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Obesity, Growth Hormone and Exercise

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DOI: 10.1007/s40279-013-0064-7 Source: PubMed

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Sports Med (2013) 43:839849

DOI 10.1007/s40279-013-0064-7

REVIEW ARTICLE

Obesity, Growth Hormone and Exercise

Gwendolyn A. Thomas William J. Kraemer
Brett A. Comstock Courtenay Dunn-Lewis
Carl M. Maresh Jeff S. Volek

Published online: 30 June 2013

Springer International Publishing Switzerland 2013

Abstract Growth hormone (GH) is regulated, suppressed

and stimulated by numerous physiological stimuli. However, it is believed that obesity disrupts the physiological
and pathological factors that regulate, suppress or stimulate
GH release. Pulsatile GH has been potently stimulated in
healthy subjects by both aerobic and resistance exercise of
the right intensity and duration. GH modulates fuel
metabolism, reduces total fat mass and abdominal fat mass,
and could be a potent stimulus of lipolysis when administered to obese individuals exogenously. Only pulsatile
GH has been shown to augment adipose tissue lipolysis
and, therefore, increasing pulsatile GH response may be a
therapeutic target. This review discusses the factors that
cause secretion of GH, how obesity may alter GH secretion
and how both aerobic and resistance exercise stimulates
GH, as well as how exercise of a specific intensity may be
used as a stimulus for GH release in individuals who are
obese. Only five prior studies have investigated exercise as
a stimulus of endogenous GH in individuals who are obese.
Based on prior literature, resistance exercise may provide a
therapeutic target for releasing endogenous GH in individuals who are obese if specific exercise programme
variables are utilized. Biological activity of GH indicates
that this may be an important precursor to beneficial
changes in body fat and lean tissue mass in obese individuals. However, additional research is needed including
G. A. Thomas
School of Nursing, Yale University, New Haven, CT, USA
G. A. Thomas
W. J. Kraemer (&)
B. A. Comstock

C. Dunn-Lewis
C. M. Maresh
J. S. Volek
Human Performance Laboratory, Department of Kinesiology,
University of Connecticut, 2095 Hillside Road, Unit 1110,
Storrs, CT 06269, USA
e-mail: William.Kraemer@uconn.edu

what molecular GH variants are acutely released and

involved at target tissues as a result of different exercise
stimuli and what specific exercise programme variables
may serve to stimulate GH in individuals who are obese.

1 Introduction
The role of exercise in addressing complications and
chronic disease associated with obesity is a much studied
topic. However, the biological mechanisms by which
exercise may promote fat loss and increase health in individuals who are obese are less studied, particularly as it
pertains to exercise prescription and identifying optimal
exercise programmes for maximal health benefits. We
review the evidence for growth hormone (GH) dysfunction
in individuals who are obese, its role as a lipolytic mechanism of particular concern for individuals who are obese,
and resistance exercise programme variables that may elicit
pulsatile GH responses that promote beneficial adaptations.
Thus, the purpose of this review is to (1) present knowledge of the pathophysiology of GH; (2) examine how
obesity affects the regulation, activity and molecular
character of GH variants in circulation; and (3) to examine
exercise as a method of promoting GH in circulation in
individuals who are obese if properly prescribed. We provide a comprehensive review using PubMed, EMBASE
and SportDiscusTM literature through March 30, 2011. The
studies included were found using the following search
terms: growth hormone, growth hormone stimulation,
growth hormone and secretion, growth hormone
receptor; growth hormone and obesity; growth hormone
binding protein growth hormone metabolism, growth
hormone and biological activity, growth hormone and
exercise, growth hormone and aerobic exercise, growth

840

hormone and resistance exercise, exercise intensity and

growth hormone, acute exercise and growth hormone,
immunoreactive growth hormone and exercise, bioactive
growth hormone and exercise and growth hormone and
obesity and exercise. Further searching was performed by
using the related citations function of PubMed and
scanning of the reference lists. Studies were excluded if
they were non-English language papers, if the articles were
abstracts or did not have implications for GH release as
pertaining to obesity and exercise. The following inclusion
criteria were used, human subjects who were adults (aged
[18 years) and in the exercise-induced GH stimulation in
obesity section, those adults who had a body mass index
(BMI) C30 kg/m2.

