. Brain cells die at a fairly constant rate
until age 60, while liver and kidneys lose 40 to 50% of their function between ages 30 and 70. By the seventh
decade, the average female has lost 30% of bone mass, while men only 15%. Gerontologists have often
considered these aging patterns to represent the “normal” and “expected” decreases in structure and
function.
Aging and Muscular Strength

Men and women generally achieve maximum strength between ages 20 to 30 years, when muscular cross-
sectional area achieves maximum size. Thereafter, strength progressively declines for most muscle groups, so
by age 70 a 30% decrement occurs in overall strength.
Decrease in Muscle Mass

Reduced muscle mass represents the primary factor responsible for age-associated strength decreases. The
smaller muscle mass reflects a loss of total muscle protein induced by inactivity, aging, or the combined
effects of both. Some loss in muscle fiber number also takes place with aging. For example, the biceps muscle
of a newborn contains about 500,000 individual fibers, while the same muscle for a man age 80 has 300,000
fibers or 40% less.
Muscle Trainability Among the Elderly

Regular exercise training facilitates protein retention and blunts the loss of muscle mass and strength with
aging. Healthy men between age 60 and 72 years who participated in a 12-week standard resistance training
program showed that muscle strength increased progressively throughout the program, averaging about 5%
each exercise session – a training response similar to young adults. Many exercise specialists who work with
the elderly maintain that improving strength represents a highly effective way to maintain muscle mass,
increase mobility, and reduce injury incidence.
Aging and Joint Flexibility

With advancing age, connective tissue (cartilage, ligaments, and tendons) becomes stiffer and more rigid,
which reduces joint flexibility. It remains uncertain whether these changes result from biologic aging per se or
reflect the impact of chronic disuse through sedentary living and/or degenerative tissue diseases of specific
joints. Regardless of the cause, appropriate exercises that regularly move joints through their full range of
motion increase flexibility 20 to 50% in men and women at all ages.
Endocrine Changes With Aging

Part of the aging process relates altered endocrine function, particularly the pituitary, pancreas, adrenal,
and thyroid glands. About 40% of individuals aged 65 and 75 years, and 50% of those older than age 80, have
impaired glucose tolerance leading to non-insulin dependent diabetes (adult-onset or type 2 diabetes). This
represents the most common form of the disease and afflicts 1 in 17 Americans; nearly one-half of these cases
remain undiagnosed. Impaired glucose metabolism leading to high blood glucose levels in type II diabetes
results from:
 Decreased effect of insulin on peripheral tissue (insulin resistance)

 Inadequate insulin production by the pancreas to control blood sugar (relative insulin deficiency)
 Combined effect of the above
These factors are influenced by genetic predisposition, obesity, sedentary lifestyle and aging.
Aging and Nervous System Function

A 37% decline in number of spinal cord axons and a 10% decline in nerve conduction velocity reflect
cumulative effects of aging on central nervous system function. Such changes partially explain the age-related
decrements in neuromuscular performance. Partitioning reaction time into central processing time and
muscle contraction time indicates that aging most affects stimulus detection and information processing to
produce a response.
Aging and Pulmonary Function

Whether regular exercise throughout one’s life overrides pulmonary system “aging” remains unknown.
Cross-sectional studies indicate that dynamic pulmonary capacity of older endurance-trained athletes exceeds
that of sedentary peers. Although longitudinal studies will provide a definitive answer, available data
suggests that regular physical activity retards pulmonary function deterioration associated with aging.
Aging and Cardiovascular Function

Different indices of cardiovascular function decline with age. Below, we review some of these changes and
the effects of exercise on altering the rate of decline.
Maximal Oxygen Uptake

Maximal oxygen uptake (VO2max) declines steadily after age 20, decreasing by 35 to 40% at age 65 (slightly
less than 1% per year). A slower rate of decline occurs for individuals who maintain an active lifestyle that
includes regular aerobic training , without a decline in fat-free body mass. Physical activity, however, does
not entirely prevent aging’s effect on VO2max, even when adjusting for a person’s quantity of muscle.
Deterioration in VO2max with aging probably results from cumulative effects including age-associated loss
of muscle mass, increases in body fat, and altered cardiovascular and pulmonary functions. The reductions in
aerobic power per kg of active muscle with aging can only reflect reduced oxygen delivery and/or reduced
oxygen extraction at the active muscle. In contrast, skeletal muscle oxidative capacity and capillarization
remain similar in older and younger individuals with comparable physiologic characteristics and training
histories. The well-documented reduction in cardiac output (both maximum heart rate and stroke volume)
represents the most likely explanation for the decrease in VO2max per kg of active muscle accompanying aging.
A System Responsive to Training at Any Age

Among the healthy elderly, exercise training enhances the heart’s capacity to pump blood and increases
aerobic capacity to the same relative degree as younger adults. Nine to 12 months of endurance training in
healthy older adults increased VO2max 19% in men and 22% in women. These values represent the high end of
the typical training response for young adults. Regular aerobic training for middle-aged men over a 20-year
period significantly delayed the usual 10 to 15% decline in exercise capacity and aerobic fitness. At age 55,
these active men maintained nearly the same values for blood pressure, body mass, and VO 2max as at age 35;
by age 70, their VO2max equaled values for individuals 25 years younger! These remarkable findings attest to
the adaptability of the aerobic system to training at any age.
Aging and Endurance Performance

Comparing endurance performance times among individuals of different ages points up the dramatic
effects of exercise training on preserving cardiovascular function throughout life. Figure 2 shows the world-
record marathon times for males and females of different ages, starting at about age 4 and into the mid-80s
(the world record was just set on April 1, 2002; 2:05:38, not shown here.)
The world record time of
340.2 minutes for the 86-year
old male corresponds to a 12.9
min per mile pace; for the-80
year old female, the world
record time equals 328.6 (12.5
min per mile pace.) This
represents a remarkable 26.2-
mile average running speed
for men and women in their
eighth decade of life.
Performances of this quality
attest to the tremendous
cardiovascular capabilities of
the healthy elderly who
continue to train regularly as
Figure 2. World record marathon times for men and women of different ages.
they grow older.
Aging and Body Composition

Excess body fat accumulation usually begins in childhood or develops slowly during adulthood. Middle-
aged men and women invariably weigh more than their college-age counterparts of the same stature (with
differences in body fat accounting for the weight difference). Scientists do not know if gains in body fat
during adulthood represent a normal biologic pattern. Observations of physically active older individuals
suggest that, while the typical individual grows fatter with age, those who remain physically active counter
the normal loss in fat-free body mass without increasing body fat percentage.
Figure 3 (next page) shows how body composition changes over a 20-year period for 21 elite master’s
runners. Despite maintaining a relatively constant body mass during the prolonged period of exercise
training (T1=70.1 kg; T2 = 69.4 kg; T3 = 70.8 kg), gains occurred in body fat and fat-free body mass declined.
The roughly 3% body fat unit increase per decade paralleled similar increases in waist girth. These data
support an argument that some alterations in body composition and body fat distribution represent a normal
aging response.
Regular Exercise: A Fountain Of Youth?

Although exercise may not necessarily represent a “fountain of youth,” regular physical activity not only
retards the decline in functional capacity associated with aging and disuse, but often reverses the loss of
function regardless of when a person becomes active.
Medical experts have debated if a

lifetime of regular exercise
contributes to good health and
perhaps longevity compared with a
sedentary “good life.” Because older
fit individuals exhibit many
functional characteristics of younger
people, one could argue that
improved physical fitness and a
vigorous lifestyle retards biological
aging and confers health benefits
later in life.
One group of researchers
investigated the diseases and
longevity of former college athletes.
This seemed like an excellent group
with which to study possible links
between exercise and longevity,
because collegiate athletes usually
have longer involvement in habitual
physical activity prior to entering
Figure 3. Changes in percent body fat (D) and (E) fatfree body mass for 21 college than nonathletes, and they
endurance athletes who continued to train over a 20year period, starting at may remain more physically active
age 50. following graduation. These and
more recent findings suggest that participation in athletics as a young adult does not assure significant
longevity.
Enhanced Quality To Longer Life: Harvard Alumni Study

Research concerning current lifestyles and exercise habits of 17,000 Harvard alumni who entered college
between 1916 and 1950 indicates that only moderate aerobic exercise, equivalent to jogging three miles a day,
promotes good health and longevity. Men who expended 2000 kCal weekly had up to one-third lower death
rates than classmates who did little or no exercise. To achieve a 2000 kCal energy output weekly requires
moderate additional physical activity such as a daily 30 to 45-minute brisk walk, run, cycle, swim, cross
country ski, or aerobic dance. The following summarizes the results of the study of alumni:
 Regular
exercise counters the life-
shortening effects of
cigarette smoking and
excess body weight
Figure 4. Reduced risk of death with regular exercise.
 Even for people with high blood pressure (a primary heart disease risk), those who exercised regularly
reduced their death rate by one-half
 Regular exercise countered genetic tendencies toward an early death. For individuals who had one or
both parents die before age 65 (another significant risk), a lifestyle that included regular exercise
reduced the risk of death by 25%
 A 50% reduction in mortality rate occurred for those whose parents lived beyond 65 years
Figure 4 (previous page) shows that among physically active people, a person who exercises more has a
reduced risk of death. For example, men who walked 9 or more miles a week showed a 21% lower mortality
rate than men who walked 3 miles or less. Exercising in light sports activities increased life expectancy 24%
over men who remained sedentary. From a perspective of energy expenditure, the life expectancy of Harvard
alumni increased steadily from a weekly exercise energy output of 500 kcal to 3500 kcal, the equivalent of six
to eight hours of strenuous weekly exercise. In addition, active men lived an average of one to two years
longer than sedentary classmates. (Other research estimates a life expectancy increase of about 10 months
with regular exercise.)
No additional health or longevity benefits accrued beyond weekly exercise of 3500 kcal. Men who
performed extreme exercise actually had higher death rates than less active colleagues (another example of
why more does not necessarily indicate better exercise benefits).
Improved Fitness: A Little Goes a Long Way

A study of more than 13,000 men and women over an eight-year interval indicates that even modest
amounts of exercise substantially reduce the risk of death from heart disease, cancer, and other causes. The
study evaluated fitness performance by directly, rather than relying on verbal or written reports of regular
physical activity habits. To isolate the effect of physical fitness per se, the researchers considered factors of
smoking, cholesterol and blood sugar levels, blood pressure, and family history of coronary heart disease.
Figure 5 (below) , based on age-adjusted death rates per 10,000 person-years, illustrates that the least fit group
died at a three-times greater rate than the most fit subjects.
The most striking finding was that the group rated just above the most sedentary category derived the
greatest health benefits. The decrease in death rate for men from the least fit to the next category equaled 38
(64.0 vs. 25.5 deaths per 10,000 person-year), whereas the decline from the second group to the most fit
category equaled only seven. Women obtained similar benefits as men. The amount of exercise required to
move from the most sedentary category to the next more fit category (the jump showing the greatest health
benefits) occurred for moderate-intensity exercise like walking briskly for 30 minutes several times weekly.
Figure 5. Physical fitness and longevity. The greatest reduction in death rate risk occurs when going from the
most sedentary category to a moderate fitness level.
According to available evidence, if life-extending benefits of exercise exist, they are associated more with
preventing early mortality than improving overall life span. While the maximum life span may not extend
greatly, more active people survive to a “ripe old age” with only moderate exercise.
Coronary Heart Disease

1.5 million Americans will have a heart attack this year and about one-third of them will die. While deaths
from CHD have declined more than 35% since 1970, heart disease still remains the leading cause of death in
the Western world. Although death rates for women lag about 10 years behind men, the gap has closed fast,
particularly for women who smoke. For every American who dies of cancer, nearly three die of heart-related
diseases. This health disaster produces staggering economic losses – $130 billion in 1996 from medical costs,
loss of earnings, and lost productivity. And this does not include the emotional impact of losing a loved one
in the prime of life.
A Life-Long Process
Almost all people show some evidence of CHD, which can be severe in seemingly healthy young adults.
This degenerative process probably
begins early in life, as fatty streaks
emerge in the coronary arteries of
children as young as age five. Little
harm exists for most people until the
coronary arteries become markedly
narrowed. Figure 6 shows that
atherosclerosis involves degenerative
changes in the inner lining of the
arteries that supply the heart muscle.
The action and chemical
modification of various compounds,
including oxidation of cholesterol in
Figure 6. [Left] Cross section of a normal coronary artery. [Right], deterioration low-density lipoproteins, initiates a
of coronary artery in atherosclerosis; deposits of fatty substance roughen the complex process that ultimately
vessel’s center. causes bulging lesions in the arterial
wall. The lesions initially take the
form of fatty streaks. With further damage and proliferation of underlying smooth muscle cells, vessels
progressively congest with lipid-filled plaques, fibrous scar tissue, or both. This change reduces the vessels’
capacity for flood flow, causing the myocardium to receive diminished oxygen (ischemia) from inadequate
blood flow.
The roughened, hardened lining of the artery frequently causes the slowly flowing blood to clot. When a
blood clot (thrombus) forms, it plugs one of the smaller coronary vessels, causing necrosis (death) of a portion
of the myocardium. When this occurs, the person can suffer a heart attack or myocardial infarction. With only
moderate blockage (but with blood flow reduced below the heart’s requirement), the person may experience
temporary chest pain termed angina pectoris. The pains usually magnify during exertion because increased
physical activity causes a great demand for myocardial blood flow. Angina attacks provide vivid evidence of
the importance of adequate oxygen supply to the myocardium.
Women at Risk
Women have increased their risk for developing CHD. Since 1910, more American women have died of
heart disease than any other cause. Because women develop heart disease 10 to 15 years later in life than men,
they more likely have heart attacks when past middle age. Only 1% of women under age 45 develop CHD,
while 13% above age 75 show clinical heart disease manifestations. This sex-age difference in heart disease
episodes makes CHD appear as a more pervasive and dramatic problem in men; a heart attack for a 75-year-
old woman seems less shocking than for a male “wage earner” who suffers an attack in the prime of life.
Increased CHD for women in later years partly relates to loss of protection offered by estrogen, which
declines markedly after menopause. Despite limited heart disease research on women, available evidence
indicates that disease symptoms, progression, and outcome differ in women and men. Some interesting sex-
related heart disease differences include:
 Following a heart attack, women usually die sooner
 Women who survive a heart attack frequently experience a second episode
 Women become more incapacitated by heart disease-related pain and disability
 Women are less likely to survive coronary artery by-pass surgery
Several factors seem clear: A similar process probably exists for CHD development in men and women,
i.e., fatty deposits narrow coronary arteries and reduce blood flow to the myocardium. Hormonal differences
may also affect blood clot formation, coronary artery smooth muscle cell proliferation, and the tendency of
coronary vascular walls to spasm in the final stages preceding a heart attack. Moreover, CHD diagnosis may
differ in women and men. Diagnostic tests, like the treadmill stress test and ECG response, have limited use
with women because men have provided the subject pool for test validation. A diagnostic gap also occurs
because some physicians do not treat heart disease signs in women as aggressively as in men. Consequently,
they do not prescribe coronary angiography (the most valid way to diagnose CHD) as often following a
positive stress test.
Despite a lower CHD risk, premenopausal women are not immune from heart disease, particularly if they
smoke. Cigarette smoking accounts for almost one-half of all heart attacks in women before age 55. Smoking
as few as four cigarettes daily doubles a women’s CHD risk. Hypertension also exists in more than 50% of
women over age 55 who suffer a heart attack; after age 65 it affects two-thirds of female victims. Elevated
blood sugar afflicts women more often than men. The presence of either Type 1 or Type 2 diabetes raises a
woman’s CHD risk to equal that for a nondiabetic man of the same age, and puts her risk of dying from a
heart attack even greater than the man’s. Use of birth-control pills also raises a woman’s CHD risk.
Risk Factors For Coronary Heart Disease

Various personal characteristics and environmental factors identified over the past 45 years indicate a
person’s susceptibility to CHD. In general, the greater the number of the risk factors, the more likely coronary
artery disease exists or will emerge in the near future. This does not mean that a specific risk factor causes
disease, as diverse factors may act and interact in a cause-and-effect manner. However, risk factor
identification and prudent modification improves an individual’s chances to avoid CHD.
The following risk factors can be modified:
1. Cigarette smoking 5. Abdominal-visceral adiposity
2. Physical inactivity 6. Diabetes mellitus
3. Hypertension 7. Obesity
4. Elevated blood lipids 8. High fat diet
9. ECG abnormalities 13. High uric acid levels

