Impaired Muscle Performance

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Learning outcomes:
At the end of this unit the student will be able to:
Explain the consequences associated with sarcopenia in
an aging population and
collate the studies describing ways physical therapists
can counter the associated adverse changes.

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Consequences of Sarcopenia
The age-related loss of muscle, coined sarcopenia in
1989.
The loss of skeletal muscle mass is accompanied by the
loss of muscle strength, rate of force development, and
muscle power.
Sarcopenia contributes to deficits in mobility, a decline
in functional capacity, and a reduction in skeletal
muscle oxidative capacity.
These muscle impairments, in combination with a
greater fat mass, contribute to the greater risk of falling,
frailty, and the development of comorbid conditions
such as insulin resistance or type 2 diabetes that
adversely impact health.

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Because muscle mass represents the protein reserve of

the body, sarcopenia is associated with a diminished
ability to meet the extra demand of protein synthesis
that is so often necessary with disease and injury in old
age.

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Changes in Muscle Structure and

Function Associated with Aging

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Impaired Regeneration of Muscle and the

Progressive Denervation /Reinnervation Process.
A primary mechanism attributed to the development of
sarcopenia in those aged 60 to 65 years and older is a
progressive denervation and reinnervation process
involving the alpha motor neurons.
A 50% decline in available motor neurons6,20-22 and a
diminished number and availability of satellite cells
that parallel the age-related temporal changes in muscle
size and strength have been noted.
Fiber type grouping also characterizes aging as
remaining alpha motor neurons enlarge their own
motor unit territory.

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When coupled with the reduction in alpha motor

neurons and motor units, a reduced motor coordination
and strength results, which may underlie age-related
mobility impairments.
In addition, muscle fiber regeneration is impaired more
in type II fibers than type I in large part due to the
degradation of the myogenic satellite stem cells.
Compounding these age-related losses are reports of
substantially lower basal mixed, myofibrillar, or
mitochondrial muscle protein synthesis rates in older
adults versus younger ones.

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Deficits in Absolute and Specific Force

Generation.
Consistent with the current interpretation of sarcopenia,
older individuals become weaker over time.
These strength deficits, however, do not necessarily
match the magnitude of atrophy that has occurred.
In part, this may be explained by the fact that muscle
generally becomes weaker even if atrophy is avoided,
which suggests that force production, separate from
muscle atrophy, also is impaired with aging.
It appears that the age-related impairment in muscle
force is only partially explained by the loss in muscle
mass.

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Muscle Activation Deficits.

The declining force production abilities with aging

occur at a faster rate than the decline in muscle mass;
hence, neural alterations are also thought to contribute
to muscle weakness by reducing central drive to the
agonist muscles and by increasing coactivation of the
antagonist muscles.

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Deteriorating Muscle Quality and

Metabolism.
A reduction in muscle quality due to infiltration of
fat and other noncontractile material such as connective
tissue, coupled with changes in muscle metabolism,
also contribute to the deteriorating muscle condition
and advancing frailty with age.
In addition, oxidative damage accumulated over time is
thought to lead to mitochondrial DNA mutations,
impaired mitochondrial function, muscle proteolysis,
and myonuclear apoptosis.

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Changes in Metabolic Function Associated

with Aging
Whole body resting metabolic rate (RMR)
progressively declines at a rate of 1% to 2% per decade
after 20 years of age.
This change is linked with age-associated decreases in
metabolically active whole-body fat-free mass.

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Altered Endocrine Function and Its

Consequences.

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Cytokines and Adiposity

Aging, as well as several chronic medical conditions
(chronic obstructive pulmonary disease [COPD], heart
disease, cancer, diabetes) that are prevalent with
increasing age, is associated with a gradual increase in
the production of proinflammatory cytokines
(responsible for accelerating inflammation and
regulating inflammatory reactions), chronic
inflammation, and loss of lean body mass.
Associations between elevated levels of tumor necrosis
factora (TNF-a), interleukin 6 (IL-6), C-reactive
protein (CRP) muscle mass, and muscle strength have
been reported, though the role of these cytokines
appears complex.