2 Growth Hormone (GH)

GH is a family of pleiotropic polypeptide variants that are
released in a pulsatile manner (at least for the 22 kD isoform) from the anterior pituitary with over 100 forms
[1, 2]. Heterogeneity of the GH molecules arises at the
level of the GH gene, messenger RNA (mRNA) splice
variants, post-translational processing, GH metabolism
(such as proteolytic fragments of GH), disulfide linked GH
aggregates of the 22 kD monomeric form, and glycosylated
forms [3]. Due to this heterogeneity, multiple isoforms of
GH may produce different and divergent biological activities, presenting challenges in understanding the bioactivity
of GH [4]. Particularly important to the understanding of
GH are the factors that regulate, suppress or stimulate GH
release. The majority of the literature has used the 22 kD to
define the responses and function of GH and thus unless
specified it is the 22 kD isoform being examined in this
review.
Physiological and pathological factors such as age, sex,
body composition, quality of sleep, nutritional status and
changed breathing patterns such as hyperventilation or
breathholding can significantly alter the pulsatile secretion,
which can then in turn influence the biological effects of
GH [5, 6]. Recent research in humans has demonstrated
that continuous GH administration augments hepatic and
muscle insulin-like growth factor 1 (IGF) 1, whereas pulsatile GH administration augments adipose tissue lipolysis
[7]. In healthy lean individuals, GH secretion occurs in
three to six pulses in a 24-h period, which have multiple
peripheral tissue effects [8, 9]. Exercise and fasting can
increase GH secretion, while excess glucose and lipids can
inhibit GH release in humans [8, 10]. The pattern of GH
release, as well as its variants, has been shown to mediate
lipid, carbohydrate and protein metabolism in body tissues
and growth processes [11, 12]. Several factors regulate
normal GH secretion including GH releasing hormone

G. A. Thomas et al.

(GHRH), and an inhibitory hormone, somatostatin (SRIH)

and, to a lesser extent, ghrelin. One of the most potent
stimulators of pulsatile GH is exercise dosage, which can
not only modify the activity but also the molecular character of GH variants in circulation [5, 13]. Such GH
stimulation may offer an additional therapeutic approach
for weight loss.
Individuals who are obese have been shown to have a
reduction in spontaneous GH secretion to physiological
stimuli by as much as 6 % for each unit increase in body
mass index (BMI) [13]. In addition, the biological benefits
of GH in humans who are obese may not be determined by
the overall magnitude of a single GH output, but rather by
the more complex pulsatile patterns of GH presentation to
peripheral tissues as typically occurs throughout a 24-h
period [7]. Given that exercise can act as a potent stimulus
of pulsatile secretion of GH, increasing circulating GH
through exercise might be an effective way to reduce total
and abdominal/visceral fat mass in obese individuals and
improve cardiometabolic risk [7, 8].
2.1 GH Stimulation, Regulation and Activity
2.1.1 Normal Diurnal Patterns in the Regulation of GH
Normal nocturnal GH secretion usually occurs around
midnight and is associated with slow-wave sleep, with
maximal GH concentrations occurring minutes after the
onset of slow-wave sleep [14]. The neuroendocrine
mechanism of this release is still under debate, but it is
often described as a cortisol-mediated mechanism [14]. It
has been well established that glucocorticoids suppress GH
secretion [15]. The secretory pattern of cortisol is reciprocal to GH (high in the morning and low at night) a
pattern that mediates GH secretion. Individuals with metabolic syndrome and visceral obesity have disturbed or
lower quality sleep reported as differences in slow-wave
sleep. Adults who are obese also can develop sleep apnoea,
which can further degrade sleep quality and diminish
nocturnal GH secretion due to diminished slow-wave
sleep [16].
2.1.2 Metabolic Substrates in the Regulation of GH
More recently, GH has been identified as a modulator of
fuel metabolism. Metabolic substrates such as amino acids,
glucose and lipids all serve as a feedback mechanism to the
hypothalamus and pituitary [17]. In normal healthy
humans, fasting has been shown to stimulate somatotroph
secretion, which could be due to a reduction in the negative
IGF-1 feedback action, as well as CNS-mediated mechanisms [18, 19]. Human subjects have shown an initial
suppression of GH for 13 h after administration of oral

