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Sports Med 2005; 35 (4): 339-361
R
EVIEW
A
RTICLE
0112-1642/05/0004-0339/$34.95/0
2005 Adis Data Information BV. All rights reserved.
Hormonal Responses and Adaptations
to Resistance Exercise and Training
William J. Kraemer
1,2
and Nicholas A. Ratamess
3
1 Human Performance Laboratory, Department of Kinesiology and Department of Physiology
and Neurobiology and School of Medicine, University of Connecticut, Storrs,
Connecticut, USA
2 School of Biomedical and Sports Science, Edith Cowan University, Joondalup, Western
Australia, Australia
3 Department of Health and Exercise Science, The College of New Jersey, Ewing, New
Jersey, USA
Contents
Abstract ....................................................................................340
1. Testosterone ............................................................................341
1.1 Acute Responses to Resistance Exercise ................................................341
1.2 Chronic Changes in Resting Concentrations of Testosterone .............................343
1.3 Modification of Androgen Receptor Content ...........................................344
1.4 Response of Luteinising Hormone ......................................................344
1.5 Testosterone Precursors ...............................................................345
1.6 Sex Hormone-Binding Globulin ........................................................346
2. Growth Hormone (GH) Super Family ......................................................346
2.1 Acute Response to Resistance Exercise ................................................346
2.2 Chronic Changes in Resting GH Concentrations ........................................348
2.3 GH Binding Protein ...................................................................348
3. Cortisol ................................................................................348
3.1 Acute Response to Resistance Exercise ................................................349
3.2 Chronic Adaptations in Resting Cortisol Concentrations .................................349
3.3 Testosterone/Cortisol Ratio ............................................................350
3.4 The Glucocorticoid Receptor and Resistance Training ...................................350
4. Insulin-Like Growth Factors (IGFs) .........................................................350
4.1 Acute IGF-1 Response to Resistance Exercise ...........................................351
4.2 Chronic Circulating IGF-1 Adaptations to Resistance Training.............................351
4.3 Muscle Isoforms of IGF-1 and Adaptations to Resistance Training .........................351
4.4 IGF Binding Proteins ..................................................................351
5. Insulin ..................................................................................352
6. Catecholamines ........................................................................352
7. Other Hormones ........................................................................352
7.1 β-Endorphins ........................................................................352
7.2 Thyroid Hormones ....................................................................353
7.3 Fluid Regulatory Hormones............................................................353
7.4 Leptin ..............................................................................353
7.5 Peptide F ...........................................................................354
7.6 Estrogens ...........................................................................354
8. Overtraining and Detraining .............................................................354
9. Circadian Patterns ......................................................................355
10. Concurrent Strength and Endurance Training ..............................................356
11. Conclusion .............................................................................356
340 Kraemer & Ratamess
Resistance exercise has been shown to elicit a significant acute hormonal
Abstract
response. It appears that this acute response is more critical to tissue growth and
remodelling than chronic changes in resting hormonal concentrations, as many
studies have not shown a significant change during resistance training despite
increases in muscle strength and hypertrophy. Anabolic hormones such as testos-
terone and the superfamily of growth hormones (GH) have been shown to be
elevated during 15–30 minutes of post-resistance exercise providing an adequate
stimulus is present. Protocols high in volume, moderate to high in intensity, using
short rest intervals and stressing a large muscle mass, tend to produce the greatest
acute hormonal elevations (e.g. testosterone, GH and the catabolic hormone
cortisol) compared with low-volume, high-intensity protocols using long rest
intervals. Other anabolic hormones such as insulin and insulin-like growth fac-
tor-1 (IGF-1) are critical to skeletal muscle growth. Insulin is regulated by blood
glucose and amino acid levels. However, circulating IGF-1 elevations have been
reported following resistance exercise presumably in response to GH-stimulated
hepatic secretion. Recent evidence indicates that muscle isoforms of IGF-1 may
play a substantial role in tissue remodelling via up-regulation by mechanical
signalling (i.e. increased gene expression resulting from stretch and tension to the
muscle cytoskeleton leading to greater protein synthesis rates). Acute elevations
in catecholamines are critical to optimal force production and energy liberation
during resistance exercise. More recent research has shown the importance of
acute hormonal elevations and mechanical stimuli for subsequent up- and
down-regulation of cytoplasmic steroid receptors needed to mediate the hormonal
effects. Other factors such as nutrition, overtraining, detraining and circadian
patterns of hormone secretion are critical to examining the hormonal responses
and adaptations to resistance training.
Resistance exercise and/or training elicits a mi- mately leading to a specific response such as an
increase in muscle protein synthesis.
lieu of acute physiological responses and chronic
adaptations that are critical for increasing muscular
Perhaps the most influential mediating factor in
strength, power, hypertrophy and local muscular
the acute responses and subsequent adaptations is
endurance.
[1]
Of primary importance to acute exer- the resistance exercise stimulus. Proper resistance
cise performance and subsequent tissue remodelling exercise prescription and manipulation of the acute
is the role(s) played by the neuroendocrine sys- programme variables (e.g. intensity, volume, rest
tem.
[2]
Hormonal elevations in response to resis- intervals, exercise selection and sequence, repetition
tance exercise take place in a unique physiological velocity, frequency) ensures an optimal neuroen-
environment. Acute elevations in circulating blood docrine response.
[2,3]
Programme design will incor-
hormone concentrations (i.e. resulting from either porate three fundamental concepts of progression
increased secretion, reduced hepatic clearance, plas- (e.g. progressive overload, variation and specificity)
ma volume reductions, reduced degradation rates) that attempt to maximise adaptations of the neuro-
present a greater likelihood of interaction with re- muscular system.
[1]
For example, with progressive
ceptors on either the target tissue cell membrane overload, motor unit recruitment will increase.
[4]
(e.g. peptides) or with nuclear/cytoplasmic receptors Recruitment of a greater number of muscle fibres
located within the target tissue (e.g. steroid recep- enables greater hormone-tissue interaction within
tors). Coinciding with blood hormonal concentra- the realm of a larger percentage of the total muscle
tions is the number of available receptors for bind- mass. Consequently, tissue activation is a precursor
ing and subsequent cellular changes. Interaction to anabolism. Therefore, the training programme as
with the receptor initiates a milieu of events, ulti- well as genetic predisposition, sex, fitness level and
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 341
the potential for adaptation all play significant roles It is the unbound fraction of testosterone that is
in the hormonal response to resistance exercise.
biologically active and able to interact with andro-
Several hormones are discussed in this review.
gen receptors (AR). The response of free testoster-
Emphasis is placed upon those anabolic and catabol-
one has been shown to parallel total testosterone in
ic hormones most relevant to tissue remodelling.
some studies,
[11,12,22]
whereas a lack of response or
Tissue remodelling is a dual process in that catabol-
reductions have been demonstrated in others.
[23,24]
ism initiates the process during resistance exercise
Recently, Tremblay et al.
[11]
reported elevated free
and anabolism predominates in the recovery period
testosterone concentrations following resistance ex-
leading to growth and repair. Thus, both catabolic
ercise. Interestingly, the acute elevation was greater
and anabolic hormones play key roles in this pro-
in resistance-trained men than endurance-trained
cess. Adaptations to resistance training entail four
men, thereby indicating a beneficial chronic adapta-
general classifications:
tion from resistance training. These data partially
1. acute changes during and post-resistance exer-
support Kraemer et al.