10. Elevated homocysteine levels 14. Pulmonary function abnormalities
11. High-strung, nervous personality 15. Tension and stress
12. Psychosocial characteristics of work (e.g., low
job control and low pay)
The following risk factors are considered fixed, i.e., they cannot be modified.
1. Age 4. Race
2. Gender 5. Male pattern baldness
3. Heredity
Quantifying the importance of each CHD risk factor in relation to the others becomes difficult because
many of the factors interrelate. For example, blood lipid abnormalities, diabetes, heredity, and obesity often
go hand-in-hand. In addition, increasing daily physical activity generally lowers body weight, body fat, blood
lipids, tension, stress, and risk for developing type 2 diabetes.
Four “treatable” factors (elevated serum lipids, high blood pressure, physical inactivity, and cigarette
smoking) represent primary risk factors for CHD. Body fat and personality type provide less predictive value
than these four. Although some risk factors link closely with CHD, the associations do not necessarily infer
causality. In some instances, risk factor reduction may not offer effective protection from the disease.
Nonetheless, a prudent approach to preventing CHD assumes that eliminating or reducing one or more risk
factors decreases the likelihood of contracting CHD.
RISK FACTORS IN CFHILDREN

OR YOURAND
INFORMATION
ADOLESCENTS
Multiple CHD risk factors (obesity, elevated blood lipids, physical inactivity, cigarette
smoking, and a family history of heart disease) frequently occur in young children and
adolescents. In addition, the risks often interrelate as the fattest children generally have the
highest cholesterol and triglyceride levels and lowest of physical activity levels. Schools must
initiate programs aimed at reducing risk factors in children and adolescents, but current efforts
have fallen short, particularly regarding tobacco use. The 1998 Youth Risk Behavior Study from
the Centers for Disease Control and Prevention reported that cigarette use among black, white,
and Hispanic high school students jumped considerably between 1991 and 1997. Moreover,
there was a precipitous 80% increase from 1991 to 1997 in percentage of black males who
smoked. The tobacco industry’s advertising and marketing campaign to attract new smokers
(coupled with renewed glamorization of tobacco products in movies, TV, and music videos)
apparently overwhelm school efforts at risk intervention at an early age.
Age, Sex, and Heredity
After age 35 in males and age 45 in females, the chances of dying from CHD increase progressively and
dramatically. Consequently, age per se represents a significant CHD risk factor. From the perspective of
causality, however, chronological age symbolizes more of an associative risk because of its close link to other
more likely “causal” risk factors like hypertension, elevated blood lipids, and glucose intolerance.
Between ages 55 and 65, about 13 of every 100 men and 6 of 100 women die from CHD. At most ages,
women fare much better than men. For example, in middle age, a man has about a sixfold greater chance of
dying from a heart attack. American women still lead all other countries in heart disease; the specific “gender
advantage” decreases significantly after menopause. This has fueled speculation that hormonal differences
between the sexes provide CHD protection for women. For some unknown reason, heart attacks that strike at
an early age tend to run in families.
Blood Lipid Abnormalities

Overwhelming evidence links high blood lipid levels with increased heart disease risk.
Cholesterol and Triglycerides

Table 1 and 2 presents serum cholesterol, triglyceride and lipoprotein levels, above which young and older
adults should seek advice on treatment. In general, a cholesterol value of 200 mg•dL-1 or lower represents a
desirable level. A cholesterol of 230 mg•dL-1 increases heart attack risk to about twice that of a person with
180 mg•dL-1, and a value of 300 mg•dL-1 increases the risk fourfold. The term hyperlipidemia refers to an
increased lipid level in blood plasma.
Table 1. Serum cholesterol and lipoprotein classifications
Total Cholesterol Classification
>200 mg•dL1 (5.2 mmol•L1) Desirable
200239 mg•dL1 (5.36.2 mmol•L1) Borderline high
< 240 mg•dL1 (6.2 mmol•L1) High cholesterol
LDL Cholesterol Classification

>130 mg•dL1 (3.4 mmol•L
F1OR YOUR) INFORMATION
1
Desirable
130159 mg•dL (3.44.1 mmol•L )
1
Borderline high
< 160 mg•dL (4.1 mmol•L )
1 1
High
HDL Cholesterol Classification
>35 mg•dL (0.9 mmol•L )
1 1
Low
Table 2. Serum triglyceride classifications
Serum
Classification Comments
Triglycerides
>200 mg•dL1 Normal
Check for accompanying
200400 mg•dL1 Borderline high
dyslipidemias
4001000 Check for accompanying
High
mg•dL1 dyslipidemias
Increased risk for acute
<1000 mg•dL1 Very high
pancreatitis
Importance of Cholesterol Forms

Cholesterol and triglycerides represent the two most common lipids associated with CHD risk. Recall
from Lecture 3 that these lipids remain insoluble in water so they do not circulate freely in blood plasma.
Rather, they transport combined with a carrier protein to form a lipoprotein. This lipoprotein varies in size
depending on the quantity of protein and lipid it contains. Hyperlipidemia refers to a general elevation in
blood lipids, while hyperlipoproteinemia more meaningfully describes elevation in the specific lipoproteins.
The distribution of cholesterol among various lipoproteins more powerfully predicts heart disease than
total plasma lipids. This helps to explain how one person with a high total cholesterol may not develop CHD,
while it develops in another person with lower cholesterol. Specifically, elevated high-density lipoproteins
(HDL), which contain the largest quantity of protein and least cholesterol, relate to low heart disease risk. In
contrast, elevated cholesterol-rich low-density lipoproteins (LDL) represent an increased risk.
SHOULD CHILDREN HAVE CHOLESTEROL MEASURED?

Guidelines issued by the National Cholesterol Education Program conclude “yes” if a family
history of high cholesterol or heart disease exists (particularly if a parent suffered a heart attack
before age 50). Shockingly, this parental “cardiac proneness” includes up to one-fourth of the
United States adult population! Research with children aged 10 to 15 years indicates that
lifestyle habits like regular exercise, improved cardiovascular fitness, and a prudent nutritional
profile contribute to favorable lipid profiles similar to effects seen with adults.
LDL transports cholesterol throughout the body for delivery to cells, including those of the arteries’
smooth muscle walls. It oxidizes there and ultimately contributes to the artery-narrowing process of
atherosclerosis. Whereas LDL carries cholesterol to tissues and contributes to arterial damage, HDL acts as a
scavenger, gathering cholesterol from cells (including cells in arterial walls) and returning it for metabolism
to the liver and excretion in the bile.

Research continues to clarify HDL’s protective effect and what factors raise its levels. For one thing,
cigarette smoking adversely affects plasma HDL concentrations. This may account for the significant CHD
risk with smoking. From an exercise perspective, endurance athlete’s posses’ relatively high HDL levels;
favorable alterations also occur in sedentary people who engage in either moderate or vigorous aerobic
training. Concurrently, exercise decreases LDL, which produces the net effect of a considerably improved
ratio of HDL-to-LDL, or HDL-to-total cholesterol. The exercise effect occurs independent of the diet’s lipid
content or the exerciser’s body composition. Moderate consumption of alcohol (equivalent to about 2 oz. or 30
mL of 90 proof alcohol, three 6 oz. glasses of wine, or a bit less than three 12 oz. cans of beer) reduces an
otherwise healthy person’s risk of heart attack. The cardioprotective mechanism may relate to alcohol’s effect
in raising HDL and lowering LDL, and blunting arterial smooth muscle cell proliferation. Excessive alcohol
consumption offers no lipoprotein benefit; it also greatly increases risk of liver disease and cancer.
CHOLESTEROL RATIOS IMPORTANT?

An effective way to evaluate lipoprotein status divides total cholesterol by HDL cholesterol.
This ratio represents a superior index of heart disease risk than either total cholesterol or LDL-
cholesterol level. An HDL:Cholesterol ratio greater than 4.5 indicates high risk for heart
disease, whereas an optimal ratio equals 3.5 or lower.
Factors That Affect Cholesterol and Lipoprotein Levels
Different variables affect cholesterol and lipoprotein levels. Variables that cause favorable effects include:
 Weight loss (through food restriction or  Moderate alcohol consumption

exercise)  Variables that cause undesirable effects
 Regular aerobic exercise (independent of include:
weight loss)  Cigarette smoking
 Increased intake of water-soluble fibers (e.g.,  Diet high in saturated fat and preformed
fibers in beans, legumes, and oat bran) cholesterol
 Increased dietary polyunsaturated to  Emotionally stressful situations
saturated fatty acid ratio and
 Certain oral contraceptives
monounsaturated fatty acids
 Sedentary lifestyle
 Increased intake of unique polyunsaturated
fats in fish oils  ObesityPhysical Activity
A critique of 43 studies of the relationship between physical inactivity and CHD concluded that lack of
regular exercise contributes to heart disease in a cause-and-effect manner, with the sedentary person at
almost twice the risk as the most active individual. The strength of this protective association equaled that
observed between CHD and hypertension, cigarette smoking, and high serum cholesterol. This places physical
inactivity as the greater heart disease risk, considering that more people lead sedentary lives than have one or more of the
other risks. Although vigorous exercise does entail a small risk of sudden death during the activity, the
important longer-term health benefits of regular physical activity far outweigh any potential acute risk.
Hypertension
More than 35 million Americans currently have systolic blood pressures over 140 mm Hg (systolic
hypertension) or diastolic pressures that exceed 90 mm Hg (diastolic hypertension). These values form the
lower limit for the classification of borderline high blood pressure. One out of every five people experience
chronic abnormally high blood pressure sometime during their lives. Uncorrected hypertension leads to heart
failure, heart attack, stroke, or kidney failure.
Hypertension, often labeled the “silent killer,” generally progresses unnoticed for decades before
inflicting its deadly blow. The cause(s) of hypertension remains unknown in more than 90% of cases. Statistics
indicate that the optimal blood pressure for longevity averages about 110 mm Hg systolic and 70 mm Hg
diastolic. Anything higher results in increased cardiovascular disease risk. For example, a man with systolic
blood pressure above 150 mm Hg has more than twice the heart disease risk as someone with 120 mm Hg.
Many people have a genetic predisposition toward hypertension that increases their tendency to retain salt,
heightens the reactivity of their blood vessels to stress, and causes higher levels of chemicals that constrict
peripheral vasculature.
Cigarette Smoking
In terms of health status, the more a person smokes, the poorer the future health status. Cigarette smoking
represents one of the strongest predictors of CHD. In fact, the probability of death from heart disease for
smokers nearly doubles compared to nonsmokers. Risk for CHD (and lung cancer) increases the more one
smokes, the deeper one inhales, and the stronger the cigarette’s tars and noxious by-products. Also, smokers
experience nearly 5 times the risk for stroke as nonsmokers, and those who smoke a pack or more a day have
an 11-times greater chance of suffering a specific type of sudden, deadly stroke that strikes younger men and
women.
Surprisingly, CHD risk from smoking translates to two to three times more deaths than excess mortality
from lung cancer. Even exposure to second-hand smoke increases CHD risk. Three hours of second-hand
smoke exposure equals smoking one pack of cigarettes. The good news: if a smoker for 40 years stops, CHD
risk returns to that of a “never smoker” within five years, regardless of age.
Obesity
Obesity’s association with many diseases makes the quantitative importance of excess body fat per se as a
health risk difficult to determine. However, the death rate for men weighing 30% in excess of ideal weight
exceeds the risk for a normal-weight individuals by 70%. The overfat condition often accompanies multiple
risk factors like hypertension and elevated serum lipids. In addition, an obese person usually consumes a
highly atherogenic diet rich in saturated fatty acids and cholesterol. Gaining weight also increases chances for
developing impaired glucose tolerance (type 2 diabetes).
Weight loss and accompanying body fat reduction generally contribute to normalizing plasma cholesterol
and triglycerides, and exert beneficial effects on blood pressure and type 2 diabetes. Age-related gains in
body mass partly explain the expected increase in blood pressure with age. Obesity does not rate as a primary
CHD risk factor, yet one cannot deny its role as an important contributing factor.
Personality and Behavior Patterns

A distinct personality susceptible to heart disease may exist. The coronary-prone behaviors (hard-driving,
ambitious, impatient, short-tempered, hostile, and restless) typify what psychologists call the Type A
personality. Unrelenting pressures, drives, deadlines, anxieties, depression, and a constant struggle against
the limitations of time comprise the Type A stress syndrome, with its accompanying excessive stimulation of
the body’s “fight or flight” hormonal response, which may impair cardiovascular health.
The opposite style, exemplified by the equally capable but easy going, no pressure, “laid back” Type B
personality, functions under no time pressure. The absence of Type A behaviors characterizes this personality
type. Generally, most people classify as neither all Type A nor all Type B, but rather a blend of both patterns.
The precise manner in which personality and behavior influence CHD development remains unknown, let
alone whether one’s basic personality “type” can significantly influence a disease process. One desirable
strategy would recognize, manage, and effectively direct excess stress elsewhere. To this end, regular exercise
blended with behavior modification can channel potentially harmful behaviors into ones that produce
positive “spin-off.” Interestingly, laughter may play an important role in the stress response and positively
influence disease processes. Individuals who laugh easily, spontaneously, and hard on a regular basis have
lower CHD incidence, recover faster from surgery, and generally remain less susceptible to disease.

EXERCISE IS GOOD MEDICINE
Studies of the health and exercise habits of Harvard alumni indicate that physically
active men had about one-half the risk of colon cancer as inactive classmates. The
protection disappeared if the men stopped exercising. One mechanism proposes that
exercise protects against cancer by speeding passage of food residues through the
digestive tract, this reduces the colon’s exposure to potential carcinogens in food.
LECTURE #10
STUDY GUIDE
1. Atherosclerosis
2. Borderline hypertension
3. CHD risk factors
4. Coronary heart disease
5. Harvard alumni study
6. Heart attack
7. High-density lipoproteins
8. Hyperlipidemia
9. Hyperlipoproteinemia
10. Low-density lipoproteins

11. Myocardial infarction
12. Primary CHD risk factors
13. Surgeon General’s Report on Physical Activity and Health
14. Systolic hypertension
15. Modifiable risk factors
16. Type A personality
17. Type B personality
STUDY QUESTIONS
The Graying of America

Give 2“facts” about the aging of our population.
1.
2.

Describe differences between the concepts of exercise and physical activity.
The New Gerontology

How long can one expect to live healthfully?
The Concept of Healthspan and Successful Aging

Describe “healthspan”.
Describe “successful aging”.

Describe the differences between the terms exercise and physical activity.
Surgeon General’s Report On Physical Activity and Health

List the three objectives of the Surgeon General’s Report on Physical Activity.
1. 3.
2.
Safety of Exercising
What is the most prevalent injury caused by exercise.
Aging and Bodily Function

At what age does “aging” seem to occur?
Aging and Muscular Strength

How much loss of muscular strength occurs by age 70?
Decrease in Muscle Mass

Reduced muscle mass triggers what age-associated decrease in physiologic function?
Muscle Trainability Among the Elderly

How much can the elderly increase their strength with a proper resistance-training program?
Aging and Joint Flexibility

Describe the change in joint flexibility with aging.
Endocrine Changes With Aging

List three “hormonal systems” most affected by aging.
1. 3.
2.
Aging and Nervous System Function

Describe the general effect of aging on the nervous system.
Aging and Pulmonary Function

Describe how aging affects pulmonary function.
Aging and Cardiovascular Function

Maximal Oxygen Uptake
Give the estimated maximum heart rate for a 59-year old person. Show your calculations.
List two reasons that VO2max declines with age.

1. 2.
A System Responsive to Training at Any Age

How much can a middle age person expect to increase VO2max with proper training?
Other Age-Related Variables

Give three reasons for age-related decrements in HRmax.
1. 3.
2.
Aging and Body Composition

How much weight does the average 20-year old male gain by age 60?
Regular Exercise: A Fountain Of Youth?

List five health benefits of regular physical activity.
1. 4.
2. 5.
3.
Enhanced Quality to a Longer Life: A Study of Harvard Alumni

Describe major findings of the study of Harvard Alumni.
Coronary Heart Disease

What percentage of total deaths do diseases of the heart and blood vessels cause?
A Life-Long Process
At what age can fatty streaks develop in the coronary arteries?
Women at Risk
Write four statements that summarize the heart disease risk for females emphasizing unique sex
differences in risk factors.
1. 3.
2. 4.
Risk Factors for Coronary Heart Disease

List the major modifiable and fixed coronary heart disease risk factors.
Modifiable risk factors
Fixed risk factors
Age, Sex, and Heredity

Why do women possess a “gender advantage” for avoiding heart disease?
Blood Lipid Abnormalities

Cholesterol and Triglycerides
List desirable cholesterol and triglyceride levels for adults.
Cholesterol
Triglyceride
Importance of Cholesterol Forms
List four different lipoproteins.