Obesity and Growth Hormone

glucose and a subsequent rise in serum GH concentration

35 h afterwards [20]. Glucose has been shown to have a
rapid inhibitory effect on GH release as, after glucose load,
healthy volunteers demonstrate a GH response to GHRH
and GH secretagogues (GHS) infusion [21, 22]. Alternately, hypoglycaemia causes acute GH secretion as
demonstrated in the insulin induced hypoglycaemia test
[17]. In addition to the aforementioned factors, the amount
of GH secretion and its pattern of release are also regulated
metabolically by glucose, arginine and non-esterified fatty
acids (NEFA) [23], and are therefore affected by nutritional
status. Understanding the underlying mechanisms behind
GH secretion and the targets of GH activity is vital to
understanding the role of GH in the metabolism.
2.1.3 Neuropeptide Regulation
An interplay between several physiological stimuli leads to
GH inhibition and secretion, and peripheral feedback
controls GH secretion [14]. In the hypothalamus, secretion
is regulated by three hypothalamic peptide hormones:
GHRH a 44 amino-acid peptide required for the initiation
of GH pulses, SRIH or somatotropin release inhibiting
factor (SRIF) that modulates the amplitude of GH and
ghrelin, a 28 amino acid peptide that affects GH secretion
through the GHS receptor (GHS-R) in the hypothalamus
and in circulation [24]. This action is mediated in the
hypothalamus via GHRH and less strongly by direct effect
on the anterior pituitary [24]. GHRH and ghrelin act synergistically to stimulate GH release. However, ghrelin can
only release stored GH, whereas GHRH can increase its
synthesis [25]. GHRH and SRIH release are not completely
understood, but are hypothesized to be regulated by
a-adrenergic, dopaminergic, serotoninergic, cholinergic
and histaminergic inputs [14]. A model of GH secretion
and activity is presented in Fig. 1.
2.1.4 GH Receptor (GHR)
The GH receptor is a 620 amino acid of the class I cytokine
receptor superfamily expressed in hepatocytes, muscle,
bone, kidney, mammary glands and adipose tissue [26, 27].
Transcriptional, translational and post-translational factors
such as nutritional status and endocrine system status can
influence the synthesis of GHRs and thus influence GH
sensitivity [2830]. For example, fasting and glucose
starvation have decreased GHR mRNA, GH deficiency can
decrease the number of GHR and insulin can decrease the
GHR binding [28]. Due to the high prevalence of GHR in
adipose tissue, it is possible that overexpression of GHR, or
the extracellular domain of GHR (GH binding protein
[GHBP]), may be affecting GH secretion in obese versus
lean individuals [31, 32].

841

2.1.5 GH Binding Protein

GHBP concentrations are closely tied to concentration
levels of GHR. GHBP is the extracellular domain of
GHR and is generated by GHR proteolysis, and plasma
GHBP concentrations are believed to reflect the GHR
abundance in the liver [33]. Two distinct GHBPs have
been identified in plasma: high- and low-affinity GHBP.
The high-affinity GHBP is a 60 kD protein identical to
the extracellular domain of the GHR. It has a high
affinity for the 22 kD form of GH. Once 22 kD GH is
secreted, it rapidly associates with the high-affinity
GHBP and therefore over 50 % of GH is complexed with
GHBP [34]. GHBP may play an important role in
understanding the differences in lower GH values in
individuals who are obese. Obesity is associated with
high concentrations of GHBP, whereas in normal weight
individuals, GHBP is positively correlated with body fat
percentage and intra-abdominal visceral fat [35]. GHBP
concentration has been shown to be varied with nutritional and metabolic status [34].
2.2 GH Biological Activity
2.2.1 Substrate Metabolism
GH has pleiotropic effects on carbohydrate, lipid and
protein metabolism. GH influences both lean and fat
mass in humans and exerts its effects by several means
that include transcriptional regulation and acute changes
in catalytic activity of several key enzymes. A single GH
pulse increases circulating concentrations of free fatty
acids (FFA) and ketone bodies (acetoacetic acid,
b-hydroxybutyric acid and acetone), which reflects stimulation of lipolysis and ketogenesis [36, 37]. GH has
been shown to have potent metabolic effects on target
tissues. It has been well established that GH in adipose
tissue promotes lipolysis and has been used as a therapy
to reduce total fat mass and abdominal fat mass [5, 14,
38, 39]. Additionally, GH dramatically reduces lipogenesis in adipose tissue, resulting in significant fat loss,
with a concomitant gain of muscle mass [40]. The net
effect of GH stimulation on downstream targets is presented in Fig. 2.
2.3 GH Physiological Dysregulation in Obesity
Individuals who are obese display disruptions in several
aspects of the GH. More specifically, they have a reduced
GH half-life, lower frequencies of GH secretion (both
spontaneous and stimulated), lower 24-h GH production
concentrations and higher GH clearance rates [41].
Reductions in spontaneous GH secretion (as much as 6 %