[25]
who reported significant
cise;
elevations in serum free testosterone in both young
2. chronic changes in resting concentrations;
and elderly men. However, the magnitude of eleva-
3. chronic changes in the acute response to a resis-
tion was greater after 10 weeks of periodised
tance exercise stimulus;
strength training compared with the pre-training re-
4. changes in receptor content.
sponse, thereby suggesting that a resistance training
Other factors such as nutritional intake, training
base may enhance the acute response to a workout.
experience, sex, age and/or maturity, interaction
In addition, a significant elevation in resting serum
with other modalities of exercise and diurnal varia-
free testosterone was observed in the young men.
tions, as well as the resistance training programme,
Free testosterone has been shown to be elevated by
affect the endocrine responses and adaptations to
25% in young women following acute resistance
resistance training are also discussed.
exercise (e.g. six sets of ten repetition maximum
[RM] squats with 2-minute rest intervals);
[14]
how-
1. Testosterone
ever, no changes have been observed following re-
sistance exercise in middle-aged and elderly wo-
1.1 Acute Responses to Resistance Exercise
men.
[26]
Several factors appear to influence the acute se-
Resistance exercise has been shown to acutely
rum total testosterone responses to resistance exer-
increase total testosterone concentrations in most
cise. The magnitude of elevation during resistance
studies in men,
[5-12]
while in young women no
exercise has been shown to be affected by the mus-
change
[8]
or an elevation
[13,14]
may take place. These
cle mass involved (i.e. exercise selection),
[27,28]
in-
elevations have been attributed to plasma volume
tensity and volume,
[29-36]
nutritional intake,
[9]
train-
reductions, adrenergic stimulation,
[15]
lactate-stimu-
ing experience,
[11,37]
and is independent of the indi-
lated secretion
[16,17]
and potential adaptations in tes-
vidual’s absolute level of muscular strength.
[37]
tosterone synthesis and/or secretory capacity of the
Large muscle-mass exercises such as the Olympic
Leydig cells in the testes.
[18]
It appears that its role in
lifts,
[38]
deadlift
[39]
and jump squats
[27]
have been
augmentation of other hormonal mechanisms (e.g.
shown to produce large elevations in testosterone
growth hormone [GH], insulin-like growth factor-1
compared with small muscle-mass exercises. These
[IGF-1]) in anabolic processes,
[19]
as well as the
large muscle-mass exercises have been shown to be
effect of testosterone on the nervous system (i.e.
potent metabolic stressors
[35,40]
and a strong meta-
testosterone can interact with receptors on neurons
bolic component may be a stimulus for testosterone
and increase the amount of neurotransmitters re-
release.
[16]
Based on these data, it appears that
leased, regenerate nerves, increase cell body size
programmes designed to stimulate testosterone se-
and dendrite length/diameter)
[20,21]
may be of prima-
cretion should be structured around large muscle-
ry interest when examining the potential benefits to
mass exercises.
enhancing acute force production.
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
342 Kraemer & Ratamess
Table I. The effects of intensity and volume on the acute total testosterone response
Study Protocol Results
Weiss et al.
[7]
Three sets of four exercises to failure, 80% of 1RM with 2 min RI Sig. ↑ in T
Ratamess et al.
[35]
1 × 10 squats, 80–85% 1RM NC
6 × 10 squats, 80–85% 1RM, 2 min RI Sig. ↑ in T
Raastad et al.
[31]
70% of 3–6RM vs 100% of 3–6RM Sig. ↑ in T; 100% >70%
Schwab et al.
[32]
4 × 6 squats (90–95% of 6RM) 31% ↑ in T
4 × 9–10 (60–65% of load used for high intensity) 27% ↑ in T
Bosco et al.
[34]
20 sets of 2–4 reps vs 10 sets of 2–3 reps of half squats Sig. ↑ in T
NC
H
¨
akkinen and 20 sets of 1RM squats NC
Pakarinen
[33]
10 sets of 10 reps with 70% of 1RM Sig. ↑ in T
Gotshalk et al.
[36]
One vs three sets of 10RM for eight exercises Sig. ↑ in T; 3 > 1
Kraemer et al.
[29,30]
Eight exercises, 3–5 × 5RM vs 10RM with 1- and 3-min RI Sig. ↑ in T; T ↓ as load ↓ and RI ↑
NC = no change; reps = repetitions; RI = rest interval; RM = repetition maximum; sig. = significant; T = testosterone; ↓ indicates decrease;
↑ indicates increase.
Little is known concerning the testosterone re- stantial elevations in total testosterone (see table I).
sponse to varying the sequence of exercises during
Schwab et al.
[32]
reported significant elevations in
resistance training. It has been suggested that large
testosterone during two squat protocols. However,
muscle-mass exercises be performed prior to small
testosterone did not significantly increase until after
muscle-mass exercises.
[1]
The hypothesis is that per-
the fourth set was completed. When resistance is
formance of large muscle-mass exercises (i.e. squat,
held constant, the larger acute testosterone response
deadlift, power clean) early in the workout may
is observed in the protocol consisting of a higher
produce significant elevations in testosterone, which
number of sets.
[34-36]
Similarly, if repetitions are held
potentially may expose smaller muscles to a greater
constant then the protocol with higher loading tends
response than that resulting from performance of
to produce the greatest acute testosterone re-
small muscle-mass exercises only. This hypothesis
sponse.
[31]
However, Ahtiainen et al.
[12]
recently re-
was recently examined. Hansen et al.
[28]
measured
ported no differences in the acute testosterone re-
muscle strength changes in the elbow flexor muscles
sponse between two protocols of similar repetition
following 9 weeks of resistance training. However,
number, but intensity was slightly greater in one
one group performed a workout consisting of elbow
protocol that incorporated forced repetitions. The
flexion exercises only and a second group per-
interaction between these variables has yielded in-
formed lower-body exercises prior to the elbow
teresting results favouring those programmes with a
flexion exercises. Performing elbow-flexion exer-
higher glycolytic component (e.g. moderate intensi-
cises only failed to acutely elevate testosterone sig-
ty, high volume, relatively short rest intervals).
nificantly. However, testosterone was significantly
Guezennec et al.
[41]
reported minor elevations in
elevated when lower-body exercises were per-
testosterone during conventional strength training
formed first, and muscle strength increased to a
greater extent as well when both lower- and upper- (i.e. 3–4 sets of 3–10 repetitions at 70–95% of 1RM,
body exercises were performed. These data provide
2.5-minute rest periods). However, when load was
support for performing large muscle mass, multiple-
increased further and repetitions decreased to three,
joint exercises early in a workout and smaller mus-
a limited testosterone response was observed. Krae-
cle-mass exercises later in the workout when train-
mer et al.
[42]
reported significant elevations in testos-
ing to enhance muscle strength.
terone following five sets of 15–20 repetitions of the
squat, despite using loads of 50% of 1RM. Kraemer
The intensity and volume of the resistance train-
et al.
[29,30]
reported that a bodybuilding programme
ing programme has been shown to affect the acute
(moderate load, high volume) with short rest periods
testosterone response. Protocols of sufficient inten-
sity and volume have been shown to produce sub- produced greater testosterone responses than high-
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 343
load, low-volume training with long (3-minute) rest lating concentrations of testosterone in response to
periods. low dietary fat intake and a diet with a high protein/
carbohydrate ratio.
[27]
Elevations in insulin concen-
The effect of training frequency on the acute
trations have coincided with decreased testosterone
testosterone response has not been adequately ad-
in another study examining protein/carbohydrate
dressed. H
¨
akkinen et al.
[24]
reported a greater testos-
supplementation.
[6]
Thus, a possible interaction be-
terone response during afternoon sessions compared
tween insulin and testosterone warrants further
with morning sessions in elite weightlifters during
study.
multiple training sessions per day. However, it is
difficult to interpret hormonal data at different times
1.2 Chronic Changes in Resting
of day as diurnal variations are very influential. In
Concentrations of Testosterone
addition, total training volume is influential as se-
rum testosterone concentrations returned to normal
Changes in resting testosterone concentrations
when training frequency was reduced to one
during resistance training have been inconsistent or
workout per day.