1. 3.
2. 4.
Physical Activity
How much greater is heart disease risk for a sedentary compared to a physically active person?
Hypertension
Indicate the lower borderline limit for the classification of high blood pressure.
Systolic
Diastolic
Cigarette Smoking
List three facts about cigarette smoking and the risk of developing CHD.
1. 3.
2.
Obesity
Discuss how obesity contributes as a multiple CHD risk factor.
Personality and Behavior Patterns

Describe personality characteristics of individuals who exhibit Type A and Type B behavior.
Type A
Type B
PRACTICE QUIZ
1. The difference between physical fitness e. none of the above

and physical activity: 6. Hyperlipidemia:
a. nothing a. elevated HDL and LDL
b. has to do with amount of activity b. relates to disease of pancreas
performed
c. controlled with high protein diet
c. has to do with absence of disease
d. elevated blood lipids
d. has to do with length of life
e. none of he above
7. HDL, LDL, VLDL:
2. The oldest old:
a. lipoproteins
a. age 85 and older
b. vitamins
b. age 70 and older
c. proteins
c. age 100 and older
d. enzymes
d. cannot exercise
8. HDL:Cholesterol ratio:
3. Physiology measures:
a. greater than 4.5 indicates high risk of
a. decline with age, but not at the same heart disease
rate
b. less than 4.5 indicates high risk heart
b. decline with age at the same rate disease
c. start to decline after age 15 y c. not important as a heart disease risk
d. stop declining for the oldest old d. chronic exercise decreases
e. none of the above e. none of the above
4. Harvard alumni study: 9. True or False: Physical activity can be
a. concerned with quality and quantity of thought of as an independent heart disease
life as affected by exercise habits risk factor:
b. showed that vigorous exercise was a. True
necessary for longevity b. False
c. showed that nutrition was more 10. Type A personality:
important than exercise in predicting
a. calm, easy going, laid back
longevity
b. increased risk for heart disease
d. showed that football players die young
c. usually are older
d. usually do not exercise
5. CHD
a. coronary heart disease
b. child health diseases
c. comorbidity, health, death
d. relates to exercise training techniques
LECTURE #11
TRAINING MUSCLES TO BECOME STRONGER
Introduction
Weightlifting began as a spectator sport in America in the early 1840s, practiced by “strongmen” who
showcased their prowess in traveling carnivals and sideshows. By the mid-1880s, measuring muscular
strength became more commonplace, particularly in schools and colleges as one of several indicators of an
individual fitness. In 1897 at a meeting of College Gymnasium Directors, strength test contests were
established to determine overall body strength based on measures of back, leg, arm, and chest strength. The
first 5 colleges to rank in the 1898–1899 contest were Harvard, Columbia, Amherst, Minnesota, and Dickinson.
By the mid-1900s, physical culture specialists, body builders, competitive weight lifters, field event
athletes, and some wrestlers used “weightlifting” exercises. Most other athletes, however, refrained from
lifting weights for fear it would slow them and increase muscle size so they would lose joint flexibility and
become “muscle-bound.” Research in the late 1950s and early 1960s silenced this myth by showing that
muscle-strengthening exercises did not reduce movement speed or flexibility. In longitudinal experiments
with untrained healthy subjects, heavy-resistance exercises actually increased speed and power.
In this lecture I explore the underlying rationale of strength (resistance) training, including physiologic
adjustments as muscles become stronger with training. The discussion centers on how to measure muscle
strength, strength differences between men and women, and different resistance training regimens.
Objectives
 Describe the following four methods to assess muscular strength: (a) cable tensiometry, (b)
dynamometry, (c) one-repetition maximum, and (d) computer-assisted isokinetic dynamometry.
 Compare absolute and relative upper and lower body muscular strength in men and women.
 Define concentric, eccentric, and isometric muscle actions, including examples of each.
 Provide general recommendations for appropriate frequency, overload, and sets and repetitions for
dynamic exercise resistance training.
 Explain specificity of training response for muscular strength related to enhanced sports performance.
 Describe how psychological and muscular factors influence maximum strength capacity.
 Describe delayed-onset muscle soreness (DOMS).
Foundations For Studying Muscular Strength

The scientific foundations for incorporating strength training as part of an athlete’s competitive training
can be traced to the Chinese in 3600 BC. In the Chou dynasty (1122-249 BC), conscripts had to pass weight-
lifting tests before they became soldiers. Weight training also took place in ancient Egypt and India;
sculptures and illustrations depict athletes training with heavy stone weights. Women also practiced weight
training; wall mosaics recovered from Roman villas showed young girls exercising with hand-held weights.
During the “Age of Strength” in the sixth century, weight lifting competitions often took place between
soldiers and athletes. Galen, the famous early Greek physician (Lecture 2), refers to exercising with weights
(halters) in his various writings.
The quest to develop muscular strength led to different “systems” of resistance training. The first
“modern” text detailing a strength training system appears to be the 1561 text by Sir Thomas Elyot, “The Boke
Named The Govuenour” (Elyot’s treatise establishes a detailed curriculum of study, including intellectual and
artistic pursuits and physical education, about the role of gymnastics and strength development standards to
which a governor should aspire). In the 1860s, Archibald MacLaren, a Scotsman, compiled the first system of
physical training with dumbbells and barbells for the British army.
Objectives of Resistance Training

The study of strength development provides practical applications in six areas: Weight lifting and power
lifting competition
1. Body building (for aesthetic goals
2. Fitness and health enhancement
3. Physical therapy; rehabilitation from injury
4. Sport-specific resistance training
5. Understanding muscle function and structure
6. Definition of Terms in Resistance Training
Terms and jargon abound in the area of resistance training, yet certain terms consistently appear in the
research literature. Below is listed a selection of common resistance training terms.
Cheating. Breaking from strict form (e.g., rather than maintaining an erect upper body when performing a
standing arm curl, a slight body swing at the start the movement allows the person to lift a heavier
weight (or the same weight more times). Cheating increases injury if performed improperly.
Circuit Resistance Training (CRT). Series of resistance training exercises performed in sequence with
minimal rest between exercises. More frequent repetitions with less resistance activate the
cardiovascular system to produce an aerobic training effect.
Concentric Action. Muscle shortening during force application
Dynamic Constant External Resistance (DCER). Training: Resistance training where external resistance
or weight does not change; joint flexion and extension occurs with each repetition. Formerly (but
incorrectly) referred to as “isotonic” exercise.
Eccentric Action. Muscle lengthening during force application.
Exercise Intensity. Muscle force expressed as a percentage of muscle’s maximum force-generating
capacity or some level of maximum.
Isokinetic Action. Muscle action performed at constant angular limb velocity.
Isometric Action. Muscle action without change in muscle length.

Maximal Voluntary Muscle Action (MVMA). Maximal force generated in one repetition (1-RM), or
performing a series of submaximal actions to momentary failure.
Muscular Endurance. Sustaining maximum (or submaximum) force; often determined by assessing
maximum number of exercise repetitions at a percentage of maximum strength.
Overload. A muscle acting against a resistance normally not encountered (unaccustomed stress).
Periodization. Variation in training volume and intensity over a specified time period; goal to prevent
staleness and peak physiologically for competition.
Plyometrics. Resistance training involving eccentric-to-concentric actions performed quickly so a muscle
stretches slightly prior to the concentric action; utilizes stretch reflex to augment muscle’s force-
generating capacity.
Power. Rate of performing work (Force x Distance ÷ Time, or Force x Velocity). Power applied to
weightlifting relates to mass lifted times vertical distance it moves, divided by the time to complete the
movement; if 100 lbs moves vertically 3 feet in one second, the power generated = 100 lb x 3 ft ÷ 1 s or 300
ft-lb•s-1.
Progressive Overload. Incrementally increasing the stress placed on a muscle as it produces greater force
or greater endurance.
Range of Motion (ROM). Maximum movement through an arc of a body joint.
Repetition. One complete exercise movement, usually consisting of concentric and eccentric muscle
actions or one complete isometric muscle action.
Repetition Maximum (RM). Greatest force generated for one repetition of a movement (1-RM).
Set. Pre-established number of repetitions performed.
Sticking Point. Region in an exercise movement (against a set resistance) that provides greatest difficulty
completing the movement.
Strength. Maximum force-generating capacity of a muscle or group of muscles.
Torque. Force that produces a turning, twisting, or rotary movement in any plane about an axis (e.g.,
movement of bones about a joint); commonly expressed in Newton-meters (Nm).
Training Volume. Total work performed in a single session.
Variable Resistance Training. Training with equipment that uses a lever arm, cam, or pulley to alter the
resistance to match increases and decreases in muscle force capacity throughout a joint’s ROM.
Measurement of Muscular Strength

Four methods generally assess
muscular strength, i.e., the
maximum force, tension, or torque
generated by a muscle or muscle
groups: Cable tensiometry,
dynamometry, one-repetition
maximum, and computer assisted
electromechanical and isokinetic
determinations.
Cable Tensiometry
Figure 1A shows a cable
tensiometer measuring muscular
force during knee extension.
Increased force on the cable
depresses a riser over which the
cable passes; this deflects the
pointer and indicates the subject’s
strength score. The application of
the tensiometer for strength
measurements differs considerably
Figure 1. Measurement of static strength by (A) cable tensiometer, (B) handgrip from its original use for measuring
dynamometer, and (C) backleg lift dynamometer. tension on steel cables linking
various parts of an airplane.
Cable tensiometry provides an excellent way to isolate a muscle at a specific joint angle for strength
determinations before and after training and rehabilitation. This method for strength assessment provides
another advantage because it can be applied in different movement phases to give a clear picture of the
strength (or weakness) of particular muscles acting in a range of motion (ROM). This cannot be done easily
with standard weight-lifting tests.
Dynamometry
Figures 1B and C display handgrip and back-lift dynamometers to assess static strength. Both devices
operate on the principle of compression. Application of external force to the dynamometer compresses a steel
spring and moves a pointer. By knowing how much force must move the pointer a given distance, one can
determine how much external “static” force has been applied to the dynamometer.
One-Repetition Maximum
The one-repetition maximum (1-RM) technique serves as a dynamic method for measuring muscular
strength. To test 1-RM for single or multiple muscle groups, the initial weight should be close to but below
maximum lifting capacity. Depending on the muscle group, increments in weight lifted range from 1 to 5 kg.
The 1-RM maneuver requires concentric and eccentric muscle actions, but only the concentric phase of the
action evaluates 1-RM.
Computer-Assisted Electromechanical and Isokinetic

Determinations
Microprocessor technology integrated with exercise equipment provides a unique way to quantify
muscular force during a variety of movements. Modern instrumentation measures force, acceleration, and
velocity of body segments in various movement patterns. Force platforms can measure the external
application of muscular force by limbs during jumping. Other electromechanical devices measure forces
generated during all movement phases of cycling, rowing, supine bench press, seated and upright leg press,
and exercises for other trunk, arm, and leg movements weight an individual can bench press or squat.
Strength Testing Considerations

The following factors affect strength testing, regardless of assessment method. It is necessary to:
 Give standardized instructions.
 Allow a warm-up of uniform duration (e.g., 3 to 5 minutes) and intensity (e.g., 50% of previously
established 1-RM depending on muscle group).
 Provide adequate practice several days before testing to minimize a “learning” component that could
compromise initial results or inflate evaluation of true training effects.
 Ensure constancy of limb position and/or measurement angle.
 Provide several trials (repetitions) to establish a criterion score.
 Administer strength tests with established reliability (reproducibility) of scores.
 Consider individual differences in body size and composition when evaluating strength scores among
individuals and groups.
Physical Testing in the Occupational Setting

No one “best” measure of muscular strength exists. Each individual possesses an array of muscular
“strengths” and “powers.” Often, these expressions of physiologic function and performance are not co-
related to each other. Likewise, a person has diverse capabilities for expressing aerobic capacity, depending
on the muscle mass exercised. In the occupational setting, a 12-minute run to infer aerobic capacity for fire
fighting or lumbering (both requiring significant upper body aerobic function), or static grip or leg strength to
evaluate the diverse strengths and powers required in such occupations, would be physiologically unwise in
light of current knowledge of performance specificity. Measurement in the occupational setting requires
attention not only to faithfully replicating specific job tasks, but also measuring the physiological demands of
the work for intensity, duration, and pace.
Important Issues for Training Muscles to Become

Stronger
Training muscles to become stronger requires different principles and adherence to specific guidelines.
Overload and Intensity

Muscular strength training requires application of the overload principle by use of weights (dumbbells or
barbells), immovable bars, straps, pulleys, or springs, and oil, air, and water hydraulic devices. In each case,
the muscle responds to the intensity of the overload rather than to the actual form of overload.
The amount of overload is usually expressed as a percent of the maximum force-generating capacity (1-
RM) of a non-fatigued muscle or muscle group. Performing a voluntary maximal muscle action means the
muscle must move against as much resistance as its present capacity level allows. Although a partially
fatigued muscle cannot generate the same force as a non-fatigued muscle, the last repetition in a set to
momentary failure still represents a voluntary maximal muscle action. Muscular overload in resistance
training usually requires voluntary maximal muscle actions.
Three approaches (either singularly or in combination) apply muscular overload in resistance training:
1. Increase load or resistance
2. Increase number of repetitions
3. Increase speed of muscle action
Muscular overload, referred to as training intensity, represents the most important concept in strength
development; it relates to the necessity for training above a minimum threshold level to induce a training
response. Minimal intensity
for overload occurs between
60 to 70% of 1-RM. This
means that performing a large
number of repetitions with a
light resistance generally
produces minimal strength
gains.
Muscle Actions
Concentric action represents
the most common form of
muscle action; it occurs in
dynamic activities where the
muscle shortens and joint
movement occurs as tension
develops. Figure 2A
illustrates a concentric
muscular action by raising a
dumbbell from the extended
to flexed elbow position.
Because a concentric muscle
action produces actual muscle
Figure 2. Muscular force during (A) concentric (shortening), (B) eccentric shortening, the word
(lengthening), and (C) isometric (static) actions. “contraction” frequently
describes this process.
Eccentric action (also called lengthening, stretching, or plyometric) occurs when external resistance
exceeds muscle force, and the muscle lengthens while developing tension. Figure 2B shows a weight slowly
lowered against the force of gravity. The muscles of the upper arm increase in length as they provide braking
action to prevent the weight from crashing to the floor.
Isometric action (also called static or stationary) occurs when a muscle attempts to shorten but cannot
overcome the resistance. Considerable muscular force can be generated during an isometric action with no
noticeable muscle lengthening or shortening or joint movement. Figure 2C illustrates an isometric muscular
action.
The term isotonic commonly describes concentric and eccentric muscle actions because movement occurs
in both cases. The term isotonic comes from the Greek isotonos (iso meaning the same or equal; tonos, tension
or strain.) Actually this term should not be applied to most dynamic muscle actions that involve movement
because the muscle’s force-generating capacity varies as the joint angle changes; thus, force output does not
remain constant through the ROM. Dynamic constant external resistance (DCER) provides a more useful
term for strength (resistance) training in which external resistance or weight does not change, but lifting
(concentric) and lowering (eccentric) phases occur during each repetition. DCER implies that the external
weight or resistance remains constant throughout the movement.
Force:Velocity Relationship
Different physical activities require different amounts of strength (force) and power. Absolute or peak
force generated in a movement depends upon the speed of muscle lengthening and shortening. Figure 3
shows the force:velocity relationship for concentric and eccentric actions. Muscles shorten at different
velocities (horizontal axis of graph) depending on the load placed on them. As the load increases, maximum
velocity decreases. Conversely, a muscle’s force-generating capacity (vertical axis of graph) rapidly declines
with increased shortening velocity. This explains the difficulty in attempting to move a heavy weight rapidly.
A concentric action becomes
a lengthening (eccentric) action
when the external load exceeds
a muscle’s maximum force
capacity (noted as point 0 on the
vertical axis.) Rapid eccentric
actions generate the greatest
muscular force. This may
explain muscle damage and
delayed muscle soreness while
doing eccentric exercise. Force
at zero velocity shortening
(isometric action) exceeds all
forces generated with concentric
actions. Muscle fiber type also
influences the force-velocity
relationships; fast-twitch muscle
fibers produce greater muscle
force at fast movement speeds
than slow-twitch fibers.
Power-Velocity
Relationship
Figure 4 (next page) shows
an “inverted U” relationship
between a muscle’s maximal power output and its speed of limb movement. Peak power rapidly increases
with increasing velocity to a peak velocity region. Thereafter, maximal power output decreases because of the
significant reduction in maximum force at faster movement speeds (Figure 15-4.) Thus, each muscle group
has an optimum movement speed to produce maximum power. At any movement velocity, greater peak
power occurs in fast-contracting fibers than slow-contracting fibers due mainly to the biochemical differences
between fibers.
Load:Repetition
Relationship
The total work accomplished by
muscle action depends on the
load (resistance) placed on the
muscle. One can perform high
repetitions with light loads, but
few repetitions with near maximal
loads.
Sex Differences In
Muscular Strength
Two approaches can determine
whether true sex differences exist
in muscular strength.
Absolute basis (as total force
exerted)
Relative basis (as force exerted in
relation to body mass, fat-free
body mass, or muscle cross-
sectional area)
Figure 4. Power-velocity relationship. Power (work per unit time) increases
as a function of movement velocity to a peak velocity region.
Absolute Strength
When comparing absolute
strength (total force in pounds or kilograms), men achieve considerably higher strength scores than women
for all muscle groups, regardless of test mode. Sex differences in strength are particularly apparent for upper
body strength evaluations; women exhibit about 50% less strength than men. In lower body strength, women
achieve 20 to 30% below the scores of male counterparts. Exceptions usually include strength-trained female
track and field athletes and bodybuilders who train diligently with overload resistance exercise to
significantly increase the strength of specific muscle groups.
Relative Strength
Human skeletal muscle in vitro generates 16 to 30 Newton’s (N) maximum force per square centimeter of
muscle cross-sectional area (MCSA) regardless of sex. In the body (in vivo), force-output capacity varies
depending on the arrangement of bony levers and muscle architecture.
Individuals with the largest MCSA generate the greatest muscular force. The strong, linear relationship
between strength and muscle size (r = 0.95) indicates little difference in arm flexor strength for the same size
muscle in men and women.
RESISTANCE TRAINING FOR CHILDREN