842

G. A. Thomas et al.

Fig. 1 A model of stimulation

and activity of GH. Dashed
lines indicate inhibition and
solid lines indicate stimulation.
FFA free fatty acids, GH growth
hormone, GHBP GH binding
protein, GHRH GH releasing
hormone, IGF-1 insulin-like
growth factor-1

Hypothalamus

Somatostatin

GHRH

Ghrelin

Pituitary

Liver

Fig. 2 Net effect of GH

stimulation on downstream
targets. GH has multiple effects
on adipose tissue, liver and
muscle tissue targets. Inhibitory
factors include glucose, FFAs
and somatostatin, stimulatory
factors include fasting, exercise,
decreased FFAs and decreased
glucose. FFA free fatty acids,
GH growth hormone, GHRH
GH releasing hormone, HSL
hormone sensitive lipase, IGF
insulin-like growth factor,
IGFBP IGF binding proteins,
LPL lipoprotein lipase, up
arrow indicates increase, down
arrow indicates decrease

(+)

FFA

GHBP

GH

IGF-1

Target
tissue

Adipose tissue

Hypothalamus

(-)
GHRH

Fasting, FFA,
glucose, exercise

Glucose, FFA,
somatostatin

Pituitary

GH

Adipose
tissue

Glucose uptake
Lipolysis (HSL)
Lipogenesis
Re-esterfication of FFA
= Adiposity

for each unit increase in BMI) and the half-life of circulating GH have been reported in obese individuals [13].
Importantly, GH has been shown to return to normal
secretory concentrations with loss of adiposity.

Liver

RNA synthesis
Protein synthesis
Gluconeogenesis
IGFs
IGFBP

Muscle

Glucose uptake
Amino acid uptake
Protein synthesis
LPL activity
= Lean body mass

Studies that administer GH for periods longer than

12 weeks have been shown to be the most successful in
reducing adiposity [4148]. Although the dosage of GH
administration has been varied, lower dosages seem to be

Obesity and Growth Hormone

843

effective in reducing both fat mass and abdominal fat

mass. GH administration has been successful in reducing
abdominal/visceral fat deposits and could prove to be
beneficial at reducing obesity-related co-morbidities
caused by increased abdominal/visceral adipose tissue
[49]. Low-dose GH treatments in addition to calorie
restriction have been shown to accelerate body fat loss
and GH secretion [50]. Kim et al. [50] and Johannsson
et al. [41] have both demonstrated that low dose GH
administration and calorie restriction can favorably affect
visceral fat levels and may be useful in reducing some of
the metabolic complications associated with visceral
obesity. However, GH treatment therapies for weight loss
have had mixed results [51]. Recombinant GH (rGH)
therapies are also not without risk, as they have been
linked to arthralgia, peripheral oedema and paresthesia,
as well as increases in fasting plasma glucose and fasting
insulinaemia [52]. Interventions that promote chronic
disease states such as diabetes mellitus are not feasible
strategies for individuals already at considerable risk for
glucoregulatory disorders. Utilizing a self-management,
low-risk method such as exercise to stimulate GH would
therefore be very beneficial in individuals who are obese.
A model of GH secretion and activity in obesity is
presented in Fig. 3.