[43]
non-existent in men and women,
[48-51]
although sig-
The acute response of testosterone has been
nificant elevations have been reported in both pre-
shown to be influenced by the age, training experi-
pubertal and pubertal boys.
[52]
In fact, similar resting
ence of the individuals, sex, as well as baseline
concentrations between untrained women and na-
values. College-aged men typically display a signifi-
tional-level elite female weightlifters have been re-
cant acute response, whereas the response may be
ported.
[47]
Rather, it appears that resting concentra-
limited in younger high-school aged men.
[39]
Junior
tions reflect the current state of muscle tissue such
weightlifters (14–18 years of age) with >2 years of
that elevations or reductions may occur at various
lifting experience have been shown to produce a
stages depending on substantial changes in the vol-
greater acute testosterone response than those with
ume and intensity of training,
[45,53]
although no
<2 years of experience.
[38]
The response in adults
changes have also been observed during periodised
has been less pronounced such that no changes in the
resistance training.
[49]
Elevated resting testosterone
acute response have been observed with additional
concentrations have been reported in some stud-
training experience.
[44]
This was recently demon-
ies,
[25,45,53-55]
whereas several studies have shown no
strated by Ahtiainen et al.
[45]
who reported no differ-
differences
[5,23,26,48,56-58]
or reductions.
[45]
Examina-
ences in the acute response between strength-trained
tion of elite Olympic weightlifters has shown no
and non-strength-trained men before and after 21
significant differences occurring over a 1-year peri-
weeks of training. Older individuals have been
od;
[23]
however, elevations were reported following
shown to produce significant elevations of testoster-
a second year of training.
[53]
Recently, Ahtiainen et
one; however, the absolute concentrations are sig-
al.
[45]
reported significantly higher free and total
nificantly lower than that of younger individuals.
[25]
testosterone concentrations during a 7-week high-
The acute testosterone response in women appears
volume training phase compared with pre-training
limited
[8,34,46,47]
as only few studies have shown sig-
values. However, reductions were observed when
nificant elevations.
[13,14]
In direct comparison, men
volume was reduced and intensity was increased
have shown acute elevations in testosterone but not
over a subsequent 7-week training period. We have
women immediately following the same proto-
reported similar findings where no changes in rest-
col.
[7,8]
Rather, it appears other anabolic hormones
ing testosterone concentrations were observed dur-
such as GH may be more influential for promoting
ing 2 weeks of high-volume overreaching but reduc-
muscle hypertrophy in women.
tions were observed during a subsequent 2-week
The acute testosterone response to resistance ex- high-intensity, lower-volume phase (unpublished
ercise appears to be influenced by nutritional sup- observation). In addition, Raastad et al.
[59]
reported a
plementation. Carbohydrate/protein supplementa- 12% reduction in resting testosterone concentrations
tion has been shown to limit the testosterone re- during a heavy training phase. Thus, substantial
sponse to resistance exercise.
[9]
The rationale is changes in volume and intensity may elicit transient
unclear but a previous study reported reduced circu- changes in resting testosterone concentrations; how-
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
344 Kraemer & Ratamess
ever, values may return to baseline when the indi- between baseline AR content in the vastus lateralis
vidual returns to ‘normal’ training. and 1RM squat, thereby suggesting that AR content,
in part, assists in mediating strength changes during
1.3 Modification of Androgen
resistance training.
[35]
Receptor Content
The resistance exercise stimulus appears to medi-
ate the magnitude of acute AR modifications. The
The presence of AR in tissues has been shown to
effect of resistance exercise volume on AR content
correlate highly with the known functions of andro-
was recently examined. Ratamess et al.
[35]
compared
gens. The AR concentration in rat skeletal muscle
two protocols (one vs six sets of ten repetitions)
depends on several factors including muscle fibre
consisting of the squat exercise to examine potential
type, contractile activity and the concentrations of
acute modifications in AR content 1 hour post-
testosterone.
[60,61]
Resistance training or exercise in
exercise. No differences were observed in AR con-
general, has been shown to modulate AR con-
tent following the single set protocol. However, the
tent.
[62,63]
In rats, resistance training elicits a signifi-
higher-volume protocol elicited significant down-
cant increase in androgen binding capacity in the
regulation of AR content. Considering that ARs are
extensor digitorum longus muscle but reduces an-
protein molecules and protein catabolism increases
drogen binding capacity in the soleus, thereby dem-
during resistance exercise,
[69]
our data demonstrated
onstrating a fibre-type specific effect of training.
[64]
that when sufficient volume is reached, AR protein
Electrical stimulation of the rat gastrocnemius in-
content may initially down-regulate (despite large
creased AR content by 25% within 3 days (with a
elevations in circulating testosterone) prior to the
concomitant increase in muscle mass) but plateaued
up-regulation that has been observed in other stud-
at 5 days when the stimulation remained the
ies.
[67]
The relationship between the magnitude of
same.
[65]
However, administration of an AR antago-
initial down-regulation and the subsequent compen-
nist in rats (i.e. oxendolone) during 2 weeks of
satory up-regulation that occurs several hours later
electrical stimulation attenuated 70% of the stimula-
warrants further investigation. However, we have
tion-induced hypertrophy observed compared with a
also discovered that ingestion of a protein/carbohy-
vehicle control group.
[66]
Collectively, these data
drate supplement before and after the workout atten-
demonstrate the importance of the androgen-AR
uates the AR down-regulation with higher-volume
interaction during training to maximise hypertro-
resistance exercise observed 1 hour post-exercise
phy.
(unpublished observation). Thus, nutritional inter-
Resistance training has been shown to up-regu-
vention plays a critical role in AR modification post-
late AR content following resistance exercise in
resistance exercise.
humans. Bamman et al.
[67]
reported that AR messen-
ger RNA (mRNA) in the vastus lateralis increased
1.4 Response of Luteinising Hormone
63% and 102%, respectively, 48 hours following
eight sets of eight repetitions of either eccentric Luteinising hormone (LH) is a protein hormone
(~110% of 1RM) or concentric (~85% of 1RM) secreted from the basophilic cells of the anterior
squats. Kadi et al.
[68]
cross-sectionally examined 17 pituitary, which is the primary regulator of testoster-
power lifters, nine of whom were cycling anabolic one secretion from the Leydig cells of the testes.
[18]
steroids and reported that power lifters had a higher Blood concentrations of LH are positively related to
percentage of AR-positive myonuclei in the trapezi- the intensity and volume of resistance training.
[23,70]
um muscles compared with untrained controls. Pow- Resting concentrations of LH did not change signifi-
er lifters administering anabolic steroids had a cantly in men and women during 16–24 weeks of
greater percentage of AR-positive myonuclei than strength and power training
[50,56]
but slight eleva-
drug-free power lifters. Interestingly, no differences tions have been shown in strength athletes during
were observed between power lifters and controls intense training periods
[71]
and in resistance-trained
for percentage of AR-positive myonuclei in the vas- men compared with endurance-trained men.
[11]
Bus-
tus lateralis muscle during baseline measurements. so et al.
[70]
compared a 4-week intensive training
We have recently shown significant correlations programme in elite weightlifters with a 2-week re-
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 345
duced training period and reported a reduction in sponses. Both acute elevations
[78,81]
and a lack of
testosterone concentrations with a concurrent eleva- acute elevation in testosterone have been report-
tion in LH during the intense training phase. It was ed.
[82]
hypothesised that the decrease in testosterone con-
Leder et al.