While resistance training for children has gained in popularity, its benefits and possible risks remain
relatively unknown. Because skeletal development is not complete in young children and adolescents,
obvious concern arises about the potential for bone and joint injury with heavy muscular overload.
Furthermore, one might question whether resistance training can induce significant strength improvements at
a relatively young age because the hormonal profile continues its progressive development (particularly for
the tissue-building hormone testosterone). Limited evidence indicates that closely supervised resistance
training programs using concentric-only muscle actions with high repetitions and low resistance significantly
improve children’s muscular strength with no adverse effect on bone or muscle.
The following guidelines should be used regarding strength training with children.
Age Strength Training Guidelines
5-7 Introduce child to basic exercises with little or no weight;

develop the concept of a training session; teach exercise
techniques; progress from body weight calisthenics, partner
exercises, and lightly resisted exercises; keep volume low.
8-10 Gradually increase the number of exercises; practice exercises
technique for all lifts; start gradual progressive loading of
exercises; keep exercises simple; increase volume slowly;
carefully monitor tolerance to exercise stress.
11-13
Teach all basic exercise techniques; continue progressive
loading of each exercise; emphasize exercise technique;
14-15 introduce more advanced exercises with little or no resistance.
Progress to more advanced resistance programs; add sport-
specific components; emphasize exercise techniques; increase
16+ volume.
Entry level into adult programs after all background
experience has been gained
Systems of Resistance Training

Five fundamentally different but interrelated systems of training result in muscular strength development:
1. Isometric training
2. Dynamic constant external resistance training
3. Variable resistance training
4. Isokinetic training
5. Plyometric training
Isometric Training (Static Exercise)

Isometric strength training gained popularity between 1955 and 1965. Research in Germany during this
time showed an increase in isometric strength of about 5% a week from only a daily, single, two-thirds
maximum isometric action for six-seconds duration! Repeating this action five to 10 times produced greater
increases in isometric strength. Gains in strength from this simple exercise overload seemed beyond belief,
and subsequent research demonstrated that isometric strength gains progressed at a much slower rate.
Research also showed that gains in strength from isometrics related to repetitions, duration of muscle action,
and training frequency.
Research since 1965 has revealed the following information regarding isometric training:
 Maximal voluntary isometric actions (100% maximum) produce greater gains in isometric strength
than submaximal isometric actions.
 Duration of muscle activation directly relates to increases in isometric strength.
 One daily isometric action does not increase isometric strength as effectively as repeated actions.
 An optimal isometric training program consists of daily repeated isometric actions.
 Isometric training does not provide a consistent stimulus for muscular hypertrophy.
 Gains in isometric strength occur predominantly at the joint angle used in training.
A drawback to isometric training is difficulty in monitoring training results. Because essentially no
movement occurs, it is difficult to determine objectively if the person’s strength actually improves and
whether he or she applies an appropriate overload force during training. Isometric force measurement
requires specialized equipment (e.g., strain gauge or cable tensiometer) not readily available at most exercise
facilities.
Dynamic Constant External Resistance (DCER) Training

This popular system of resistance training involves lifting (concentric) and lowering (eccentric) phases
with each repetition using weight plates (barbells and dumbbells) or exercise machines that feature different
applications of muscle overload.
Progressive Resistance Exercise

Researchers in rehabilitation medicine following World War II devised a method of resistance training to
improve the force-generating capacity of previously injured limbs. Their method involved three sets of
exercise, each consisting of 10 repetitions done consecutively without rest. The first set involved one-half the
maximum weight lifted 10 times or one-half 10-RM; and the second set used three-quarters 10-RM; the final
set required maximum weight for 10 repetitions or 10-RM. As patients trained and became stronger, 10-RM
resistance increased periodically to match strength improvements. This technique of progressive resistance
exercise (PRE) , a practical application of the overload principle, forms the basis for most strength
conditioning programs.
Variations of PRE
Variations of PRE have determined an optimal number of sets and repetitions, including frequency and
relative intensity of training, to improve strength. The findings can be summarized as follows:
 Performing between 3-RM and 9-RM is the most effective number of repetitions to increase muscular
strength.
 PRE training once weekly with only 1-RM for one set increases strength significantly after the first week
of training, and each week up to at least the sixth week.
 No particular sequence of PRE training with different percentages of 10-RM produces more effective
strength improvement, provided each training session consists of one set of 10-RM.
 Smaller strength increases occur when performing one set of an exercise rather than two or three sets,
and three sets produces greater improvement than two sets.
 For beginners, significant strength increases occur with only one training day weekly, but the optimum
number of training days per week with PRE remains unknown.
 When PRE training uses several different exercises, training four or five days a week may be less
effective for increasing strength than training two or three times weekly. More frequent training may
prevent sufficient recuperation between exercise sessions, which could retard neuromuscular
adaptation and strength development.
 A fast rate of movement for a given resistance generates greater strength improvement than lifting at a
slower rate. Neither free weights nor concentric-eccentric-type weight machines or “isotonic” devices
produce inherently superior results compared with other strength development methods.
Variable Resistance Training

A limitation of typical DCER weight-lifting exercise is failure of muscles to generate maximum force
through all phases of the movement. Variable resistance training equipment alters resistance to movement by
use of a lever arm, irregularly shaped metal cam, or pulley to match increases and decreases in force in
relation to joint angle (lever characteristics) throughout a ROM. This adjustment facilitates strength gains
allowing near-maximal force production throughout a ROM.
Research has shown that a single cam cannot possibly compensate fully for individual differences in
mechanics and force applications at all phases of the particular movement. Variations in limb length, point of
attachment of muscle tendons to bone, body size, and strength at different joint angles all affect maximum
force generated throughout a ROM. In most cases, cams produce too much resistance during the first half and
too little resistance during the second half of flexion and extension exercises. Despite these limitations, cam
devices produce strength improvements comparable to other types of equipment.
Isokinetic Training
Isokinetic resistance training differs from isometric and DCER methods; it employs a muscle action
performed at constant angular limb velocity. Unlike dynamic resistance exercise, isokinetic exercise does not
require a specified initial resistance; rather, the isokinetic device controls movement velocity. The resisting
force offered by the isokinetic machine cannot be accelerated; any force applied against the device’s lever
results in an opposing force, which thwarts any increase in movement velocity. The muscles exert maximal
force throughout the ROM while shortening (concentric action) at a specific velocity. Advocates of isokinetic
training argue that ability to exert maximal force throughout the full ROM optimizes strength development.
Also, concentric-only actions minimize muscle and joint injury and resulting pain.
Plyometric Training
Athletes who require specific powerful movements (e.g., football, volleyball, sprinting, and basketball)
perform exercise training termed plyometrics. With plyometric training, movements make use of the inherent
stretch-recoil characteristics of skeletal muscle and neurological modulation via the stretch or myotatic reflex.
Consider walking: When the foot first hits the ground, the quadriceps initially act (stretch) eccentrically, then
briefly isometrically, before the shortening phase of a muscle’s action begins. The term stretch-shortening
cycle describes the sequence of sequentially linked eccentric-isometric-concentric muscle actions. When
stretching occurs rapidly, stored elastic energy in muscle fibers and initiation of the myotatic reflex combine
to produce a powerful concentric action.
Vertical jumping provides an example of the stretch-shortening cycle to enhance performance. During a
normal vertical jump, the jumper bends at the knees and hips (eccentric action of extensors), pauses briefly
(isometric action), and rapidly reverses direction (concentric action) to jump upward as high as possible. If
this same movement stops for several seconds following the knee bend (just before reversing movement
direction), the subsequent jump (concentric action) produces a lower jump height compared with a
performance that uses the complete stretch-shortening cycle.
Figure 6. Examples of stretchshortening cycle (plyometric) exercises. A, strength development;
B, depth jumping; C, reactive ability.
Practical Applications
A plyometric training drill incorporates one’s body mass and the force of gravity to provide the all-
important rapid prestretch, or “cocking” phase to “activate” the stretch reflex and the muscle’s natural elastic
recoil elements. Lower-body plyometric drills include a standing jump, multiple jumps, repetitive jumping in
place, depth or drop jumps (from 1 to 4-ft. heights), and various modifications of single and double leg
jumps. Repeating these exercises regularly supposedly provides both neurological and muscular training to
enhance power performance of specific muscles. Figure 6 shows examples of plyometric exercises for strength
development, using resistance and other apparatus, including general jumping exercises and depth jumps.
Comparison of Training Systems

Few research studies directly compare different training systems within the same experimental protocol.
Some studies compare two different training systems (e.g., isometric versus variable resistance; isometric
versus isokinetic; isometric versus eccentric). The results generally support the specificity and individual
differences principles. When training and testing incorporate the same system, relatively large strength
increases occur, regardless of type of training system. When testing uses a different system than in training,
smaller training-induced strength increases occur, and in some experiments become nonexistent. Difficulties
arise in trying to compare different training systems because of methodological problems equating training
volume (sets and repetitions), total work, total training time, and most importantly, training intensity. This
makes it almost impossible to directly “prove” one strength training system “better” than another. Moreover,
some individuals simply respond more favorably to one system and not another.
Periodization
Periodization refers to organizing resistance training into phases of different types of exercise done at
varying intensities and volumes for a specific time period. Figure 7 displays a wave-like, basic periodization
scheme (and descriptions) with four phases or mesocycles . This system shows that phase one consists of
high volume (repetitions and sets) and low intensity exercise. During the next three phases, total exercise
volume decreases, and intensity increases. Periodization cycles can vary from one cycle to two or three cycles
Mesocycle 4
Figure 7. Basic periodization scheme comprising four transition phases. The periodization concept subdivides a macrocycle into
distinct phases or mesocycles. These in turn usually separate into weekly microcycles.
yearly. In general, each of the four phases emphasize a different component of strength development over a
competitive season.
Adaptations To Resistance Training

Resistance training produces acute responses and chronic adaptations. An acute response refers to
immediate changes (in muscle or other cells, tissues, or systems) that occur during or immediately after a
single bout of resistance exercise. For example, enzyme levels and energy stores change in response to specific
Figure 8. Six factors that impact the development and maintenance of muscle mass.
muscle actions. Chronic changes take place with repeated stimuli over the course of a training regimen.
Adaptation refers to how the body adjusts to repeated stimuli. The body responds acutely to a given stress,
while repeated exposure to the stimulus produces long-lasting changes that affect the acute response over
time (e.g., less disruption in cellular integrity [muscle damage] with a given level of exercise.)
Knowing the acute and chronic responses to resistance training facilitates exercise prescription and
program design. Adaptations to repeated muscular overload ultimately determine a training program’s
effectiveness. The time-course of adaptations varies among individuals and depends on the nature and
magnitude of prior adaptations. A resistance-training program should consider the expression of individual
differences in adaptation (training responsiveness.)
Adaptations to resistance training occur in diverse body systems from the cellular to systemic level.
Figure 8 displays six factors that impact development and maintenance of muscle mass. Unmistakably,
genetics provides the governing frame of reference that influences the effect of each other factor on the
ultimate training outcome. Muscular activity, however, contributes little to tissue growth without appropriate
nutrition to provide essential building blocks. Similarly, training outcome depends on specific hormones and
patterns of nervous system activation. Without overload, each of the other factors remains relatively
ineffective for inducing strength development.
Fast- and Slow-Twitch Muscle Fibers

Exercise physiologists have applied invasive biopsy techniques to study the functional and structural
characteristics of human skeletal muscle. The biopsy procedure uses a special needle to puncture the muscle
and obtain approximately 20 to 40 mg of tissue (the size of a grain of rice) for chemical and microscopic
analysis. Two distinct types of fiber have been identified in human skeletal muscle: fast-twitch and slow-
twitch. The proportion of each fiber type within a particular muscle probably remains fairly constant
throughout life.
Fast-Twitch Fiber
Fast-twitch muscle fiber, also known as type II fiber, possesses a high capacity for anaerobic ATP
production during glycolysis. These fibers possess a rapid contraction speed; they become activated in sprint
activities that depend almost entirely on anaerobic metabolism for energy. The metabolic capabilities of fast-
twitch fibers also become important in stop-and-go or change-off-pace sports like basketball, soccer, lacrosse,
and field hockey These sports often require rapid energy transfer through anaerobic metabolism.
Slow-Twitch Fiber
The slow-twitch or type I muscle fiber has a contraction speed about one-half as fast as its fast-twitch
counterpart. Slow-twitch fibers possess numerous mitochondria and a high concentration of enzymes
required to sustain aerobic metabolism. They demonstrate a much greater capacity to generate ATP
aerobically than their fast-twitch counterparts. As such, slow-twitch muscle fiber activation predominates in
endurance activities that depend almost exclusively on aerobic metabolism. Middle-distance running or
swimming, or basketball, field hockey, and soccer, require a blend of both aerobic and anaerobic capacities.
Both types of muscle fibers become activated in such sports.
From the preceding discussion, do you think that the predominant fiber type in specific muscles
contributes to success in a particular sport or activity?
Muscle Adaptations
Psychologic inhibitions and learning factors greatly modify muscular strength, but anatomic and
physiologic factors within the muscle determine the ultimate limit of strength development. The gross and
ultrastructural changes in muscle with chronic resistance training generally produce adaptations in the
contractile apparatus, accompanied by substantial gains in muscular strength and power. An increase in the
muscle’s external size represents the most visible adaptation to resistance training. Muscle fiber hypertrophy
(increase in size of individual fibers) usually explains increases in gross muscle size, although increased fiber
number (fiber hyperplasia) provides a hotly debated alternative hypothesis.
Muscle Fiber Hypertrophy

Increases in muscle size (hypertrophy) with resistance training for men and women can be viewed as a
fundamental biologic adaptation. Weightlifters’ and body builders’ extraordinarily large muscle size and
definition results from enlargement of individual muscle cells, mainly fast-twitch fibers. Growth takes place
from one or more of the following adaptations:
 Increased contractile proteins (actin and myosin)
 Increased number and size of myofibrils per muscle fiber
 Increased amounts of connective, tendinous, and ligamentous tissues
 Increased enzymes and stored nutrients

Not all muscle fibers undergo the same degree of enlargement with resistance training. Muscle growth
depends on the muscle fiber type activated and recruitment pattern. With initiation of heavy resistance
exercise training, alterations in various muscle proteins begin within several workouts. As training continues,
contractile proteins increase in conjunction with enlargement of muscle fiber cross-sectional area.
Muscle Remodeling: Can Fiber Type Be Changed?