Fig. 3 A model of stimulation

and activity of GH in obese
individuals. Dashed lines
indicate inhibition and solid
lines indicate stimulation. FFA
free fatty acids, GH growth
hormone, GHBP GH binding
protein, GHRH GH releasing
hormone, IGF-1 insulin-like
growth factor-1

3 Exercise as a Stimulus for GH Release in Individuals

Who are Obese
Prescribing exercise as a stimulus to create a GH response in
individuals who are obese is of significant importance, as it
may provide a non-pharmacological method to reduce adipose
tissue deposits and increase lean muscle mass. Numerous
studies have reported the influences that physical activity have
on the GH/IGF axis [3, 5360]. Both aerobic and resistance
exercise have demonstrated the ability to increase circulating
GH in lean individuals [61, 62]. However, investigations
examining responses to both modes of exercise within the
same participants have shown that greater GH concentrations
occur in response to a resistance exercise stimulus [61]. In
addition, in response to an aerobic exercise stimulus it has
been prolifically established that obese individuals concentrations are blunted [62]. Therefore, several factors must be
considered when examining acute exercise as a potential
stimulus for GH secretion in individuals who are obese that
include the acute programme variables (exercise order, exercise choice, load, volume and rest period lengths) used in the
exercise session and the form of GH measured. Understanding
these factors may be of use to properly prescribe the optimal
exercise stimulus that can increase GH concentrations in circulation in individuals who are obese.

Hypothalamus

Somatostatin

GHRH

Ghrelin

Pituitary

GHBP
GH

IGF-1

Liver

Target
tissue

OBESITY

Adipose tissue

FFA

844

3.1 Acute Aerobic and Resistance Exercise

and GH Release
Acute resistance and aerobic exercise of the right intensity
and duration is known to significantly increase GH in
human plasma in all age groups [63]. Resistance exercise
protocols that stimulate large muscle mass, use moderate
loads (10 repetition maximum [RM]) and have relatively
short rest periods and high total work have been shown to
maximize the GH response to exercise [64]. Felsing et al.
[65] demonstrated that exercising at the lactate threshold or
at 4060 % of maximum oxygen uptake (VO2max) for a
constant rate of 10 min must be reached before a significant increase in GH concentration is detectable. However,
recent research has also shown that protocols that utilize
high-intensity interval/sprint exercise can elicit a GH
response [66]. Peak GH concentration from both aerobic
and resistance training protocols has been shown to range
from 5 to 25 lg
L-1 in both young men and women.
During and after exercise, GH can influence or be influenced by a variety of physiological demands that include
increased blood lactate concentrations, increased hydrogen
ion concentrations, changes in oxygen demand/availability,
afferent signals from muscle metabolic receptors, motor
centre activity, catecholamines, a proprioceptive mechanism and changes in core temperature [67].
3.2 Exercise as the Stimulus for GH Release
Exercise-induced GH secretion begins 1020 min after
exercise onset, with peak concentrations occurring immediately post-exercise or a little thereafter [1, 3, 56, 6870].
Numerous research groups have studied the response of
GH release at different exercise intensities and have shown
that there is a linear dose response between exercise
intensity and GH secretion [10]. Research has shown that
an optimal exercise stimulus significantly increases GH
concentration in circulation in all age groups, even those
who are experiencing age-related GH reductions [57, 58,
63, 64, 7176]. However, research has not been able to
elucidate the effects of exercise on the molecular form of
the secreted GH or its biological activity [3]. Understanding which exercise programme variables promote the
greatest biological activity of GH may be important in
exercise prescription for individuals who are obese.
3.3 Exercise Stimulus and Form of GH Release
Our current understanding of the GH forms stimulated by
exercise has developed primarily through the use of
enzyme immunoassay and radioimmunoassay whose usage
presents an incomplete picture of the GH response to
exercise [55]. It should also be noted that the difference in