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Mitochondrial Dysfunction.
The aging-associated damage to muscle mitochondrial
DNA (mtDNA) may reduce the rate of muscle cell
protein synthesis, adenosine triphosphate (ATP)
synthesis, and ultimately may lead to the death of
muscle fibers and loss of muscle mass.
Consistent with other metabolic changes that are seen
with aging, because these mitochondrial abnormalities
have also been shown to be at least partially reversible
with exercise.

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Apoptosis.
Age related loss of myocytes via apoptosis has been
suggested to be a key mechanism behind the muscle
loss associated with human aging as well, though this
evidence is preliminary.
Recent data demonstrate that physical exercise can
mitigate skeletal muscle apoptosis in aged animals.
These basic science considerations should prompt the
clinician to consider exercise as not only a counter to
loss of physical fitness and function, but perhaps also a
mode of slowing down the apoptotic pathways
underlying sarcopenia.

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Diseases and Conditions Associated with

Skeletal Muscle Decline.

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Influence of Genetics.

Genetic epidemiologic studies suggest that between

36% and 65% of an individuals muscle strength and
up to 57% of their lower extremity performance can be
explained by heredity.

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MUSCLE COUNTERMEASURES
FOR OLDER INDIVIDUALS
Resistance training for individuals age 65 years and
older induces predictable increases in muscle strength,
muscle power, and mobility function in communitydwelling older persons, nursing home inhabitants, and
the hospitalized older adults.
Significant improvements in strength and mobility
function have also been reported in individuals 80
years of age and older.

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Adaptations in Muscle Strength and

Mobility Levels with Resistance Exercise.
Without a doubt, older individuals who participate in at
least 6 to 12 weeks of resistance training will improve
their strength and mobility function.
Strength improvements range from 25% to well over
100%.
The effects of age may be influenced by gender,
duration of training, or muscle groups investigated.

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Adaptations in Muscle Power with

Resistance Exercise.
Resistance training that specifically targets muscle
power (40% to 70% 1 RM, as fast as possible) has a
significant impact on physical functioning as well as
muscle power production and muscle strength.
Leg muscle power is especially important when
considering that muscle power declines more sharply
than strength in older individuals.
Previous literature suggests that 4 to 16 weeks of
power training results in robust (100% to 150%)
improvements in leg muscle power in both healthy and
impaired older individuals..

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Adaptations in Muscle Size and

Composition with Resistance Exercise.
The impact of resistance training on muscle
hypertrophy, an expected outcome in the young, is less
predictable in older individuals, especially those older
than age 80 years.
Older women (mean age 85 years) have also been
reported to have a blunted hypertrophy response at both
the whole muscle and fiber level.
This limited hypertrophic response may or may not be
important clinically as muscle size has been reported to
be less influential than muscle power and strength on
functional mobility.

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Resistance Exercise via Negative,

Eccentrically Induced Work.
There is evidence suggesting that resistance training
that exploits the high-forceproducing capabilities of
eccentric muscle activity are both feasible and effective
for older individuals.
Because eccentric resistance training can produce high
forces at relatively low energetic costs, eccentrically
biased resistance training programs are especially
useful in an older population.

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Nutritional Intake as a Countermeasure

for Sarcopenia
In addition to decreased physical activity, inadequate
protein intake may also contribute to sarcopenia.
Nutritional intake, like exercise, is a modifiable
countermeasure that may help to minimize loss of lean
muscle tissue and muscle strength in older adults,
though there is significant controversy as to the
amount, quality, and timing of protein supplementation
in this population.

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Currently, it is recommended that all meals for older

adults contain a moderate amount(20% to 35% energy)
of high-quality protein.
Protein supplementation immediately before or
immediately after a resistance training session has been
reported to be more successful at enhancing muscle
hypertrophy.

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References:
Andrew A. Guccione, Rira A. Wong, Dale Avers, 2012
Geriatric Physical Therapy, 3rd ed, Elsevie
Timothy L. Kauffman, John O. Barr, Michael L. Moran
2007 Geriatric Rehabilitation Manual, 2 nd ed, Churchill
Livingstone
ACSMs guidelines for exercise testing and
prescription.9th edition.

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Thank you

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