Fourteen men performed three sets of 6-RM leg squats three times per week to evaluate the effects of eight
weeks of resistance training on muscle fiber size and composition in leg extensor muscles. Biopsies from the
vastus lateralis before and after training showed significant increases in the volume of fast-twitch fibers.
However, no change resulted in the percentage distribution of fast- and slow-twitch muscle fibers. This
finding supported previous short-term studies of overload training and muscle fiber type. Several months of
resistance training in adults does not alter basic fiber composition of skeletal muscle. It remains unknown
whether specific training early in life, or prolonged training such as engaged in by Olympic-caliber athletes,
actually changes a muscle fiber’s inherent twitch (speed of shortening) characteristics. Current consensus
maintains that genetic factors determine an individual’s predominant muscle fiber distribution. Significant
muscle fiber type transformation (i.e., transforming Type I to Type II fibers) probably does not occur in
healthy individuals.
Muscle Hypertrophy and Testosterone Levels

It is a popular belief that the male sex hormone testosterone facilitates muscle hypertrophy with resistance
training. Testosterone, the chief male hormone, binds with special receptor sites on muscle and other tissues
to contribute to male secondary sex characteristics. These include sex differences in muscle mass and strength
that develop at puberty’s onset. Variation in testosterone level would then explain individual differences in
muscular enlargement with resistance training, and the alleged smaller hypertrophic response of women to
muscular overload. Research to date, however, does not support such notions. Essentially no correlation
exists between plasma testosterone levels and body composition and muscular strength in men and women.
Muscle Hypertrophy: Male Versus Female

Computed topography scans to directly evaluate muscle cross-sectional area show that men and women
experience a similar hypertrophic response to resistance training. Men achieve a greater absolute change in
muscle size because of a larger initial total muscle mass, but no difference in muscle enlargement on a
percentage basis. Other comparisons between elite male and female bodybuilders have verified these
observations. The limited data from short-term experiments suggest that women can use conventional
resistance training and gain strength and size on a similar percentage basis as men without developing overly
large muscles (i.e., absolute change in girth).
Muscle Fiber Hyperplasia

Do the actual number of muscle cells increase ( hyperplasia ) with resistance training? Research in the
early 1980s showed that overload training of cat skeletal muscle caused development of new muscle fibers.
Hyperplasia occurred through proliferation of satellite cells (cells between the basement layer and plasma
membrane of muscle fibers) or longitudinal splitting (a relatively large muscle fiber splits into two or more
smaller, individual “daughter” cells.) However, species differences may influence a muscle’s response to
overload training; massive cellular hypertrophy in humans with resistance training does not occur in many
animal species. Thus, cellular proliferation represents their compensatory adjustment.
Cross-sectional studies of body builders with large limb circumferences and muscle mass failed to show
that they possessed significant hypertrophy of individual muscle fibers. While these athletes could have
inherited an initially large number of small muscle fibers (which then “hypertrophied” to normal size with
training), the findings certainly raise the possibility of significant hyperplasia in humans under certain
circumstances. Muscle fibers may adapt differentially to the high-volume, high-intensity training used by
body builders compared with the lower-repetition, heavy-load system favored by strength and power
athletes. Under most conditions, hyperplasia does not represent the primary human skeletal muscle
adaptation to overload. However, some hyperplasia may occur when Type II fibers reach their upper size
limit.
Connective Tissue and Bone Adaptations

Supporting ligaments, tendons, and bone tissues strengthen as muscle strength and size increase. Changes
in ligaments and tendons parallel the rate of muscle adaptation, while bone changes more slowly, perhaps
over a six-to-twelve month period. Connective tissue proliferates around individual muscle fibers; this
thickens and strengthens the muscles’ connective tissue harness. Such adaptations from resistance training
protect joints and muscles from injury and justify resistance exercise for preventive and rehabilitative
purposes.
Training volume and intensity influence the effect of resistance training on the cardiovascular system.
Subtle yet important differences exist between myocardial enlargement from resistance training
(physiological hypertrophy) and enlargement from chronic hypertension (pathological hypertrophy). In the
pathologic condition, ventricular wall thickness increases beyond normal limits regardless of assessment
method and evaluative criteria. Dilation and weakening of the left ventricle, a frequent response to chronic
hypertension, does not accompany the compensatory increase in myocardial wall thickness with resistance
training. The hearts of these athletes usually exceed the size of untrained counterparts, but heart size
generally falls within the upper range limits of normal in relation to various measures of body size or cardiac
function.
Resistance exercise causes a greater, acute rise in blood pressure than lower-intensity dynamic
movements, but does not produce any long-term increase in resting blood pressure. Weight lifters and body
builders with hypertension probably have existing essential hypertension, experience chronic overtraining
syndrome, use steroids, or possess an undesirable level of body fat or other hypertension risks established for
the general population.
Body Composition Adaptations

For the most part, small decreases occur in body fat, with minimal increases in total body mass and fat-
free body mass. The largest increases amount to about 3 kg (6.6 lb.) over ten weeks, or about 0.3 kg weekly,
with results about the same for men and women. Body composition data for other strength training systems
show similar results. Thus, no one resistance training system appears superior to another for changing body
composition.
Organizing A Resistance Training Program

Individuals without prior resistance-training experience generally follow a program designed to produce
all-around strength improvements. Competitive athletes have different needs, and they organize their
strength-training regimen into phases with different types of exercises done at varying intensities and
volumes. A resistance-training program consists of four aspects:
1. Goal setting
2. Selecting the appropriate training system
3. Determining optimal resistance
4. Program organization
Muscle Soreness and Stiffness

Following an extended layoff from exercise, most of us have experienced pain, aches, soreness, tenderness,
stiffness or an “uncomfortable” feeling in exercised muscles and joints. Temporary soreness can persist
several hours immediately following unaccustomed exercise, whereas residual delayed-onset muscle
soreness (DOMS) may appear 24-hours later and last up to two weeks, depending on its severity. DOMS can
range from mild (24 hours post-exercise) to severe (5 days post-exercise.) Any one of at least six factors may
cause DOMS:
 Minute tears in muscle tissue damage cells, which release chemical substances (e.g., histamines,
prostaglandins, bradykinin, proteolytic enzymes, potassium ions, anaerobic metabolites) that stimulate
free nerve endings and produce pain.
 Osmotic pressure changes cause fluid retention (swelling) in surrounding tissues.
 Muscle spasms or cramps (sudden, involuntary, severe contraction in a shortened position) occur.
 Overstretching and tearing of portions of the muscle’s connective tissue harness (muscle-tendon
junction) or the muscle’s external surface occur. Structural damage to the internal myofibrils occurs in
the region of the Z-line. Damage to this region, called Z-line streaming, may involve mechanical factors
induced by high-force eccentric muscle actions.
 Alterations in the cell’s mechanism for calcium regulation occur.
 Inflammation responses (increases in white blood cells and interlukin-1 beta, and monocyte and
leukocyte accumulation) occur.
DOMS and Eccentric Muscle Action

Although the precise cause of muscle soreness remains unknown, the degree of discomfort largely
depends on intensity and duration of effort and, most importantly, the type of exercise performed. High-
force/high-tension eccentric muscle actions (actively resisting muscle lengthening) generally cause the
greatest postexercise discomfort. This effect does not relate to lactate buildup, because level running
(primarily concentric actions) produces no residual soreness despite significant elevations in blood lactate. In
contrast, downhill running (primarily eccentric actions) causes moderate-to-severe DOMS without
significantly elevating lactate during or following exercise.
Cell Damage
The first bout of repetitive, unaccustomed physical activity disrupts the integrity of the cells’ internal
environment. This can produce microlesions and subsequent temporary ultrastructural muscle damage in a
pool of stress-susceptible or degenerating muscle fibers. Damage becomes more extensive several days after
exercise than in the immediate postexercise period. A single bout of moderate concentric exercise provides a
significant prophylactic effect on the development of muscle soreness in subsequent high-force eccentric
exercise, with the effect persisting up to six weeks. Such results support the wisdom of initiating a training
program with repetitive, moderate concentric exercise to protect against the muscle soreness that occurs
following exercise with an eccentric component.
VITAMIN E HELPS REDUCE DOMS

Vitamin E acts as an important antioxidant to thwart free radical damage via lipid peroxidation, which
increases the vulnerability of the cell and its constituents. A recent study showed that supplements of 800 IU
of vitamin E taken every day for seven days before 45 minutes of downhill running minimized muscle
damage and reduced inflammation and soreness compared to a control group that received a placebo.
This study demonstrated that heavy resistance exercise increases free radical formation, and that
supplementing with vitamin E minimizes damage to muscle fiber membranes. The proposed mechanism
remains unknown concerning why intensive resistance exercise increases free radical formation. Research
with animals suggests mitochondrial hyperoxia may increase free radical formation during aerobic exercise.
For intense muscular activities that emphasize high force production, human research also suggests that
reperfusion with blood at the muscle site following exercise may trigger increased free radical formation.
Additional research should focus on different modes of high-force exercise, including variations in intensity,
duration, and frequency, and vitamin E supplementation on muscle morphology.
Theories Explaining DOMS

Several theories attempt to explain DOMS, including:
 Spasm
Due to extreme overload the muscle goes into periodic spasms that result in soreness
 Tear
Minute tears, or ruptures, of individual fibers cause the delayed soreness
 Excess metabolite
Prolonged exercise that follows a layoff causes metabolite accumulation in muscle; fluid retention
occurs because the metabolites trigger osmotic changes in the cellular environment; swelling
caused by increased osmotic pressure excites sensory nerve endings and causes pain
 Connective tissue damage
Eccentrically exercised muscles damages connective tissue
Figure 19 outlines probable steps in DOMS development and recuperation.
Figure 9. Proposed sequence for developing

DOMS following unaccustomed exercise.

1. Absolute muscular strength
2. Adaptation
3. Circuit resistance training (CRT)
4. Concentric action
5. Delayed-onset muscle soreness (DOMS)
6. Drop-jumping
7. Dynamic constant external resistance (DCER)
8. Dynamometry
9. Eccentric muscle action
10. Force:velocity relationship
11. Isokinetic muscle action

12. Isometric muscle action
13. Muscle hyperplasia
14. Muscular hypertrophy
15. One-repetition maximum
16. Overload principle
17. Periodization
18. Plyometrics
19. Progressive resistance exercise (PRE)
20. ROM
21. Spasm hypothesis
22. Strength training specificity
23. Tear theory

STUDY QUESTIONS
Foundations For Studying Muscular Strength

List four areas for which the study of muscular strength development provides practical
applications.
1. 3.
2. 4.
Objectives of Resistance Training

List three objectives of resistance training for overall fitness and exercise performance.
1. 3.
2.
Measurement of Muscular Strength

List four methods for measuring muscular strength.
1. 3.
2. 4.
Cable Tensiometry
List one advantages of cable tensiometry testing.
One-Repetition Maximum
Define 1-RM.
Strength Testing Considerations

Name three factors that affect strength testing.
1. 3.
2.
Important Issues for Training Muscles to Become Stronger

Overload and Intensity
How is the amount of overload usually expressed in resistance training?
List three approaches to applying overload in resistance training.

1. 3.
2.
List and describe the three types of muscle action.

Action Description
1.
2.
3.
Force-Velocity Relationship
Draw a graph showing the force-velocity relationship for concentric and eccentric actions.
Force
Lengthening Shortening
Velocity
Power-Velocity Relationship
Draw and label a graph showing the relationship between power and velocity.
Sex Differences in Muscular Strength

Absolute Strength
What are the sex differences in absolute muscular strength of the upper and lower body?
Upper Lower
Relative Strength
Quantify the maximum muscle force (N) generated by human skeletal muscle per square cm of
muscle cross-sectional area.
Resistance Training For Children

List three considerations before initiating a children’s resistance training program.
1. 3.
2.
Systems of Resistance Training

List five different systems for muscular strength development.
1. 4.
2. 5.
3.
Isometric Training (Static Exercise)

List four facts regarding isometric strength training.
1. 3.
2. 4.
Dynamic Constant External Resistance Training

Progressive Resistance Exercise
Briefly describe the principles of the progressive resistance exercise system.
Variable Resistance Training

List three factors that why a single variable resistance “cam” does not allow for individual
differences in mechanics and force applications.
1. 3.
2.
Isokinetic Training
Explain in you own words the unique aspects of isokinetic resistance training compared to more
“standard” forms of resistance training.
Plyometric Training
What performance would benefit most from plyometric training?
Practical Applications
Describe an example of plyometric training for a track sprint athlete.
Comparison of Training Systems

Comparisons of strength training systems generally support the _____________ and
___________________ principles of strength training.
Periodization
Describe the purpose of fractionating the resistance training cycle in periodization.
Adaptations to Resistance Training

Describe differences between acute and chronic adaptations.
Fast-Twitch Fiber
List two characteristics of fast-twitch (type II) muscle fibers
1.
2.
What energy system most often supports fast-twitch muscle fiber activity?
Slow-Twitch Fiber
List two characteristics of slow-twitch or (type I) muscle fibers.
1.
2.
Muscle Fiber Hypertrophy

List four muscle adaptations that help to explain muscle growth form resistance training.
1. 3.
2. 4.
Muscle Remodeling: Can Fiber Type Be Changed

Describe changes in the percentages of fast and slowtwitch fibers resulting from training.
Muscle Hypertrophy: Males Versus Female

Discuss whether the skeletal muscle of women can hypertrophy to the same extent as men with
regular resistance training.
Muscle Fiber Hyperplasia

Summarize the current state of knowledge regarding muscle fiber hyperplasia with resistance
training.
Explain why typical resistance training does not provide an adequate stimulus to improve
cardiovascular status.
What happens to blood pressure with resistance training?
Body Composition Adaptations

Is resistance training important for causing changes in body composition?
Muscle Soreness and Stiffness

List four possible causative factors for delayed onset muscle soreness.
1. 3.
2. 4.
DOMS and Eccentric Muscle Action

Why do eccentric actions contribute to greater muscle damage and resulting soreness than
concentric actions?
PRACTICE QUIZ
1. Isometric action: c. inversely proportional to resistance
a. muscle action without change in muscle d. same as DCER
length e. none of the above
b. same as eccentric action 5. Concentric action:
c. same as concentric action a. lengthening action
d. opposite of eccentric action b. same as isokinetic action
e. none of the above c. shortening action
2. DCER: d. involves no joint movement
a. external resistance does not change e. none of the above
b. external resistance changes by 1-RM 6. Eccentric action:
c. same as isometric action a. lengthening action
d. same as isokinetic action b. same as isokinetic action
e. none of the above c. shortening action
3. Dynamometer: d. involves no joint movement
a. used to measure isokinetic strength e. none of he above
b. used to measure static strength 7. Power:
c. used to measure range of motion a. usually expressed in joules
d. same as 1-RM b. force x distance ÷ by time
e. none of the above c. distance x time ÷ force
4. Training intensity: d. resistance x distance moved
a. same as muscular overload e. none of the above
b. proportional to number of contractions 8. PRE:
a. same as fartlek training

b. uses eccentric actions only
c. uses concentric actions only
d. uses isometric actions only
9. True or False: Isokinetic resistance training
differs from isometric and DCER methods.
a. True
b. False
10. Muscle hyperplasia:
a. increase in muscle cell number
b. increase in muscle cell size
c. increase in size of myofibrils
d. decrease in muscle fiber number
LECTURE #12
BODY COMPOSITION: ASSESSMENT AND HUMAN
VARIATIONS
Introduction
This lecture discusses the gross composition of the human body and present the rationale underlying
various direct and indirect methods to partition the body into two basic compartments, body fat and fat-free
body mass. It also presents simple, non-invasive methods to analyze an individual’s body composition.
Americans consume more fat per capita than any other nation. They also consume more than 90% of the
foods high in saturated fatty acids and processed, high-glycemic carbohydrates. A national preoccupation
with food and effortless living causes more than 110 million men and women (and more than 10 to 12 million
children and teenagers) to become “over fat” and in need of weight reduction. If these individuals consumed
600 fewer calories daily to reduce to a “normal” body fat level, the annual energy savings would equal the
yearly residential electricity demands of Boston, Chicago, San Francisco, and Washington, DC, or the
equivalent of more than 1.3 billion gallons of gasoline to fuel about 1 million autos for one year!
Objectives
 Summarize inadequacies of the “height-weight” tables.
 Outline characteristics of the “reference man” and “reference woman,” including specific values for
storage fat, essential fat, and sex-specific essential fat.
 Define fat-free body mass.
 Define minimal weight.
 Describe Archimedes’ principle applied to human body volume measurement.
 Compare the body composition values of average young men and women with elite competitors in
endurance running, wrestling, weight lifting, and bodybuilding.
 List significant health risks of obesity.
 Define fat cell hypertrophy and fat cell hyperplasia, and explain how each contributes to obesity.
 Outline how “unbalancing” the energy balance equation affects body weight. Explain the effectiveness
of specific exercise for localized fat loss.
Gross Composition of the Human Body