G. A. Thomas et al.

the magnitude of bGH compared to iGH is dramatic with

bGH concentrations (e.g., ranging from 2,000 to over
12,000 lg
L-1) compared with iGH (e.g. ranging from 2 to
just over 30 lg
L-1) depending upon the exercise stimuli.
Previous investigations have thus established that resistance exercise can increase circulating immunoreactive GH
(iGH) concentrations in lean individuals [53, 54] but it is
less understood if bioactive GH (bGH) is also affected.
Acute exercise has been shown to modify both the activity
and molecular character of GH variants in circulation [55].
The seven studies that have examined bGH and iGH in
response to acute exercise and are summarized in Table 1.
McCall et al. [77, 78] first observed an increase in (bGH),
but not (iGH) in men following acute physical activity. The
differences in GH response in these studies may, however,
be attributable to different assays, as they offer different
target endpoints of interaction and thus divergence can
exist for both the magnitude and response of GH to an
exercise stimulus [3, 7981].
Hymer et al [3] demonstrated increases in the iGH, but
no differences in the bGH. Kraemer et al. conducted a
series of assessments of bGH in healthy untrained women
[56, 57, 59]. In all three studies, iGH increased post-acute
heavy resistance exercise and there were no acute changes
in bGH. Kraemer et al. [8, 57] speculated that the discrepant findings for bGH between McCalls research and
the Hymer and Kraemer studies may be due to sex differences or cortisol differences. Women have greater basal
concentrations of GH, which may make the exercise
induced stimulation, particularly of bGH, more difficult. In
addition, cortisol concentrations in McCalls research were
considerably lower than those for the heavy resistance
exercise protocols in the Hymer and Kraemer studies,
which may be suppressing bioactivity [57]. Based on this
information, it can be concluded that GH response to acute
exercise is dependent on sex, the specific exercise training
programme used, the training status of the individuals and
the form of GH being examined.
3.4 Acute Aerobic and Resistance Exercise and GH
Release in Obese versus Lean Individuals
Only five studies have examined the exercise-induced
response of GH to acute exercise protocols in individuals
who are obese. These studies are outlined in Table 2. The
majority of these studies examined aerobic, but not resistance, exercise protocols. Kanaley et al. [82] examined GH
responses to treadmill exercise in non-obese versus women
who were obese. Exercise-induced GH response over 6 h
was greater for non-obese women than for women who are
obese. Wong and Harber [83] examined exercise-induced
GH response to cycling in lean versus men who were
obese. They observed no differences in a resting control

Strongest
women (10)
Weakest
women
out of 100
sample (10)
Women (74)

Kraemer et al.
[59], 2003

20.1
21.0

Healthy, untrained

Healthy, untrained

24.5

23.6

Healthy, untrained

Healthy, untrained

23

23

24

Healthy, untrained

Healthy, astronauts
undergoing space
flight

Healthy, undergoing
bed rest

Training status

Acute resistance exercise

protocol; 3 9 10, 8595 %
with 120 and 90-s rest

Acute resistance exercise;

6 9 10 squats with 2-min rest

Chronic and acute resistance exercise:

Acute: done at baseline and after
24 week follow-up; consisted
of 6 9 10 squats with 2-min rest
Chronic: 24 weeks of one of four
exercise protocols or a control group

Acute resistance exercise;

6 9 10 squats with 2-min rest

Acute resistance exercise;

6 9 10 squats with 2-min rest

Unilateral isometric plantar flexor

contractions

Unilateral isometric plantar flexor

contractions

Exercise protocol

Bioactive: rat tibial line bioassay; DSLs

immunofunctional ELISA
Immunoreactive: DSL ELISA bioactive:
rat tibial line bioassay and GHBP

Immunoreactive: NIDDK polyclonal RIA;

Nichols monoclonal IRMA

Immunoreactive: NIDDK polyclonal RIA;

Nichols monoclonal IRMA
Bioactive: rat tibial line bioassay

Immunoreactive: Nichols IRMA

Bioactive: rat tibial line bioassay; DSLs
immunofunctional ELISA

Immunoreactive: NIDDK polyclonal RIA;

Nichols monoclonal IRMA
Bioactive: rat tibial line bioassay; DSLs
immunofunctional ELISA

Immunoreactive: immunoassayable GH
Bioactive: rat tibial line bioassay

Immunoreactive: RIA GH
Bioactive: rat tibial line bioassay

Assays employed

NOC post-exercise on NIDDK, Nichols

IRMA, and immunofunctional
: iGH in response to exercise in both
groups; : GHBP and ; bGH in obese

: NIDDK post-exercise for all groups; :