[83]
have shown that during small (i.e.
tributed to the elevation in LH. An acute bout of
100mg) and large (i.e. 300mg) administered doses
resistance exercise does not induce LH secretion,
[43]
of oral androstenedione, the majority of androstene-
although a delayed response has been demonstrated
dione undergoes hepatic metabolism to testosterone
later into the recovery period;
[11]
therefore sug-
and then to testosterone metabolites prior to release
gesting that acute elevations in serum testosterone
into systemic circulation. The net effect is a large
concentrations during resistance exercise are due to
production of testosterone metabolites despite only
other regulatory mechanisms (e.g. reduced clear-
small or no elevations in testosterone. Further sup-
ance, plasma volume shifts).
port for these data were provided by Brown et al.
[84]
who examined a low dose of sublingual andros-
1.5 Testosterone Precursors
tenediol administration (60mg) and reported signifi-
cant elevations of both total and free testosterone
The biosynthetic pathway of testosterone con-
(that were not observed during oral administration)
tains many steps. Theoretically, supplementation
for 180 minutes (with a peak occurring at 60 min-
with such testosterone precursors may enhance tes-
utes) post-administration. These data indicate that
tosterone concentrations (by reducing the number of
small to moderate oral doses of prohormones pro-
conversion steps) and subsequent acute resistance
duce minimal, if any, elevations in testosterone in
exercise performance. Some of these precursor
young men. However, the subsequent elevations in
molecules that have been investigated include dehy-
testosterone metabolites, estradiol, estrone, and re-
droepiandrosterone (DHEA) [prasterone], 4-andros-
ductions in HDLs potentially pose health risks that
tendione, 4-androstenediol, 5-androstenediol, 19-
need to be considered prior to prohormone use.
norandrostenediol, 19-norandrostenedione and 1-
Long-term studies have shown no further im-
androstene-3β-17β-diol.
[72,73]
Studies have shown
provement in muscle strength or hypertrophy with
that low doses (50–100 mg/day) of these
DHEA/androstenedione/androstenediol supplemen-
prohormones do not increase circulating testoster-
tation (150–300 mg/day) over 8–12 weeks of resis-
one concentrations in young, healthy men
[74-78]
al-
tance training.
[74,77,82,85-87]
Baseline testosterone
though elevations of DHEA, androstenedione and
values measured during this time did not change
LH have been observed in addition to less desirable
significantly, although significant elevations in an-
responses such as elevations in estrone, estradiol,
drostenedione/androstenediol, DHEA sulfate (PB
and reductions in high-density lipoproteins (HDLs).
008), estrone and estradiol were reported.
[85]
In addi-
In fact, the magnitude of estradiol elevation has been
tion, 5 days of oral androstenedione supplementa-
shown to be dose-dependent.
[78]
It has been suggest-
tion (100 mg/day) did not elevate protein synthe-
ed that this range of administration was too low
sis.
[88]
Therefore, the potential ergogenic effects of
considering that young, healthy men have much
precursor hormones remain to be seen and require
higher resting testosterone concentrations than wo-
further examination particularly since many individ-
men and older men.
[72]
uals consume higher than the recommended dose.
Interestingly, low-dose supplementation of an-
drostenedione has been shown to elevate testoster- Adrenal androgens may play a greater role in
one in post-menopausal women
[79]
and higher doses women considering the low levels of testosterone
(~300mg) have been shown to elevate free testoster- present. Women tend to have a slightly larger con-
one by 37% in middle-aged men.
[80]
However, in version percentage of circulating DHEA and its
young men, supplementation with 200–300 mg/day precursor DHEA sulfate to androstenedione and tes-
of 4-androstenediol, 4-androstenedione and/or sup- tosterone at the tissue level
[89]
and typically have
plements consisting of multiple prohormones (i.e. higher baseline concentrations of androstenedione
300mg of androstenedione plus 150mg of DHEA, as than men.
[7]
However, androstenedione is signifi-
well as other ingredients) has shown variable re- cantly less potent than testosterone. Few studies
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
346 Kraemer & Ratamess
have examined the acute response to resistance exer- are also released such as a 20kD isoform missing
cise. Weiss et al.
[7]
reported 8–11% elevations in residues 32–46, a 5kD isoform consisting of resi-
circulating androstenedione in both men and women dues 1-43 and a 17kD isoform consisting of residues
following a programme consisting of four exercises 44–191.
[92]
In addition, other monomeric, dimeric,
for three sets to failure with 80% of 1RM and 2- protein-bound GH and aggregates of GH have been
minute rest intervals. Tremblay et al.
[11]
reported identified, which are included this GH superfami-
elevations in DHEA sulfate during resistance exer- ly.
[92]
The physiological roles of these variants are
cise and this response was greater in resistance- now under investigation but appear to function simi-
trained men than endurance-trained men. No larly to the 22kD molecule in promoting tissue anab-
changes
[26]
and reductions
[48]
in baseline concentra- olism.
tions of androstenedione, DHEA and DHEA sulfate
2.1 Acute Response to Resistance Exercise
have been reported during 24 weeks of resistance
training. However, baseline concentrations of
The 22kD GH molecule has been the focus of
DHEA sulfate were elevated after 8 weeks of resis-
most resistance exercise studies. Exercise,
[93-95]
es-
tance training in young women and this elevation
pecially resistance exercise,
[96]
has been shown to
correlated significantly to increases in lean body
acutely elevate many of the GH variants. Recently,
mass.
[90]
The impact of acute and chronic changes in
Hymer et al.
[97]
examined a common protocol used
the concentrations of testosterone precursors war-
in our laboratory (e.g. six sets of ten repetitions of
rants further investigation.
the squat with 75% of 1RM with 2-minute rest
intervals) and reported significant elevations in GH
1.6 Sex Hormone-Binding Globulin
variants <30kD and 30–60kD in size in women. In
addition, Kraemer et al.
[98]
using the same protocol
Circulating androgens are predominately bound
in women reported differential acute responses in
to the transport protein sex hormone-binding globu-
GH variants based on muscular strength. A sub-
lin (SHBG). A change in SHBG concentrations may
group of the ten strongest women showed the high-
influence the binding capacity of testosterone and
est resting concentrations of all GH fractions, al-
the magnitude of free testosterone available for dif-
though the ten weakest women displayed the highest
fusion across the cell membrane to interact with
concentrations of the <30kD fractions. Similar acute
membrane-bound steroid receptors. Recent studies
responses were observed in strong and weak women
have identified SHBG receptors on cell membranes
in >30kD fractions although the weaker women
and a possible receptor-mediated role for SHBG in
showed a greater <30kD response. These results
mediating androgen actions through a cyclic adeno-
indicate that other molecular weight variants of GH
sine monophosphate mechanism.
[91]
Differential re-
appear responsive to resistance exercise; however,
sponses have been observed during resistance train-
further research is warranted in order to elucidate
ing. Acute elevations have been reported
[35,37]
in
the impact of these elevations. The remainder of this
some but not all studies,
[24]
whereas reductions
[23]
section will focus on the often-studied 22kD GH
and no changes in resting SHBG concentrations
molecule.
have been reported following 3–24 weeks of resis-
Resistance exercise has been shown to elevate
tance training,
[26,50,51,56,58]
following 1 week of inten-
the concentrations of human GH through 30 minutes
sive Olympic weightlifting
[43]
and over a 2-year
post-exercise similarly in men and women, although
period in elite Olympic weightlifters.
[53]
the resting concentrations of GH are significantly
higher in women.