A full understanding of human body composition requires consideration of complex interrelationships
among its chemical, structural, and anatomical components. Figure 1 displays a five-level, multicomponent
model for quantifying body composition. Each level of the model becomes progressively more complex as
biological organization increases (atoms –––> molecules –––> cells –––> tissue systems –––> whole body.) The
model’s essential feature views each level as distinct, with measurable characteristics or subdivisions. This
allows the researcher to focus on a particular aspect of body composition related to specific or general
biological effect including changes in molecular, cellular, or tissue composition from body weight gain or loss,
or diverse forms of exercise training.
Figure 1. Fivelevel, multicomponent model to assess and interpret body composition. Each component within a level
becomes more complex with an increase in the body’s level of biological organization.
Analysis of body composition most often focuses on the tissue and whole body level, primarily because of
methodological and practical limitations. Due to marked sex differences in several of the body’s
compositional components, a convenient framework for understanding body composition employs the
concept of a reference man and reference woman developed by Dr. Behnke (Figure 2.)
Height-Weight Tables
Height-weight tables serve as statistical landmarks to commonly assess the extent of “overweightness.”
They use the average ranges of body mass in relation to stature where men and women aged 25 to 59 years
have the lowest mortality rate. Height-weight tables do not consider specific causes of death or quality of
health before death. Different versions of the tables recommend different “desirable” weight ranges, with
some considering frame-size, age, and sex.
Reference Man and Reference Woman
Figure 2. Body composition of the reference man and reference woman.
The reference man is taller by 10.2 cm and heavier by 13.3 kg than the reference woman, his skeleton
weighs more (10.4 vs. 6.8 kg), and he possesses a larger muscle mass (31.3 vs. 20.4 kg) and lower total fat
content (10.5 vs. 15.3 kg.) These differences exist even when expressing the amount of fat, muscle, and bone as
a percentage of body mass. This holds particularly for body fat, which represents 15% of the reference man’s
total body mass and 27% for females. The concept of reference standards does not mean that men and women
should strive to achieve these body composition values, or that reference values actually represent “average.”
Instead, the model provides a useful frame of reference for interpreting statistical comparisons of athletes,
individuals involved in physical training programs, and the underweight and obese.
Essential and Storage Fat

According to the reference model, total body fat exists in two storage sites or depots: essential fat and
storage fat.
Essential Fat
The essential fat depot (equivalent to approximately 3% of body mass) consists of fat stored in the marrow
of bones, heart, lungs, liver, spleen, kidneys, intestines, muscles, and lipid-rich tissues of the central nervous
system (brain and spinal cord.) Normal physiologic functioning requires this fat. In females, essential fat also
includes additional sex-specific essential fat (equivalent to approximately 9% of body mass.) More than likely,
this additional fat depot serves biologically important childbearing and other hormone-related functions.
Essential body fat likely represents a biologically established limit, beyond which encroachment could impair
health status as in prolonged semistarvation from famine, malnutrition, and disordered eating behaviors.
Storage Fat
In addition to essential fat depots, storage fat consists of fat accumulation in adipose tissue. Storage fat
includes the visceral fatty tissues that protect the various internal organs within the thoracic and abdominal
cavities from trauma, and the larger subcutaneous fat adipose tissue volume deposited beneath the skin's
surface. Men and women have similar quantities of storage fat – approximately 12% of body mass in males
and 15% in females. For the reference standards, this amounts to 8.4 kg for the reference and 8.5 kg for the
reference woman.
Fat-Free Body Mass and Lean Body Mass

The terms fat-free body mass and lean body mass refer to specific entities: lean body mass (a theoretical
entity) contains the small percentage of essential fat stores; in contrast, fat-free body mass represents the body
mass devoid of all extractable fat. In normally hydrated, healthy male adults, the fat-free body mass and lean
body mass differ only in terms of organ-related essential fat. Thus, lean body mass (LBM) calculations include
the small quantity of essential fat, whereas fat-free body mass (FFM) computations exclude total body fat
(FFM = Body mass – Fat mass.) Many researchers use the terms interchangeably; technically, however, the
differences are subtle but real.
Minimal Body Mass

In contrast to the lower limit of body mass for the reference man which includes 3% essential fat, the lower
body mass limit for females, termed minimal body mass includes about 12% essential fat (3% essential fat +
9% sex-specific essential fat.) Generally, the leanest women in the population do not have body fat levels
below 10 to 12% of body mass, a value that probably represents the lower limit of fatness for most women in
good health. The theoretical minimal body mass concept developed by Behnke, incorporating about 12%
essential fat, corresponds to a man’s lean body mass with about 3% essential fat. Information from popular
magazines and health clubs not withstanding, females cannot achieve the same low body fat content as males.
Therefore, women should not expect to “sculpt” their bodies down below 12-17% body fat. Even world-class
female body builders, triathletes, and gymnasts rarely have body fat levels below this amount.
Underweight and Thin

The terms underweight and thin are not necessarily synonymous. Measurements in our laboratories have
focused on the structural characteristics of apparently “thin” looking females. Subjects were initially
categorized subjectively as appearing thin or “skinny.” Each of the 26 women then underwent a thorough
anthropometric evaluation that included skinfolds, circumferences, and bone diameters, and percent body fat
and fat-free body mass from hydrostatic weighing.
The results were unexpected because the women’s percent body fat averaged 18.2%, about 7 percentage
points below the average 25 to 27% body fat typically reported for young adult women. Another striking
finding included equivalence in four trunk and four extremity bone-diameter measurements among the 26
thin-appearing women, 174 women who averaged 25.6% fat, and 31 women who averaged 31.4% body fat.
This meant that appearing thin or skinny did not necessarily correspond to a diminutive frame-size or an
excessively low body fat content using lower limits of minimal body mass and essential body fat proposed in
Behnke’s model.
Leanness, Exercise, and Menstrual Irregularity

Physically active women in general, and participants in “low weight” or “appearance“ sports like distance
running, body building, figure skating, diving, ballet, and gymnastics, increase their chances of menstrual
cycle disturbances. These include delayed onset of menstruation, an irregular menstrual cycle
(oligomenorrhea), or complete cessation of menses (amenorrhea.) Amenorrhea in the general population
occurs in 2 to 5% of women of reproductive age, whereas it can reach as high as 40% in some sports.
Studies of female ballet dancers support this position; as a group, ballet dancers remain quite lean and
have a greater incidence of menstrual dysfunction, eating disorders, and a higher mean age at menarche
compared with age-matched, non-dance females. One-third to one-half of female athletes in endurance-type
sports probably has some menstrual irregularity. In premenopausal women, irregularity or absence of
menstrual function increases their risk of bone loss and musculoskeletal injury when they participate in
vigorous exercise.

WHEN A MODEL IS NOT IDEAL
In 1967, only an 8% difference existed in body weight between professional fashion models and
the average American woman. Today, a model's body weight averages 23% lower than the
national average. Twenty years ago, gymnasts weighed about 20 lbs more than present day
counterparts. Thus, it comes as no surprise that disordered eating patterns and unrealistic
weight goals (and general dissatisfaction with one’s body) remain so common among females
of all ages.
In some way, the body seems to “sense” high physical stress and inadequate energy reserves to sustain a
pregnancy; in such cases, ovulation ceases. Some researchers have argued that at least 17% body fat
represents a “critical level” for onset of menstruation and 22% fat as a level required to sustain normal
menstruation. They argue that body fat below these levels triggers hormonal and metabolic disturbances that
affect the menses.
Leanness Not the Only Factor

The lean-to-fat ratio may play a key role in normal menstrual function (perhaps through peripheral fat's
role in converting androgens to estrogens, or through leptin production in adipose tissue), but so may other
factors. Many physically active females fall significantly below the supposed critical level of 17% body fat, but
have normal menstrual cycles and maintain a high level of physiologic and performance capacity.
Conversely, some amenorrheic athletes have average levels of body fat. In a study from one of our
laboratories, we compared menstrual cycle regularity for 30 athletes and 30 nonathletes, all with less than
20% body fat. Four of the athletes and three nonathletes ranging from 11 to 15% body fat had regular cycles,
whereas seven athletes and two nonathletes had irregular cycles or were amenorrheic. For the total sample, 14
athletes and 21 nonathletes had regular menstrual cycles. These data corroborate other research, and disprove
the hypothesis that normal menstrual function requires a critical body fat level of 17 to 22%.
Potential causes of menstrual dysfunction include the complex interplay of physical, nutritional, genetic,
hormonal, regional fat distribution, psychological, and environmental factors. An intense exercise bout
triggers the release of an array of hormones, some of which have antireproductive properties. Further
research needs to determine whether regular heavy exercise produces a cumulative hormonal effect sufficient
to disrupt the normal menses. In this regard, when injuries in young amenorrheic ballet dancers prevent them
from exercising regularly, normal menstruation resumes, even though body weight remains stable.
Additional predisposing factors for reproductive endocrine dysfunction among athletes include nutritional
inadequacy and an exercise-induced energy deficit with heavy training.
Based on current research, approximately 13 to 17% body fat should be regarded as an estimate of a
minimal body fat level associated with regular menstrual function. The effects and risks of sustained
amenorrhea on the reproductive system remain unknown. A gynecologist/endocrinologist should evaluate
failure to menstruate or cessation of the normal cycle because it may reflect a significant medical condition
(e.g., pituitary or thyroid gland malfunction or premature menopause.) As explained in Lecture 3, prolonged
menstrual dysfunction can have profound negative effects on the density of the body's bone mass.
Methods to Assess Body Size and Composition

Two general approaches determine the fat and fat-free components of the human body:
1. Direct measurement by chemical analysis
2. Indirect estimation by hydrostatic weighing, simple anthropometric measurements, and other simple
procedures including height and weight
DIRECT ASSESSMENT
Two approaches directly assess body composition. In one technique, a chemical solution literally dissolves
the body into its fat and non-fat (fat-free) components. The other technique requires physical dissection of fat,
fat-free adipose tissue, muscle, and bone. Such analyses require extensive time, meticulous attention to detail,
and specialized laboratory equipment, and pose ethical questions and legal problems in obtaining cadavers
for research purposes.
INDIRECT ASSESSMENT
Many indirect procedures assess body composition including Archimedes’ principle (also known as
underwater weighing.) This method computes percent body fat from body density (the ratio of body mass to
body volume.) Other procedures use skinfold thickness and girth measurements, x-ray, total body electrical
conductivity or impedance, near-infrared interactance, ultrasound, computed tomography, air
plethysmography, magnetic resonance imaging, and dual energy x-ray absorptiometry.
Hydrostatic Weighing (Archimedes’ Principle)

The Greek mathematician and inventor Archimedes (287-212 BC) discovered a fundamental principle that
is applied to evaluate human body composition. Here is a description of Archimedes’ findinds:
“King Hieron of Syracuse suspected that his pure gold crown had been altered by substitution of silver
for gold. The King directed Archimedes to devise a method for testing the crown for its gold content
without dismantling it. Archimedes pondered over this problem for many weeks without succeeding,
until one day, he stepped into a bath filled to the top with water and observed the overflow. He thought
about this for a moment, and then, wild with joy, jumped from the bath and ran naked through the
streets of Syracuse shouting, ‘Eureka! Eureka!’ I have discovered a way to solve the mystery of the King’s
crown.”
Archimedes reasoned that gold must have a volume in proportion to its mass, and to measure the volume
of an irregularly shaped object required submersion in water with collection of the overflow. Archimedes
took lumps of gold and silver, each having the same mass as the crown, and submerged each in a container
full of water. To his delight, he discovered the crown displaced more water than the lump of gold and less
than the lump of silver. This could only mean the crown consisted of both silver and gold as the King
suspected.
Essentially, Archimedes evaluated the specific gravity of the crown (i.e., the ratio of the crown's mass to
the mass of an equal volume of water) compared with the specific gravities for gold and silver. Archimedes
probably also reasoned that an object submerged or floating in water becomes buoyed up by a counterforce
equaling the weight of the volume of water it displaces. This buoyant force helps to support an immersed
object against the downward pull of gravity. Thus, an object is said to lose weight in water. Because the
object’s loss of weight in water equals the weight of the volume of water it displaces, the specific gravity
refers to the ratio of the weight of an object in air divided by its loss of weight in water. The loss of weight in
water equals the weight in air minus the weight in water.
Specific gravity = Weight in air / Loss of weight in water
In practical terms, suppose a crown weighed 2.27 kg in air and 0.13 kg less (2.14 kg), when weighed
underwater (Figure 3.) Dividing the weight of the crown (2.27 kg) by its loss of weight in water (0.13 kg)
results in a specific gravity of 17.5. Because this ratio
differs considerably from the specific gravity of gold
(19.3), we too can conclude: “Eureka, the crown must be
fraudulent!”
The physical principle Archimedes discovered
allows us to apply water submersion or
hydrodensitometry to determine the body’s volume.
Dividing a person's body mass by body volume yields
body density (Density = Mass ÷ Volume), and from
this an estimate of percent body fat.
Determining Body Density

For illustrative purposes, suppose a 50-kg woman
weighs 2 kg when submerged in water. According to
Archimedes’ principle, a 48-kg loss of weight in water
equals the weight of the displaced water. The volume
of water displaced can easily be computed because we
know the density of water at any temperature. In the
example, 48 kg of water equals 48 L, or 48,000 cm3 (1 g
of water = 1 cm3 by volume at 39.2°F.) If the woman
were measured at the cold-water temperature of
39.2°F, no density correction for water would be
necessary. In practice, researchers use warmer water
and apply the density value for water at the particular
Figure 3. Archimedes’ principle to determine the volume
and subsequently the specific gravity of the king’s crown.
temperature. The body density of this person, computed as mass / volume, would be 50,000 g (50 kg) / 48,000
cm3, or 1.0417 g•cm-3.
Computing Percent Body Fat, Fat Mass (FM), and Fat-Free Mass
(FFM)
The equation that incorporates whole body density to estimate the body's fat percentage derives from the
following three premises:
Densities of fat mass (all extractable lipid from adipose and other body tissues) and fat-free mass
(remaining lipid-free tissues and chemicals, including water) remain relatively constant (fat tissue = 0.90
g•cm-3; fat-free tissue = 1.10 g•cm-3), even with large variations in total body fat and the fat-free mass (FFM)
components of bone and muscle.
Densities for the components of the fat-free mass at a body temperature of 37°C remain constant within
and among individuals: water, 0.9937 g•cm-3 (73.8% of FFM); mineral, 3.038 g•cm-3 (6.8% of FFM); protein,
1.340 g•cm-3 (19.4% of FFM.)
The person measured differs from the reference body only in fat content (reference body assumed to
possess 73.8% water, 19.4% protein, 6.8% mineral.)
The following equation, derived by Berkeley scientist Dr. William Siri, computes percent body fat from
estimates of whole body density:
Siri Equation = [Percent body fat = 495 / Body density – 450]
The following example incorporates the body density value of 1.0417 g•cm-3 (determined for the woman
in the previous example) in the Siri equation to estimate percent body fat:
Percent body fat = 495 / Body density – 450
Percent body fat = 495 / 1.0417 – 450
Percent body fat = 25.2%
The mass of body fat (FM) can be calculated by multiplying body mass by percent fat:
Fat mass (kg) = Body mass (kg) x [Percent fat ÷ 100]
Fat mass (kg) = 50 kg x 0.252
Fat mass (kg) = 12.6
Subtracting mass of fat from body mass yields fat-free body mass (FFM):
FFM (kg) = Body mass (kg) – Fat mass (kg)
FFM (kg) = 50 kg – 12.6 kg
FFM (kg) = 37.4
In this example, 25.2% or 12.6 kg of the 50 kg body mass consists of fat, with the remaining 37.4 kg
representing the fat-free mass.
Body Volume Measurement

Figure 4 illustrates measurement of body volume by hydrostatic
weighing. First, the subject's body mass in air is accurately assessed,
usually to the nearest ±50 g. A diver’s belt secured around the waist
prevents less dense (more fat) subjects from floating toward the surface
during submersion. Seated with the head out of water, the subject then
makes a forced maximal exhalation while lowering the head beneath the
water. Using a snorkel and nose clip eases apprehension about submersion
in some subjects. The breath is held for several seconds while the
underwater weight is recorded. The subject repeats this procedure eight to
twelve times to obtain a dependable underwater weight score. Even when
achieving a full exhalation, a small volume of air, the residual lung
volume, remains in the lungs. The calculation of body volume requires
subtraction of the buoyant effect of the residual lung volume, measured
immediately before, during, or following the underwater weighing.
Body Volume Measurement By Air