Nichols
IRMApost-exercise for all groups, no
differences
in rat tibial line assay post-exercise at
baseline or
at follow-up for control group; : postexercise at
follow-up tibial line for upper body
strength and
hypertrophy groups
: Basal/resting NIDDK for OC group; :
OC relative to

: Rat tibial line bioassay post exercise

relative
to pre-exercise; no change in RIA GH
: Rat tibial line bioassay post-exercise
relative
to pre-exercise; no change in
immunoassayable GH
: NIDDK post-exercise
: Nichols IRMA post-exercise; :
immunofunctional
GH post-exercise, no differences in rat
tibial line
pre- to post-exercise
: Nichols IRMA post-exercise; :
immunofunctional
GH post-exercise, no differences between
or within
groups over time for rat tibial line assay

Acute results

bGH bioactive growth hormone, DSL Diagnostic Systems Laboratories, ELISA enzyme linked immunosorbent assay, GH growth hormone, GHBP GH binding protein, iGH immunoreactive GH, NIDDK
National Institute of Diabetes and Kidney Disease, Nichols IRMA Nichols Institute Diagnostics Immunoradiometric Assay, NOC not on oral contraceptives, OC oral contraceptives, RIA radioimmunoassay,
: indicates increase, ; indicates decrease
a
Ages are presented as mean or actual where stated

Thomas et al.
[90], 2011

Kraemer et al.
[57], 2008

Women
taking OC
(25)
Women NOC
(35)
Lean men (9)
Obese men
(9)

Women (35)

Hymer et al.
[3], 2001

Kraemer et al.
[56], 2006

43.8

Male
astronauts
(4)

McCall et al.
[78], 1999

23.6

42.3

Men (8)

McCall et al.
[77], 1997

Age
(years)a

Subjects (n)

Study, year

Table 1 Review of literature on bioactive growth hormone response to exercise in adults

Obesity and Growth Hormone

845

Non-obese women
(8)
Lower body obese
women (11)
Upper body obese
women (12)
Lean men (6)
Obese mean (7)

Kanaley et al.
[82], 1999

Lean men (9)

Obese men (9)

Thomas et al.
[86], 2011

20.1
21.0

29.8
23.2
27.3

30.6
25.4

23.3

34.5
36.1

33.3

32.9

35

Agea (years)

Sedentary \2 days a week

and \30 min/day
(not resistance trained)

Sedentary \2 days a week

and \30 min/day

Healthy, sedentary

Healthy, untrained,
\3 sessions per week

Healthy, training status

was unspecified

Training status

Resistance exercise 40-min

protocol, 2 sets of 10,
resistance not specified,
third
set to muscular exhaustion
using
85 % of 10RM, 90 s of rest
in between
Resistance exercise, 3 upper
and 3 lower body exercises;
3 sets of 10 repetitions
at 8595 % of 10RM, 120and 90-s rest

1 9 30 and 3 9 10 min
treadmill activity maintained
midway between VO2max at
lactate threshold and VO2peak

30 min at ventilatory
threshold
on cycle ergometer

30-min treadmill exercise at

70 % of VO2peak

Exercise protocol

Immunoreactive GH; DSL ELISA

Bioactive GH; rat tibial line bioassay
GHBP

Beckman-Coulter Access
Immunoassay System

Nichols Institute Diagnostics;

24 h integrated GH

RIA GH assay

Nichols Institute Diagnostics;

6 h integrated GH

Assays employed

: Immunoreactive GH in
response to exercise in both
groups; : GHBP and ; bGH in
obese

GH not different at rest between

groups; : GH for lean men
mid- and post-exercise; ;
pulsatile GH secretion in obese
men relative to lean men

GH not different in control

condition (at rest); : GH for
lean men mid- and post
exercise; ; pulsatile GH in
obese men relative to lean men
: 24 h GH post-exercise
compared with pre-exercise for
all groups; ; basal and pulsatile
GH secretion in obese relative
to non-obese

: 6 h integrated GH in response
to exercise was greater in nonobese relative to both obese
womens groups