[46]
The magnitude appears depen-
2. Growth Hormone (GH) Super Family
dent upon exercise selection and subsequent amount
The acidophilic cells of the anterior pituitary of muscle mass recruited,
[28,38]
muscle actions used
secrete molecules that make up the family of GH (i.e. greater response during concentric than eccen-
polypeptides. The most commonly studied GH tric muscle actions),
[22]
intensity,
[12,99,100]
vol-
isoform, the 22kD molecule, consists of 191 amino ume,
[36,101]
rest intervals between sets
[29,30]
and train-
acids.
[18]
Other biologically active spliced fragments ing status (e.g. greater acute elevations based on
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 347
individual strength and the magnitude of total work 1RM with 1-minute rest intervals) all consisting of
performed).
[45,102,103]
The importance of total work four exercises and reported the acute GH response
has been demonstrated as multiple-set protocols matched total work such that the most substantial
have elicited greater GH responses than single-set response was observed in the endurance protocol.
protocols.
[36,104,105]
It appears that the acute GH re- Using a similar protocol, Smilios et al.
[108]
reported
sponse to resistance exercise is highly influenced by that the acute GH response was greater following
the metabolic properties (total work) of the protocol. four sets versus two sets of resistance exercise (no
That is, protocols eliciting high blood lactate values additional elevation was observed using six sets)
(e.g. those programmes that are moderate to high in targeting hypertrophy and local muscular endur-
intensity, high in volume, stress large muscle mass, ance. The hypertrophy protocol produced a signifi-
and use relative short rest intervals) tend to produce cant elevation but less compared with the endurance
the most substantial GH responses.
[29,30,36,42,101]
High protocol. The strength protocol yielded only a small
correlations between blood lactate and serum GH elevation.
concentrations have been reported
[33]
and it has been
Ahtiainen et al.
[12]
compared two programmes of
proposed that H
+
accumulation produced by lactic
similar format with the exception that one group
acidosis may be the primary factor influencing GH
used 12RM loading and the other group used forced
release.
[46]
This finding was supported by an attenu-
repetitions in order to perform 12 repetitions with a
ated GH response following induced alkalosis dur-
heavier load and reported a more substantial GH
ing high-intensity cycling.
[106]
Hypoxia, breath hold-
response when using forced repetitions. Williams et
ing, acid-base shifts and protein catabolism have
al.
[109]
compared three protocols of high (3 × 10RM,
been reported to influence GH release.
[46]
Thus,
1-minute rest intervals, eight exercises), moderate
resistance exercise is a potent stimulus for elevating
(15 sets of ten repetitions for the leg extension,
GH so long as the threshold of volume and intensity
1-minute rest intervals), and low (3 × 10RM for the
are met.
[99]
leg extension, 1-minute rest interval) volumes, and
Several investigations have given support to the reported that only the high-volume protocol elicited
association between acidosis resulting from resis- a significant rise in GH. Goto et al.
[110]
examined a
tance exercise, total work and the acute GH re- strength protocol (five sets using 90% of 1RM with
sponse. Moderate- to high-intensity, high-volume 3-minute rest intervals) and reported a low GH
programmes using short rest periods have shown the response. However, the addition of a single set of
greatest acute GH response compared with conven- high repetitions with 50% of 1RM to the end of the
tional strength or power training using high loads, strength protocol elicited a much higher GH re-
low repetitions and long rest intervals in men.
[29,30]
sponse. These data indicate that the hormonal re-
H
¨
akkinen and Pakarinen
[33]
reported that 20 sets of sponse to a strength protocol may be maximised by
1RM in the squat only produced a slight increase in inclusion of high volume set(s) and the end of the
GH, whereas a substantial increase in GH was ob- workout.
served following ten sets of ten repetitions with 70%
It has been shown that the acute GH response is
of 1RM. Hoffman et al.
[101]
compared a low-intensi-
somewhat limited in older individuals.
[25,44,100]
In
ty, higher volume protocol (15 repetitions of the
general, GH concentrations decline with age (e.g.
squat with 60% of 1RM) to a high-intensity, low-
somatopenia) and these reductions correspond to
volume protocol (four repetitions of the squat with
periods of muscle atrophy (sarcopenia) in the elder-
90% of 1RM) and reported a significantly higher
ly. Considering the impact of these findings, at-
GH response with the higher-volume protocol.
tempts to restore GH to some extent appear war-
Zafeiridis et al.
[107]
compared a strength protocol ranted to increase muscle strength and hypertrophy.
(i.e. four sets of five repetitions using 88% of 1RM It has been suggested that a major factor contribut-
with 3-minute rest intervals), hypertrophy protocol ing to the limited GH response (other than age)
(i.e. four sets of ten repetitions using 75% of 1RM maybe the magnitude of exertion displayed. Pyka et
with 2-minute rest intervals) and an endurance pro- al.
[100]
reported lower blood lactates in the elderly
tocol (i.e. four sets of 15 repetitions using 60% of during resistance exercise, thereby supporting the
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
348 Kraemer & Ratamess
hypothesis that maximal effort is necessary for op- GH and its roles in the homeostatic control of other
timising the exercise-induced secretion of GH. In- variables, e.g. glucose. In addition, these findings
terestingly, resistance training over 12 weeks in the suggest that the acute response of GH to resistance
elderly has been shown to promote greater acute GH exercise may be most prominent for tissue remodel-
response to a resistance exercise protocol,
[44]
possi- ling. The exercise-induced increase has been highly
bly suggesting the greater response was due to an correlated with the magnitude of type I and type II
increased ability to exert oneself. muscle fibre hypertrophy (r = 0.62–0.74).
[58]
These
relationships could be indicative of a role for repeat-
The specificity of muscle action selection during
ed acute resistance exercise-induced GH elevations
resistance training may affect the acute GH response
on cellular adaptations in trained muscle. Changes
to resistance exercise. Kraemer et al.
[111]
trained
in receptor sensitivity, differences in feedback
subjects for 19 weeks performing either all concen-
mechanisms, IGF-1 potentiation and diurnal varia-
tric repetitions, concentric repetitions with double
tions may also play significant roles.
the volume, or concentric and eccentric repetitions
and the acute response to a resistance exercise proto-
2.3 GH Binding Protein
col consisting of either concentric or eccentric mus-
cle actions was measured pre- and post-exercise.
Circulating GH is complexed to mostly high-
The GH response was high for the concentric train-
affinity GH-specific binding proteins (GHBPs) that
ing groups during the concentric protocol; however,
greatly extend its half-life and enhance the overall
the acute response was greater for the eccentric
biological effects of GH. It is now known that the
protocol for the concentric/eccentric training group.
human high-affinity GHBP arises from proteolytic
These data indicate that GH secretion may be sensi-
cleavage of the extracellular domain of the GH
tive to the muscle actions used during resistance
receptor.
[113]
This process is thought to occur princi-
training. It has been shown that the anterior pituitary
pally at the liver, which is the most GH receptor-rich
may be directly innervated by nerve fibres mostly
tissue, but could occur wherever the GH receptor
with synapses on corticotroph and somatotroph
exists. Little is known concerning GHBP and resis-
cells.
[112]
It has also been suggested that ‘neural-
tance exercise. Rubin et al.
[103]
recently reported that
humoral’ regulation of GH secretion may take place
acute resistance exercise (six sets of squats with
such that a rapid neural response is observed during
80–85% of 1RM for ten repetitions with 2-minute
the initial stress with the humoral phase subsequent-
rest intervals) resulted in significant elevations of
ly occurring.
[112]
If such is the case then it may be
GHBP; however, no differences were observed be-
possible for higher brain centres, e.g. motor cortex,
tween resistance-trained and untrained individuals
to play an active role in regulating GH secretion
suggesting that chronic resistance training does not
during resistance exercise and this regulatory mech-
alter circulating GHBP or change GH receptor ex-
anism may be sensitive to specific muscle actions
pression.
used during resistance training.