Displacement
Techniques other than hydrodensitometry can measure body volume.
For example the BOD POD, a plethysmographic device for determining
body volume. The technology applies the gas law stating that a volume of
air compressed under isothermal conditions decreases in proportion to a
change in pressure. Essentially, body volume equals the chamber’s
reduced air volume when the subject enters the chamber. The subject sits
in a structure comprised of two chambers, each of known volume. A
molded fiberglass seat forms a common wall separating the front (test)
and rear (reference) chambers. A volume-perturbing element (a moving
diaphragm) connects the two chambers. Changes in pressure between the
two chambers oscillate the diaphragm, which directly reflects any change
in chamber volume. The subject makes several breaths into an air circuit to
assess thoracic gas volume (which when subtracted from measured body
volume yields body volume.) Body density computes as body mass
(measured in air) ÷ body volume (measured by BOD POD.) The Siri
equation converts body density to percent body fat.
Figure 4. Measuring body
Skinfold Measurements volume by underwater weighing.
Simple anthropometric procedures can successfully predict body fatness. The most common of these
procedures uses skinfolds. The rationale for using skinfolds to estimate total body fat comes from the close
relationships among three factors: (a) fat in adipose tissue deposits directly beneath the skin (subcutaneous
fat), (b) internal fat, and (c) body density.
Girth Measurements
Girth measurements offer an easily administered, valid, and attractive alternative to skinfolds. Apply a
linen or plastic measuring tape lightly to the skin surface so the tape remains taut but not tight. This avoids
skin compression that produces lower than normal scores. Take duplicate measurements at each site and
average the scores.
The Body Mass Index

Clinicians and researchers frequently use body mass index (BMI), derived from body mass in relation to
stature, to evaluate the “normalcy” of one's body weight. The BMI has a somewhat higher association with
body fat than estimates based simply on stature and mass.
BMI = Body mass, kg / Stature, m2
The importance of this
index is its curvilinear
relationship to all-cause
mortality ratio: As BMI
becomes larger, risk
increases for
cardiovascular
complications (including
hypertension), diabetes,
and renal disease (Figure
5). The disease risk levels at
the bottom of the figure
represent the degree of risk
with each 5-unit increase in
BMI. The lowest health risk
category occurs for BMIs in
the range 20 to 25, with the
Figure 5. Curvilinear relationship between allcause mortality and body mass index. At
extremely low BMIs, the risk for digestive and pulmonary diseases increases, while highest risk for BMIs >40.
cardiovascular, gallbladder, and type 2 diabetes risk increases with higher BMIs. For women, 21.3 to 22.1 is
the desirable BMI range;
the range for men is 21.9 to
22.4. An increased incidence of high blood pressure, diabetes, and CHD when BMI exceeds 27.8 for men and
27.3 for women.
The Surgeon General defines overweight as a BMI between 25 and 30; a BMI in excess of 30 defines
obesity, a value corresponding to a moderate category of health risk. For the first time in the Unites States,
overweight people (BMI over 25) outnumber people of desirable weight; shockingly, 59% percent of
American men and 49% of women have BMIs that exceed 24!
The prevalence of overweight status in the United States using the BMI index is 34 million adults (15.4
million males, 18.6 million females), representing about 26% of the adult population. When analyzing the
data in Figure 6 by ethnicity and sex, significantly more black, Mexican, Cuban, and Puerto Rican males and
females classify as overweight compared with white males and females. Thirty-one percent of Mexican males
displayed the most overweight based on BMI (31.2%), while BMI targeted 45.1% of black females as
overweight.
Determine Your Body Mass Index from the following table; use weight in pounds and height in feet and
inches.
Weight 100 105 110 115 120 125 130 135 140 145 150 155 160 165 170 175 180 185 190 195 200 205
lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs lbs
Height
5'0" 20 21 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40
5'1" 19 20 21 22 23 24 25 26 26 27 28 29 30 31 32 33 34 35 36 37 38 39
5'2" 18 19 20 21 22 23 24 25 26 27 27 28 29 30 31 32 33 34 35 36 37 37
5'3" 18 19 19 20 21 22 23 24 25 26 27 27 28 29 30 31 32 33 34 35 35 36
5'4" 17 18 19 20 21 21 22 23 24 25 26 27 27 28 29 30 31 32 33 33 34 35
5'5" 17 17 18 19 20 21 22 22 23 24 25 26 27 27 28 29 30 31 32 32 33 34
5'6" 16 17 18 19 19 20 21 22 23 23 24 25 26 27 27 28 29 30 31 31 32 33
5'7" 16 16 17 18 19 20 20 21 22 23 23 24 25 26 27 27 28 29 30 31 31 32
5'8" 15 16 17 17 18 19 20 21 21 22 23 24 24 25 26 27 27 28 29 30 30 31
5'9" 15 16 16 17 18 18 19 20 21 21 22 23 24 24 25 26 27 27 28 29 30 30
5'10" 14 15 16 17 17 18 19 19 20 21 22 22 23 24 24 25 26 27 27 28 29 29
5'11" 14 15 15 16 17 17 18 19 20 20 21 22 22 23 24 24 25 26 26 27 28 29
6'0" 14 14 15 16 16 17 18 18 19 20 20 21 22 22 23 24 24 25 26 26 27 28
6'1" 13 14 15 15 16 16 17 18 18 19 20 20 21 22 22 23 24 24 25 26 26 27
6'2" 13 13 14 15 15 16 17 17 18 19 19 20 21 21 22 22 23 24 24 25 26 26
6'3" 12 13 14 14 15 16 16 17 17 18 19 19 20 21 21 22 22 23 24 24 25 26
6'4" 12 12 13 14 15 15 16 16 17 18 18 19 19 20 21 21 22 23 23 24 24 25
In June 1998, the National Institutes of Health released the first Guidelines for identifying, evaluating, and
treating obesity based on BMI values. The new classifications (2000) based on BMI are as follows:
Classification BMI Score
Underweight <18.5
Normal 18.5-24.9
Overweight 25.0-29.9
Obesity Class I 30.0-34.9
Obesity Class II 35.0-39.9
Extreme Obesity >40
The above guidelines have fueled controversy because previous guidelines established overweight at a
BMI of 27 (not 25). The lowering of the demarcation value propels an additional 30 million Americans into the
overweight category. This now means that 555 of the U.S. population qualify as overweight.
The following table uses the BMI to predict disease risk. A high BMI links to increased risk of death from
all causes, hypertension, cardiovascular disease, dyslipidemia, diabetes, sleep apnea, osteoarthritis, and
female infertility.
Competitive athletes and body builders with a high BMI due to increased muscle mass, and pregnant or
lactating women, should not use BMI to infer overweightness or relative disease risk. Also, the BMI does not
apply to growing children or frail and sedentary elderly adults.
BMI and Health Risk
BMI Score Health Risk
>25 Minimal
25 - 27 Low
27 30 Moderate
30 <35 High
35 <40 Very High
>40 Extremely
High
Limitations of BMI for Athletes

As with height-weight tables, the BMI fails to consider the body's proportional composition. Specifically,
factors other than excess body fat (bone and muscle mass, and even the increased quantity of plasma volume
induced by exercise training) affect the BMI equation. A high BMI could lead to an incorrect interpretation of
overfatness in lean individuals, when in fact genetic makeup or exercise training caused the high BMI.
The possibility of misclassifying someone as overweight using BMI standards applies particularly to large-
size, field-event athletes, bodybuilders, weightlifters, upper-weight class wrestlers, and professional football
players. In contrast to professional football players, the average player in the NBA has a BMI of only 24.5.
This relatively low BMI places them in the very-low-risk category and keeps them out of the overweight
category, although they would be classified overweight by the height-weight standards.
Bioelectrical Impedance Analysis (BIA)

A small, alternating current flowing between two electrodes passes more rapidly through hydrated fat-
free body tissues and extracellular water compared with fat or bone tissue due to the greater electrolyte
content (lower electrical resistance) of the fat-free component. Consequently, impedance to electric current
flow relates to the quantity of total body water, which in turn relates to fat-free body mass, body density, and
percent body fat.
Using this technique, person lies on a flat, nonconducting surface. Source electrodes attach on the dorsal
surfaces of the foot and wrist, and Sink electrodes attach between the radius and ulna and at the ankle.
A painless, localized electrical current is
introduced, and the impedance (resistance) to
current flow between the source and detector
electrodes is determined. Conversion of the
impedance value to body density (adding body
mass and stature, sex, age, and sometimes race,
level of fatness, and several girths to the equation -
computes percent body fat.
Dual-Energy X-Ray
Absorptiometry
Dual-energy x-ray absorptiometry (DXA), a
Figure 6. Dualenergy Xray absorptiometry. Anorexic female
high-technology procedure routinely used to assess
(two left images) and a typical female (two right images)
bone mineral density permits quantification of fat whose body fat averages 25%. The anorexic weighed 44.4 kg
and muscle around bony areas of the body, (97.9 lb) with a percentage body fat of 7.5%.
including regions without bone present. DXA has
become an accepted clinical tool for assessing spinal osteoporosis and related bone disorders. DXA does not
require assumptions about the biological constancy of the fat and fat-free components inherent when using
hydrostatic weighing.
With DXA, two distinct x-ray energies (short exposure with low-radiation dosage) penetrate into bone and
soft tissue areas to a depth of about 30 cm. Specialized computer software reconstructs an image of the
underlying tissues. The computer-generated report quantifies bone mineral content, total fat mass, and fat-
free body mass. Selected body regions can also be pinpointed for more in-depth analysis (Figure 6.)
Average Values for Body Composition

Table 1 lists average values for percent body fat in men and women throughout the United States. Values
representing ±1 standard deviation provide some indication of the variation or spread from the average; the
column headed “68% Variation Limits” indicates the range for percent body fat that includes one standard
deviation, or about 68 of every 100 persons measured. For example, the average percent fat of 15.0% for
young men from the New York sample includes the 68% variation limits from 8.9 to 21.1% body fat. Thus, for
68 of every 100 young men measured, percent fat ranges between 8.9 and 21.1%. Of the remaining 32 young
men, 16 would possess more than 21.1% body fat, while the 16 other men would have a body fat percentage
less than 8.9. In general, percent body fat for young adult men averages between 12 and 15%, whereas the
average fat value for women falls between 25 and 28%.
Table 1. Average percent body fat for younger and older women and men. Taken from the literature.
Group Age Height Weight %Fat 68%

Range cm kg Variation Limits
Younger Women
North Carolina, 1962 17-25 165.0 55.5 22.9 17.5-28.5
New York, 1962 16-30 167.5 59.0 28.7 24.6-32.9
California, 1968 19-23 165.9 58.4 21.9 17.0-26.9
California, 1970 17-29 164.9 58.6 25.5 21.0-30.1
Air Force, 1972 17-22 164.1 55.8 28.7 22.3-35.3
New York, 1973 17-26 160.4 59.0 26.2 23.4-33.3
North Carolina, 1975 17-25 166.1 57.5 24.6 22.2-31.1
Army recruits, 1986 17-25 162.0 58.6 28.4 23.9-32.9
Massachusetts, 1994 17-30 165.3 57.7 21.8 16.7-27.8
Average 17.1-26.3 164.6 57.8 25.4
Older Women
Minnesota, 1953 31-45 163.3 60.7 28.9 25.1-32.8
43-68 160.0 60.9 34.2 28.0-40.5
New York, 1963 30-40 164.9 59.6 28.6 22.1-35.3
40-50 163.1 56.4 34.4 29.5-39.5
North Carolina, 1975 33-50 162.9 58.0 29.7 23.1-36.5
Massachusetts, 1993 31-50 165.2 58.9 25.2 19.2-31.2
Average 34.7-50.5 163.3 63.9 30.2
Younger Men
Minnesota, 1951 17-26 177.8 68.1 11.8 5.9-11.8
Colorado, 1956 17-25 172.4 68.3 13.5 8.3-18.8
Indiana, 1966 18-23 180.1 75.5 12.6 8.7-16.5
California, 1968 16-31 175.7 74.1 15.2 6.3-24.2
New York, 1973 17-26 176.4 71.4 15.0 8.9-21.1
Texas, 1977 18-24 179.9 74.6 13.4 7.4-19.4
Army recruits, 1986 17-25 174.7 70.5 15.6 10.0-21.2
Massachusetts, 1994 17-30 178.2 76.3 12.9 7.8-18.9
Average 17.1-26.3 176.9 72.5 13.8
Older Men
Indiana, 1996 24-38 179.0 76.6 17.8 11.3-24.3
40-48 177.0 80.5 22.3 16.3-28.3
North Carolina, 1976 27-50 23.7 17.9-30.1
Texas, 1977 27-59 180.0 85.3 27.1 23.7-30.5
Massachusetts, 1993 31-50 177.1 77.5 19.9 13.2-26.5
Average 29.8-49 178.3 80.0 22.2
Determining Goal Body Mass

Excess body fat detracts from good health, physical fitness, and athletic performance. However, no one
really knows the optimum body fat or body mass for a particular individual. Inherited genetic factors greatly
influence body fat distribution, and certainly impact long-term programming of body size. Average values for
percent body fat for young adults approximate 15% for men and 25% for women. Women and men who
exercise regularly or train for athletic competition have lower percent body fat. In contact sports and activities
requiring muscular power, successful performance usually requires a large body mass with average to low
body fat. In contrast, weight-bearing endurance activities require a lighter body mass and minimal level of
body fat. Proper assessment of body composition, not body weight, should determine an athlete's ideal body mass. Goal
body mass should coincide with optimizing sport-specific measures of physiologic functional capacity and
exercise performance. A “goal” body mass target that uses a desired (and prudent) percentage of body fat can
be computed as follows:
Goal body mass = Fat-free body mass / (1.00 – % fat desired)
Suppose a 120-kg (265-lb) shot-put athlete, currently with 24% body fat, wishes to know how much fat
weight to lose to attain a body fat composition of 15%. The following computations provide this information:
Fat mass = body mass, kg x decimal %body fat
Fat mass = 120 kg x 0.24
Fat mass = 28.8 kg
Fat-free body mass = body mass, kg – fat mass, kg
Fat-free body mass = 120 kg – 28.8 kg
Fat-free body mass = 91.2 kg
Goal body mass = Fat-free body mass, kg / 1.00 – decimal %body fat
Goal body mass = 91.2 kg / (1.00 – 0.15)
Goal body mass = 91.2 kg / 0.85
Goal body mass = 107.3 kg (236.6 lb.)
Desirable fat loss = Present body mass, kg – Goal body mass, kg
Desirable fat loss = 120 kg –107.3 kg
Desirable fat loss = 12.7 kg (28.0 lb.)
If this athlete lost 12.7 kg of body fat, his new body mass of 91.2 kg would have a fat content equal to 15%
of body mass. These calculations assume no change in fat-free body mass during weight loss. Moderate
caloric restriction plus increased daily energy expenditure induces loss of body fat (and conservation of lean
tissue.)
Obesity
Obesity: A Long-Term Process
Obesity frequently begins in childhood. For these children, the chances of becoming obese adults increase
three-fold compared with children of normal body mass. Simply stated, a child generally does not “grow out
of” obesity. “Tracking” body weight through generations indicates that obese parents likely give birth to
overweight children, who grows into an obese adults whose offspring’s often become obese.
Excessive fatness also develops slowly through adulthood, with ages 25 to 44 the years of greatest fat
accretion. In one longitudinal study, fat content of 27 adult men increased an average of 6.5 kg over a 12-year
period from age 32 to 44 years. Women gain the most weight; about 14% gained 13.6 kg (30 lb) between ages
25 and 34. The typical American man (beginning at age 30) and woman (beginning at age 27) gains between 0.2 to 0.8
kg (0.5 - 1.75 lb) of body weight each year until age 60, despite a progressive decrease in food intake! Whether
“creeping obesity” during adulthood reflects a normal biologic pattern remains unknown.
Not Necessarily Overeating