Results

bGH bioactive growth hormone, DSL Diagnostic Systems Laboratories, ELISA enzyme-linked immunosorbent assay, GH growth hormone, GHBP GH binding protein, Nichols IRMA Nichols Institute
Diagnostics immunoradiometric assay, RIA radioimmunoassay, VO2max maximal oxygen consumption, VO2peak peak oxygen consumption, : indicates increase, ; indicates decrease
a
Ages are presented as mean or actual where stated

Ormsbee et al.
[85], 2009

Non-obese men
(8)
Obese men (8)
Non-obese women
(7)
Obese women (6)
Lean men (10)
Obese men (10)

Weltman et al.
[84], 2008

Wong and Harber

[83], 2006

Subjects (n)

Study, year

Table 2 Review of literature on acute growth hormone responses to exercise in obese adults

846
G. A. Thomas et al.

Obesity and Growth Hormone

condition between men who were lean or obese. However,

pulsatile GH response was blunted in men who were obese
relative to lean men following an acute cycling exercise
protocol. Weltman et al. [84] examined differences
between men and women who were lean or obese in
response to intermittent and continuous treadmill aerobic
exercise. All groups, regardless of sex or obesity status,
displayed increased 24-h GH post-exercise. However, basal
and pulsatile GH secretion was blunted in obese relative to
non-obese individuals regardless of sex.
Only two studies have examined an acute resistance,
exercise-induced GH response in individuals who are obese.
Ormsbee et al. [85] compared iGH responses in ten lean and
ten obese sedentary men who were sedentary and obese
following a 40-min resistance exercise protocol. GH concentrations were not different at rest between the groups.
Ormsbee found that GH responses were greater for lean men
who were lean while men who were obese showed a pulsatile
GH secretion that was blunted following exercise. It is
important to note that Ormsbee did not examine bGH
responses nor were other GH markers, such as GHBP,
examined as part of the study. Thomas et al. [86] compared
iGH, bGH and GHBP responses in nine lean and nine sedentary men who were obese following an acute resistance
exercise protocol that utilized a high-volume, whole-body
acute resistance exercise protocol. Thomas found that exercise-stimulated iGH was no different in men who were obese
compared with lean men. However, bGH concentrations
overall were significantly lower in the participants who were
obese compared to participants who were lean. Additionally,
individuals who were obese had significantly higher GHBP
concentrations. These results indicated that individuals who
are obese can stimulate pulsatile GH by resistance exercise if
the acute programme variables are properly manipulated.

4 Conclusions and Recommendations

Given the role of pulsatile GH in metabolism, specifically
lipolysis, the reduction of GH concentrations in individuals
who are obese presents a potential risk factor for further
adiposity. It also presents a potential difficulty for obese
individuals in adiposity reduction and weight loss. Several
questions remain as to the efficacy of GH on fat metabolism and reduction in overall adiposity. However, preliminary studies indicate that resistance exercise employing
high-volume, whole-body training may be potent mechanism for promoting GH pulsatile response, thereby
decreasing adiposity and promoting lean muscle mass in
individuals who are obese.
We would also argue that resistance exercise offers a
mechanism in which individuals who are obese are able to
exercise at the same intensity as lean individuals and could

847

experience a pulsatile GH release if the proper acute programme variables are used. It is therefore important that
sports medicine professionals focus on each acute exercise
session to produce the optimal iGH response in individuals
who are obese. An acute exercise sessions that is of highvolume and is moderate to high in intensity with short rest
intervals (\1 min), and utilizes exercises that target large
muscle mass, is the optimal stimulus to produce an acute
hormonal response of GH release [87]. Therefore, exercise
prescription should focus on these variables to influence
pulsatile iGH secretion for individuals who are obese.
Research in samples of individuals who are obese has
demonstrated that very few are meeting the recommendations for physical activity thresholds that are necessary for
decreasing chronic disease risk or promoting weight loss
[88, 89]. Given the potential long-term impact on society of
the healthcare costs associated with obesity-associated
disease, identifying specific exercise programme variables
with empirically supported mechanisms for promotion of
weight loss offers a potentially more efficient alternative
for actively engaging obese individuals to exercise.
Acknowledgments The authors have no conflicts of interest that are
directly relevant to the content of this review. This review was supported in part by the National Institute of Nursing Research (Research
Training: Self and Family Management Research (T32 NR008346).

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