3. Cortisol
2.2 Chronic Changes in Resting
GH Concentrations
Glucocorticoids are released from the adrenal
Traditional resistance training does not appear to cortex in response to the stress of exercise. Of these,
affect resting concentrations of GH. No changes in cortisol accounts for approximately 95% of all
resting GH concentrations have been observed in glucocorticoid activity. Cortisol has catabolic func-
men and women of various ages.
[25,26,55,58]
This con- tions that have greater effects in type II muscle
tention is also supported by data demonstrating sim- fibres.
[2]
About 10% of circulating cortisol is free,
ilar resting concentrations of GH in elite Olympic while ~15% is bound to albumin and 75% is bound
weightlifters
[53]
and strength athletes (i.e. body to corticosteroid-binding globulin. In peripheral tis-
builders, power lifters, weightlifters)
[45]
compared sues, cortisol stimulates lipolysis in adipose cells
with lesser-trained individuals. These findings are and increases protein degradation and decreases
consistent with dynamic feedback mechanisms of protein synthesis in muscle cells resulting in greater
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 349
release of lipids and amino acids into circulation, We have recently demonstrated that six sets of
respectively. Because of its major role in tissue ~10RM squats with 2-minute rest intervals in-
remodelling, acute and chronic changes of cortisol creased serum cortisol concentrations substantially,
during resistance training is often examined. whereas performance of only one set did not elicit
any response.
[35]
Increasing total volume by the in-
3.1 Acute Response to Resistance Exercise
clusion of higher intensity sets using forced repeti-
tions has been shown to elicit a larger cortisol re-
Studies have shown significant elevations in cor-
sponse than the same protocol performed with less
tisol and adrenocorticotropic hormone (ACTH, a
loading and no forced repetitions.
[12]
It addition, the
pituitary hormone that stimulates cortisol release
rest interval length affects the acute cortisol re-
from the adrenal cortex) during an acute bout of
sponse.
[46,117]
Kraemer et al.
[118]
reported that per-
resistance exercise
[10,24,25,38,41,46]
with the response
forming eight sets of 10RM leg press exercises with
similar between men and women
[46]
although one
1-minute rest intervals elicited a significantly
study reported an increase in cortisol in men but not
greater acute cortisol response than the same proto-
women who performed the same protocol.
[8]
The
col using 3-minute rest periods. Thus, while chronic
acute cortisol response appears to be independent of
high levels of cortisol have adverse effects, acute
training status at least in adolescent weightlifters,
[38]
elevations may be part of a larger remodelling pro-
although a recent study has shown less of a response
cess in muscle tissue.
in endurance athletes compared with resistance-
The effect of carbohydrate supplementation on
trained men performing the same resistance exercise
the subsequent acute cortisol response to resistance
protocol.
[11]
Some hormonal elevations have been
exercise has been studied. Tarpenning et al.
[119]
re-
attributed to plasma volume reductions; however,
ported that the acute cortisol response was limited
when corrected for plasma volume changes cortisol
with a 6% carbohydrate solution during resistance
concentrations still remain elevated.
[58]
In addition,
exercise, and that a carbohydrate-supplemented
it has been reported that the acute increase in cortisol
group experienced greater gains in hypertrophy over
secretion during resistance exercise may be attenu-
12 weeks of resistance training. Kraemer et al.
[9]
ated by anabolic steroid use.
[114]
reported a blunted cortisol response during 3 days of
Programmes that elicit the greatest cortisol re-
carbohydrate supplementation and resistance train-
sponse also elicit the greatest acute GH and lactate
ing. However, not all studies have shown an attenua-
response. Significant correlations between blood
tion of the acute cortisol response to resistance exer-
lactate and serum cortisol have been reported.
[35,115]
cise with carbohydrate supplementation.
[109]
It has
In addition, acute elevations in serum cortisol have
been suggested that carbohydrate supplementation
been highly correlated to 24-hour post-exercise se-
during resistance exercise reduces the demand for
rum creatine kinase concentrations.
[116]
Metabolical-
gluconeogenesis, thereby reducing the need for cor-
ly demanding protocols high in total work, i.e. high
tisol.
[120]
Although further research is warranted,
volume, moderate to high intensity with short rest
some evidence exists supporting carbohydrate sup-
periods, have elicited the greatest acute lactate and
plementation during resistance exercise for limiting
cortisol response with little change during conven-
the acute cortisol response.
tional strength/power training.
[33,46,117]
In fact, some
strength protocols have failed to elicit a significant
3.2 Chronic Adaptations in Resting
cortisol response whereas hypertrophy and endur-
Cortisol Concentrations
ance protocols performed by the same group of
subjects elicited more substantial acute elevations Resting cortisol concentrations generally reflect
through 30 minutes post-exercise.
[107,108]
The num- a long-term training stress. Chronic resistance train-
ber of sets per exercise and/or volume appears to ing does not appear to produce consistent patterns of
influence the acute cortisol response in most studies cortisol secretion as no change,
[23,26,45,49-51,53,121]
re-
but not all.
[109]
Smilios et al.
[108]
have shown that ductions
[37,48,55,56,58]
and elevations
[71]
have been re-
four to six sets of resistance exercise elicited a ported during normal strength and power training in
significantly larger cortisol response than two sets. men and women, and during short-term overreach-
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
350 Kraemer & Ratamess
ing. In animals, cortisol concentrations have ex- ministration on the glucocorticoid receptor. It ap-
plained a substantial amount of the variance ob- pears that with consistent resistance training experi-
served in muscle mass changes.
[122]
Thus, it appears ence, down-regulation of the glucocorticoid receptor
that the acute cortisol response may reflect metabol- may occur, thereby reducing the catabolic influence
ic stress whereas the chronic changes (or lack of on skeletal muscle tissue.
change) may be involved with tissue homeostasis
Eccentric resistance exercise has been shown to
involving protein metabolism.
up-regulate glucocorticoid receptor content and my-
ofibrillar proteolysis.
[126]
Recently, Willoughby et
3.3 Testosterone/Cortisol Ratio
al.
[126]
examined glucocorticoid receptor content and
mRNA 6 and 24 hours following two eccentric
The testosterone/cortisol (T/C) ratio and/or free
resistance exercise protocols (both consisting of
testosterone/cortisol ratio have been suggested to be
seven sets of ten repetitions of knee extensions with
indicators of the anabolic/catabolic status of skeletal
150% of 1RM) and reported significant up-regula-
muscle during resistance training.
[123]
Either an in-
tion at 6 and 24 hours post-exercise (with a much
crease in testosterone, a decrease in cortisol, or both
more substantial increase at 24 hours) following the
would indicate potential state of anabolism. Howev-
first bout. However, the up-regulation was signifi-
er, this appears to be an oversimplification and is at
cantly attenuated following the second bout, thereby
best only an indirect measure of the anabolic/cata-
indicating a protective training effect with exposure
bolic properties of skeletal muscle.
[18]
Some studies
to eccentric exercise. In addition, these changes
have shown changes in the T/C ratio during strength
paralleled elevations in serum cortisol (i.e. larger
and power training, and this ratio has been positively
elevations were observed immediately after, 6, 24,
related to performance improvements,
[48,56]
whereas
and 48 hours following bout 1 than bout 2). The
other studies have shown no change.
[45]
Stressful
attenuated up-regulation in glucocorticoid receptor
training (overreaching) in elite weightlifters has
content and mRNA following bout 2 also coincided
been shown to decrease the T/C ratio.
[23]
Periodised,
with attenuated up-regulation of factors of the ATP-
higher-volume programmes have been shown to
dependent ubiquitin proteolytic pathway. These data
produce a significantly greater increase in the T/C
indicate that chronic exposure to eccentric resis-
ratio than a low-volume, single-set programme.