If obesity existed as a singular disorder, with gluttony and overindulgence as causative factors, decreasing
food intake would surely be the most effective way to permanently reduce weight. Obviously, other
influences, such as genetic, environmental, social, and perhaps racial are involved. Specific factors that
predispose a person to excessive weight gain include eating patterns, eating environment, food packaging,
body image, biochemical differences related to resting metabolic rate, basal body temperature, variations in
dietary-induced thermogenesis, amount of spontaneous activity or “fidgeting,” quantity and sensitivity to
satiety hormones, levels of cellular adenosine triphosphatase, lipoprotein lipase, and other enzymes, presence
of metabolically active brown adipose tissue, and daily physical activity.
Regardless of the specific causes of obesity and their interactions, the treatment procedures devised so far
- diets, surgery, drugs, psychological methods, and exercise, either alone or in combination - have not been
particularly successful on a long-term basis. Nonetheless, optimism exists that researchers will someday
devise an effective way to prevent and treat this national health affliction.
Genetics Play a Role

While genetic makeup does not necessarily cause obesity, it does lower the threshold for its development;
it contributes significantly to differences in weight gain for individuals fed identical daily caloric excess.
Figure 7 presents data from a large number of individuals representing nine different types of relations.
Genetic factors determine about 25% of the variation among people in percent body fat and total fat mass,
while the larger percentage of variation relates to a transmissible (cultural) effect. In an obesity-producing
environment (sedentary and stressful, with easy access to food), the genetically susceptible individual gains
weight, possibly lots of it. Athletes with a genetic propensity for obesity fight a constant battle to achieve and
maintain an optimal body mass and composition for competitive performance.
Figure 7. Total transmissible variance for body fat.
A Mutant Gene?
Research with a strain of mice that enlarge
to five times normal size provides evidence to
support the important genetic contribution to
body weight and body fat deposition. The
mutation of a gene, called obese or simply ob,
probably disrupts hormonal signals that
regulate the animal’s appetite, metabolism,
and fat storage, causing energy balance to tip
towards fat accumulation.
Figure 8. Genetic model for obesity. A malfunction of the satiety
gene affects production of the satiety hormone leptin.
Underproduction of leptin disrupts proper function of the
hypothalamus (step#3), the center responsible for regulating the
body’s fat level.
Figure 8 proposes that the ob gene, normally activated in adipose tissue, produces leptin, a body fat-
signaling satiety hormone that influences the appetite control center in the hypothalamus. Normally, leptin’s
action blunts the urge to eat when caloric intake provides sufficient energy to maintain ideal fat stores. In this
way, body fat level and the brain become intimately “connected” through a physiological pathway that
regulates caloric intake. A defective gene causes inadequate leptin production. As a result, the brain receives
an improper assessment of the body’s adipose status, and the urge to eat outstrips the energy need to
maintain a desirable body fat level. This biological control mechanism fits nicely with the setpoint theory to
explain excessive body fat accumulation. This also clarifies why obese individuals find it extremely difficult to
sustain significant losses in body fat.
Physical Activity: An Important Component

Older men and women who maintain physically active lifestyles blunt the “normal” tendency to gain fat
during adulthood. For young and middle-aged men who exercised regularly, time spent in physical activity
related inversely to body fat level - the more exercise the less body fat. Surprisingly, no relationship emerged
between body fat and caloric intake. This suggests that less demanding training, not greater food intake,
produced the greater body fat levels among the active middle-aged men compared to younger, more active
counterparts.
Health Risks Of Obesity

Considerable research links obesity to diverse health risks in children, adolescents, and adults. Clear
associations exist between obesity and hypertension, diabetes, and various lipid abnormalities
(dyslipidemia), in addition to increased risk of cerebral and vascular diseases, alterations in free fatty acid
metabolism, and atherosclerosis. However, health risks do not confront every obese person, suggesting that
obesity represents a nonuniform, heterogeneous condition. Indeed, evidence accumulated over the last 15
years confirms the heterogeneous nature of obesity, not only its cause (s) but also its complications.
Nevertheless, obesity should be viewed as a chronic medical condition because multiple biologic hazards of
premature illness and death exist at surprisingly low levels of excess body fat. Some researchers believe that
even modest obesity powerfully predicts heart disease risk, equal to cigarette smoking, elevated blood lipids,
physical inactivity, and hypertension. Staggering economic expenses arise from obesity-related medical
complications; by the year 2000, 12% of the cost of illness in the US will relate directly or indirectly to
excessive body fatness.

THE RISKS OF BEING YOUNG AND FAT
Childhood obesity represents a more significant adult health risk than obesity
developed in adulthood. A 55year followup indicates that individuals who became
overweight in childhood or adolescence had significantly greater risk of a broad
range of adverse health effects compared to normalweight counterparts.
Surprisingly, with the exception of diabetes, these effects were independent of the
children’s eventual weight as an adult.
How Fat Is Too Fat?
Three criteria can evaluate a person’s level of body fatness:
1. Percent body fat
2. Fat patterning
3. Fat cell size and number
Percent Body
The demarcation between normal body fat levels and obesity often becomes arbitrary. The “normal range”
of body fat in adult men and women has been identified as at least plus or minus one unit of variation
(standard deviation) from the average population value. That variation unit equals –5% body fat for men and
women between the ages 17 and 50 years. Within this statistical boundary, overfatness corresponds to any
percent body fat value above the average value for age and sex, plus 5 percentage points. For young men,
whose fat mass averages 15% of total body mass, the borderline for obesity equals 20% body fat. For older
men, average percent fat equals about 25%. Consequently, a body fat content in excess of 30% represents
overfatness for this group. For young women, obesity corresponds to a body fat content above 30%, while for
older women borderline obesity begins at 37% body fat.
A problem with these age-specific demarcations for obesity lies in the assumption that men and women
“normally” become fatter with aging. However, this does not necessarily occur for physically active older
men and women. If lifestyle actually accounts for the greatest portion of body fat increase during adulthood,
then the criterion for overfatness could justifiably
represent the standard for younger men and

STANDARDS FOR OVERFATNESS
Men - above 20% body fat
Women - above 30% body fat
women: above 20% for men and above 30% for

women.
Gradations of obesity progress from the upper
limit of normal (20% for men and 30% for women) to
as high as 50 to 70% of body mass. Common terms
for gradations in obesity include pleasantly plump for
those just above the cut-off, to moderately obese,
excessively obese, massively obese, and morbidly obese.
The last category includes people who weigh in the
range of 170 to 275 kg (385 to 600 lb) and whose fat
content exceeds 55%. In such cases, body fat can
exceed fat-free body mass, and obesity becomes life
threatening.
Fat Patterning
Fat cells (adipocytes) display remarkable
diversity depending on their anatomic location.
Some cells efficiently “capture” excess nutrient
calories from the bloodstream and synthesize them
into triglycerides for storage, while other adipocytes
not only accumulate triglycerides but readily release
Figure 9. Male and female fat patterning including the waist
tohip girth ratio threshold for significant health risk.
this form of stored energy for use by other tissues. This explains why certain fat deposits exhibit resistance to
reduction and others expand and contract readily in response to the body’s energy balance. Research now
indicates that the patterning of adipose tissue distribution, independent of total body fat and body weight,
alters the health risk from obesity.
Studies using MRI and CT-scanning to precisely discriminate subcutaneous from visceral (intra-
abdominal) adipose tissue (V-AT) show that V-AT accumulation in excess of 130 cm2 relates to an altered
metabolic profile that includes:
 Hyperinsulinemia
 Insulin resistance and glucose intolerance
 Hypertriglyceridemia
 Reduced high-density lipoprotein (HDL) cholesterol concentrations
 Increased apolipoprotein B, the regulatory protein constituent of the harmful LDL cholesterol
Excessive insulin production and depressed insulin sensitivity that characterizes V-AT obesity not only
increases risk for noninsulin dependent diabetes mellitus, but also risk for ischemic heart disease. Thus,
visceral obesity represents an additional component of the insulin-resistant, dyslipidemic syndrome, which
represents the most prevalent cause of coronary artery disease in industrialized countries.
The notion that body fat distribution represents an important component in the clinical assessment of
obese patients first emerged in 1947, and has been confirmed in subsequent epidemiological studies. A
preferential abdominal fat accumulation, first described as android obesity (male-pattern or central obesity),
exists largely among overweight patients with hypertension, type 2 diabetes, and coronary heart disease. This
contrasts to the lower health risks of gynoid obesity (female-pattern or peripheral obesity), where the
majority of excess fat deposits in the body’s gluteal and femoral regions. Figure 9 shows examples of the
apple (android) and pear (gynoid) body shape types.
The waist-to-hip girth ratio (WHR) (Figure 9) often represents the initial clinical assessment of V-AT.
Ratios exceeding 0.80 for women and 0.95 for men indicate excessive visceral fat accumulation, which
predicts increased risk of death from coronary artery disease and other illnesses. An elevated waist-to-hip
girth ratio predicts health risk with greater accuracy than the popular measurement of body mass index
(BMI).

1. Archimedes’ principle
2. Body mass index
3. Body volume
4. Density
5. Desirable body mass
6. Essential fat
7. Fat mass
8. Skinfold
9. Fat-free body mass
10. Hydrostatic weighing
11. Lean body mass

12. Minimal weight
13. Overweight
14. Reference man
15. Reference woman
16. Sex-specific fat
17. Specific gravity
18. Storage fat
19. Underweight
20. Android obesity
21. Gynoid obesity
22. Obesity
STUDY QUESTIONS
Gross Composition of the Human Body

List three major structural components of the human body and their percentage as represented by
the reference man and woman. (Hint: Refer to Figure 18.1 in your textbook.)
Structural Component Reference Man Reference Woman
1.
2.
3.
Reference Man and Reference Woman

Compare body mass, stature, total fat, and storage and essential fat for the reference man and
women.
Reference Man Reference Women
Stature, cm
Body mass, kg
Total fat, kg
Total fat, %
Storage fat, kg
Storage fat, %
Essential fat, kg
Essential fat, %
Essential and Storage Fat

Essential Fat
Give the function and location of essential fat and sex-specific essential fat in humans.
Function Location
Essential fat
Sex-specific fat
Storage Fat
Give the function and location of storage fat in humans.
Function
Location
Fat-Free Body Mass and Lean Body Mass

What is the suggested “healthy” lower level of percent body fat in males?
Minimal Body Mass

What is the suggested “healthy” lower level of percent body fat in females?
Underweight and Thin

What precisely is meant by the terms “underweight" and "thin?”
Underweight
Thin
Leanness, Exercise, and Menstrual Irregularity

Describe the lower limit of body fat believed required for maintaining normal menstrual function?
Leanness Not the Only Factor

List four factors associated with menstrual dysfunction.
1. 2.
3. 4.
Methods to Assess Body Size and Composition

List two general procedures to evaluate body composition.
1.
2.
Direct Assessment
Describe a major limitation of the direct method of body composition assessment in humans.
Indirect Assessment
List three indirect procedures commonly used to assess body composition.
1. 3.
2.
Hydrostatic Weighing (Archimedes’ Principle)

State Archimedes principle of water displacement.
Determining Body Density

Complete the formula: Specific gravity = ______________÷______________.
Calculate the approximate body volume of a person weighing 50 kg and 2 kg when submerged
underwater.
Computing Percent Body Fat and Mass of Fat and Fat-Free Tissue
Compute the percent body fat of a person whose body density equals 1.0742 g/cc.
Give the equation and compute the fat mass for a person weighing 63.4 kg with body fat of 10.8%.
Equation
Fat mass
Body Volume Measurement

Write the equation to compute body volume by hydrostatic weighing.
Body Volume Measurement By Air Displacement

Explain the principle underlying the use of the BOD POD for body volume determinations.
Skinfold Measurements
The close relationship between these three variables provides the rationale for using skinfold
measurements to predict body composition.
1. 3.
2.
Girth Measurements
List two advantages of girth measurements over skinfolds to assess body fat.
1.
2.
The Body Mass Index

Write the formula to compute body mass index.
Limitations of BMI For Athletes

Give one limitation of the BMI and its importance to athletes?
Limitation
Importance to athletes
Average Values for Body Composition

Give the average percent body fat for college age males and females.
Males Females
Determining Goal Body Mass

Write the equation to compute desirable body mass.
A 20-year old man weighs 89 kg with 22% body fat. If this man reduces body fat to a desired 12%
level, determine (a) his new body mass, and (b) total fat mass lost? Assume all weight loss
represents fat.
New body mass
Total fat loss
Obesity
Obesity: A Long-Term Process
Discuss the trend for weight gain in adult men and women as they age.
Not Necessarily Overeating

List three factors that predispose a person to excessive weight gain.
1. 3.
2.
Genetics Play a Role

How much of the variation in weight gain among individuals can be accounted for by genetic
factors?
A Mutant Gene?
Describe the role of the mutant “obese” gene in the obesity development.
Physical Activity: An Important Component

Discuss how increases in body fat with age relate to physical inactivity than age itself.
Health Risks of Obesity

Does excess body weight or excess body fat relate more strongly to heart disease risk?
How Fat is Too Fat?

List three criteria for evaluating a person’s level of body fatness.
1. 3.
2.
Percent Body
What percent body fat level indicates borderline obesity in adult men and women?
Men
Women
Fat Patterning
List the 2 types of fat patterning
1.
2.
PRACTICE QUIZ
1. Essential body fat: 6. BMI:

a. same for males and females a. mass ÷ stature squared
b. women have more b. mass ÷ volume
c. men have more c. same as body surface area
d. non-existent d. determines amount of body fat
e. none of the above e. none of he above
2. FFM: 7. True: False. Goal body mass = FFM ÷ FM:
a. fat free mass a. True
b. fat mass b. False
c. body mass minus lean body mass 8. Leptin:
d. same for males and females a. satiety hormone
e. none of the above b. enzyme responsible for fat
3. Minimal body mass: hypercellularity
a. same for males and females c. found in muscle cells
b. women’s lower d. only found in individuals with high

BMI’s
c. men’ lower
d. body mass minus fat free mass
9. True or False: FFM = Body mass – fat mass
a. True
4. Archimedes’ principle:
b. False
a. evaluates specific gravity
10. Dyslipidema:
b. evaluates body fat
a. found in leptin cells
c. predicts optimal body weight
b. enzyme found in the obese
d. does not apply to humans
c. lean individuals don’t produce this
type of fat
5. Body density:
d. lipid abnormalities
a. weight divided by FFM
b. weight divided by fat
c. weight divided by volume
d. volume divided by weight

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MVS 110 EXERCISE PHYSIOLOGY PAGE 1

The Scientific Method and Exercise Physiology

General Goals of Science

FOR YOUR INFORMATION

Casual and Causal Relationships

FOR YOUR INFORMATION

INDEPENDENT AND DEPENDENT VARIABLES

The Surety of Science

Publishing Results of Experiments

Empirical vs. Theoretical – Basic vs. Applied Research

READING #1 STUDY GUIDE

Define Key Terms and Concepts

10. Empirical research

12. Experimental studies

13. Field of study

14. Field studies

15. Science hierarchy

16. Independent variables

17. Operational definitions

20. Theoretical research

The Scientific Method and Exercise Physiology

Give four aims of science.

Describe a dependent variable.

Casual and Causal Relationships

Nature of Experimental Studies

Give the main point of experimental studies.

Nature of Field Studies

The Surety of Science

Empirical vs. Theoretical – Basic vs. Applied Research

From Ancient Greece to the United States

The Early United States Experience

Austin Flint, Jr., M.D.: American Physician-Physiologist

Amherst College Connection

George Wells Fitz, M.D.: A Major Influence

FOR YOUR INFORMATION

Prelude to Exercise Science: Harvard’s Department of

Exercise Studies in Research Journals

The Harvard Fatigue Laboratory (1927-1946)

FOR YOUR INFORMATION

Other Early Exercise Physiology Research Laboratories

Nordic Connection (Denmark, Sweden, Norway and

Norwegian and Finnish Influence

The University of Michigan Experience

Figure 7. Barbour (Women’s) Gym [circa, 1900] attached to Waterman (Men’s) gym The roots of today’s

“There is herby created and established a University Department of Physical Education….

Other Contributors to Exercise Physiology

Reading #2 Study Guide

Define Key Terms and Concepts

3. Austin Flint, Jr., M.D.

5. David Bruce Dill

9. George Wells Fitz.

10. Harvard Fatigue Laboratory

12. Margaret Bell

13. Paul Hunsicker

14. Per-Olof Åstrand

15. The Hitchcock’s

16. Thomas K. Cureton

The Early United States Experience

Austin Flint, Jr., M.D.: American Physician-Physiologist

Amherst College Connection

George Wells Fitz, M.D.: A Major Influence

Prelude to Exercise Science: Harvard’s Department of Anatomy, Physiology, and

The Harvard Fatigue Laboratory (1927-1946)

Other Early Exercise Physiology Research Laboratories

Open-Circuit Spirometry Figure 3. Closedcircuit method uses a spirometer prefilled