[55]
tance exercise does provide a protective effect in
However, in an animal study where the T/C ratio
limiting tissue catabolism and reducing some of the
was manipulated to investigate muscle hypertrophy,
magnitude of associated muscle damage through
it was reported that the T/C ratio was not a useful
modifications of glucocorticoid receptor content.
indicator of tissue anabolism.
[122]
Thus, the use of
the T/C ratio remains questionable.
4. Insulin-Like Growth Factors (IGFs)
3.4 The Glucocorticoid Receptor and
IGFs are structurally related to insulin and medi-
Resistance Training
ate many of the actions of GH. IGFs are small
The catabolic effects of cortisol are mediated polypeptide hormones (70 and 67 amino acid resi-
through interaction with glucocorticoid receptors. dues for IGF-1 and IGF-2, respectively) that are
Consequently, cortisol and possibly androgen con- secreted as they are produced by the liver in re-
centrations appear to be critical to determining the sponse to GH-stimulated DNA synthesis.
[91]
IGFs
level of up- or down-regulation of glucocorticoid increase protein synthesis during resistance training
receptors. For many years it has been suggested that and enhance muscle hypertrophy.
[91]
The impor-
anabolic steroids may also be anti-catabolic in na- tance of these hormones, in particular IGF-1, has
ture because of competitive inhibition of binding been recently shown as immunisation to IGF-1 in
between androgens and cortisol for the glucocorti- diabetic rats prevented protein synthesis following
coid receptor.
[124]
Although evidence does support resistance exercise.
[127]
Of the two, IGF-1 has been
this contention,
[125]
further research is warranted to extensively studied and will be discussed from here
examine the anti-catabolic nature of androgen ad- on.
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 351
4.1 Acute IGF-1 Response to 4.3 Muscle Isoforms of IGF-1 and
Adaptations to Resistance Training
Resistance Exercise
IGF-1 has been shown to have autocrine/
The acute response of IGF-1 to resistance exer-
paracrine functions within muscle cells.
[132,133]
Two
cise remains unclear. Most studies have shown no
isoforms in skeletal muscle have been identified
change in IGF-1 during or immediately following an
each functioning independently.
[134]
One isoform is
acute bout of resistance exercise,
[6,9,128]
whereas a
similar to the circulating hepatic IGF-1 called
few studies have shown acute elevations during and
IGF-1Ea and the second muscle-specific isoform of
following resistance exercise.
[29,30,103]
The lack of
IGF-1 is mechano growth factor (MGF).
[133,134]
The
change has been attributed to delayed secretion of
second isoform only differs from the liver isoform
IGF-1, i.e. 3–9 hours, following GH-stimulated
by the presence of the first 49 base pairs from exon
mRNA synthesis,
[46]
as peak values may not be
5.
[134]
Overloaded muscle and subsequent mechani-
reached until 16–28 hours post-stimulated GH re-
cal damage, e.g. resistance training, appear to be
lease.
[6]
Therefore, it appears that IGF-1 elevation
prominent stimuli for these isoforms.
[67,133]
It ap-
following an acute bout of resistance exercise may
pears both isoforms increase protein synthesis and
be delayed until GH-stimulated synthesis and secre-
promote satellite cell activation.
[134]
Bamman et
tion from the liver can take place.
al.
[67]
reported significant elevations in muscle
IGF-1 mRNA following resistance exercise, particu-
larly during eccentric resistance exercise. Hameed et
4.2 Chronic Circulating IGF-1 Adaptations to
al.
[134]
examined muscle content 2.5 hours following
Resistance Training
a lower-body workout (e.g. ten sets of six repetitions
using 80% of 1RM with 2-minute rest intervals) and
No change in resting concentrations of IGF-1
reported that in young men MGF mRNA increased
have been reported during normal short-term resis-
substantially (however, no increase was observed in
tance training
[25,58]
and overreaching (unpublished
older men), whereas IGF-1Ea mRNA did not signif-
observation), unless concurrent with carbohydrate/
icantly change in young or older men. Brahm et
protein supplementation.
[9]
Resistance-trained men
al.
[135]
have shown that arterial concentrations of
have been shown to have higher resting IGF-1 con-
IGF-1 remained constant during intensive exercise.
centrations than untrained men.
[103]
However, long-
However, venous concentrations of IGF-1 in-
term studies in women have shown elevations in
creased, which may suggest that a circulating eleva-
resting IGF-1, particularly during high volume train-
tion may be accounted for by greater release from
ing.
[55,129]
Borst et al.
[130]
reported significant eleva-
the muscles (i.e. via cell disruption and greater
tions in resting serum IGF-1 following only 13
blood flow). Nevertheless, it does appear that the
weeks of a 25-week training programme. The eleva-
muscle isoforms of IGF-1 play a prominent role
tions reported by Borst et al.
[130]
were similar be-
during tissue remodelling.
tween single-set and multiple-set training groups
despite a significantly greater strength increase ob-
4.4 IGF Binding Proteins
served in the multiple-set group. Marx et al.
[55]
re-
ported significant elevations in resting IGF-1 con-
Nearly all circulating IGFs are bound to IGF
centrations in previously untrained women follow-
binding proteins (IGFBPs). These regulate IGF
ing 6 months of training. In addition, the magnitude
availability and prolong IGF circulation.
[91]
The
was greater when a high-volume, multiple-set pro-
most common is IGFBP-3. Acute resistance exer-
gramme was used. Reductions in IGF-1 (~11%)
cise has been shown to elevate IGFBP-3
[42,136]
and
have also been reported during high volume and
this response was greater following L-carnitine L-
intensity overreaching, but have returned to baseline
tartrate supplementation.
[42]
Nindl et al.
[136]
have
once the overreaching phase subsided.
[59,131]
Thus, it
shown that an acute bout of resistance exercise did
appears that the volume and intensity of training are
not influence IGF-1 specifically but affected the
important for chronic IGF-1 adaptations.
manner in which IGF-1 was partitioned among its
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
352 Kraemer & Ratamess
family of binding proteins. IGFBP-3 was elevated tude may be dependent upon the force of muscle
for the first hour following resistance exercise but contraction, amount of muscle stimulated, volume
did not differ overnight whereas IGFBP-2 was ele- of resistance exercise and rest intervals.
[117,142]
Prior
vated overnight.
[136]
Less is known concerning to intense exercise, a significant elevation in plasma
chronic circulating concentrations of IGFBP-3. epinephrine and norepinephrine has been ob-
Borst et al.
[130]
have reported a significant decline in served,
[10,30]
thereby demonstrating an ‘anticipatory
IGFBP-3 between weeks 13 and 25 of a resistance rise’. This anticipatory rise may be part of the
training programme. The impact of changes in body’s psychophysiological adjustment for prepar-
IGFBPs requires further study. ing to maximally perform during resistance exer-
cise. Chronic adaptations remain unclear, although
5. Insulin
it has been suggested that training reduces the cat-
echolamine response to resistance exercise.
[41]
How-
Insulin has been shown to significantly affect
ever, alterations in the acute response may reflect
muscle protein synthesis when adequate amino acid
the demands of the programme such that systematic
concentrations are available, especially by reducing
variation and progressive overload may obviate any
protein catabolism.
[137,138]
Serum insulin concentra-
subsequent decrease.
tions parallel changes in blood glucose, and the
response is enhanced when protein/carbohydrates
7. Other Hormones
are ingested prior to, during, or following the
workout.
[6,9,137-140]
Without supplementation, serum
7.1 β-Endorphins
insulin concentrations have been shown to decrease
during an acute bout of resistance exercise.
[31]
We
Less is known concerning the role of β-
have reported depressed fasted insulin values during
endorphins during resistance training. Elevations
4 weeks of resistance training overreaching.
[141]
Al-
have been reported during resistance exercise in
though a potent anabolic hormone when in its nor-
men and women.
[38,143,144]
However, no
mal range of physiological concentrations, insulin
changes
[145,146]
and post-exercise reductions
[147]
appears to be mostly affected by blood glucose
have also been reported. Although a threshold of
concentrations and/or dietary intake. Therefore, in-
intensity and volume is necessary for acute eleva-
gestion of carbohydrates, amino acids, or combina-
tions to occur during aerobic exercise (i.e. at least
tions of both prior to, during, and/or immediately
70% of maximum oxygen consumption
after the resistance exercise protocol is recommend-
[
˙
VO
2max
]),
[148]
a similar scenario may also be ob-
ed for maximising insulin’s effects on tissue anabo-
served during resistance exercise as protocols that
lism. Supplementation prior to or during resistance
have shown no acute elevation in β-endorphins
exercise is especially beneficial for maximising pro-
have also failed to result in acute elevations of
tein synthesis because it takes advantage of the large
cortisol.
[145]
The acute elevation has been attributed
increase in muscular blood flow and subsequent
to the magnitude of muscle mass used, rest interval
amino acid delivery.
length, intensity and volume of the resistance exer-
cise programme,
[38,116]
has correlated highly with
6. Catecholamines
blood lactate concentrations in those studies that
Catecholamines reflect the acute demands of the reported elevations,
[115,116]
and does not appear relat-
resistance exercise protocol and are important for ed to training experience or muscle strength.
[38]
In
increasing force production, muscle contraction addition, the response is greater and longer in dura-
rate, energy availability, as well as several other tion when resistance exercise is performed by indi-
functions including the augmentations of hormones viduals in negative energy balance.
[144]
Body build-
such as testosterone.
[2]
An acute bout of resistance ing type workouts (high volume, moderate load,
exercise has been shown to increase plasma concen- short rest periods) elicit the most substantial eleva-
trations of epinephrine,
[10,41,117,142]
nore- tions in plasma β-endorphin concentrations com-
pinephrine
[10,41,117]
and dopamine.
[10,117]
The magni- pared with traditional strength training (high load,
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 353
low repetitions, long rest periods).
[116]
Thus, acute er lifters perform one set of the leg press exercise to
elevations may occur during resistance exercise; exhaustion using 80% of their 1RM. Immediately
however, further research is needed to elucidate the post-exercise into 5 minutes of recovery plasma
role(s) of β-endorphins during resistance training. osmolality, atrial peptide, renin activity and angi-
otensin II were elevated. These data were the first to
7.2 Thyroid Hormones
demonstrate that fluid balance and the subsequent
hormonal response may be affected in as little as the
The role of thyroid hormones during resistance
first set of a resistance exercise workout.
training remains unclear but may be permissive in
its interaction with other hormones. In animals, the
7.4 Leptin
interaction of liothyronine (T
3
) with its receptor has
Leptin, a product of the ob gene arising from
been shown to up-regulate AR mRNA with this
adipose tissue, is a protein hormone thought to relay
effect potentiated by higher androgen concentra-
satiety signal to the hypothalamus to regulate energy
tions.
[149]
In moderately trained men and highly
balance and appetite.
[158]
Leptin concentrations are
trained rowers, significant resting reductions in thy-
highly correlated to body fat mass such that obese
roxine (T
4
),
[150]
free T
4
,
[150]
free T
3
,
[151]
and thyroid
humans have on average four times more serum
stimulating hormone (TSH)
[151]
were reported,
leptin than lean individuals.
[159]
Serum leptin con-
whereas no changes in T
3
[150]
or T
4
[151]
have also
centrations may be influenced by sex, metabolic
been reported. Pakarinen et al.
[152]
reported signifi-
hormones (e.g. stimulated by insulin and cortisol
cant reductions in TSH, T
3
and T
4
during one inten-
and inhibited by β-adrenergic agonists) and current
sive week of resistance training (two workouts per
energy requirements.
[160]
In middle-aged and elderly
day) in elite weightlifters. However, over the course
obese hypogonadal men, testosterone and anabolic
of 1 year of training in elite weightlifters, no
steroid administration have been shown to reduce
changes were observed for any thyroid hormone
age-associated increases in fat mass, percentage
until the pre-competition period, i.e. lower volume
body fat and body mass index (BMI),
[161,162]
and has
of training, where significant increases in free T
4
been shown to reduce concentrations of leptin in a
and T
3
were reported.
[153]
These hormonal changes
dose-dependent manner.
[163]
returned to baseline when the intensity increased
Many studies have shown no direct impact of
during the next training phase. It appears that resis-
exercise on leptin concentrations independent of its
tance training may alter thyroid function; however,
effect on adipose tissue,
[160]
although high levels of
the impact of these alterations remains speculative at
energy expenditure may lead to a delayed reduction.
the present time. Due to the tight homeostatic con-
Gippini et al.
[164]
reported that leptin did not corre-
trol of thyroid hormones, elevations during resis-
late with BMI in body builders and that resistance
tance training are not expected.
training did not influence leptin production indepen-
dently of changes in body composition. Simsch et
7.3 Fluid Regulatory Hormones
al.
[151]
reported reductions in resting leptin concen-
Fluid homeostasis is critical to acute exercise trations following high-intensity resistance training
performance in general, although the majority of the in highly trained rowers. Zafeiridis et al.
[107]
com-
literature has examined aerobic modalities of exer- pared three types of resistance exercise protocols: (i)
cises. Fluid regulatory hormones such as arginine strength; (ii) hypertrophy; and (iii) muscular endur-
vasopressin, atrial peptide, renin, aldosterone and ance, and reported significant reductions in leptin
angiotensin II have been shown to increase in re- through 30 minutes of recovery. However, similar
sponse to exercise with the magnitude dependent on reductions were observed in non-exercising, control
exercise intensity, duration and hydration sta- subjects, thereby demonstrating that resistance exer-
tus.
[154,155]
Resistance exercise has been shown to cise did not result in the reduction. Rather, fasting
reduce plasma volume
[35,156]
comparable to changes and/or diurnal variation appeared to be critical fac-
elicited by running and/or cycling at 80–95% of tors. We have reported similar findings after resis-
˙
VO
2max
.
[157]
Kraemer et al.
[10]
had competitive pow- tance exercise in fasted subjects.
[103]
Nindl et al.
[165]
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
354 Kraemer & Ratamess
had subjects perform a high-volume protocol (i.e. 50 tance exercise has been shown to depress peptide F 4
total sets) and reported no acute changes in leptin hours into the recovery period.
[142]
Interestingly,
concentrations. However, a delayed reduction (9–13 changes in the ratio of peptide F to epinephrine were
hours) was observed and this was accompanied by a observed suggesting that overtraining may alter the
12% increase in resting energy expenditure, thereby secretory patterns of chromaffin cells.
[171]
demonstrating that a large disruption in metabolic
7.6 Estrogens
homeostasis (e.g. >800 kcals of exercise) could elic-
it reductions in leptin independent of changes in fat
Estrogens are steroids synthesised and secreted
mass. These data indicate that the resistance exer-
primarily by the ovaries (and adrenals to a lesser
cise stimulus (i.e. interaction of volume, intensity,
extent) in women, but are also produced from aro-
rest intervals, total work, etc.) does not influence the
matisation of testicular and adrenal androgens in
acute leptin response; however, if a protocol high
men. Estrogens perform many functions in the
enough in volume is performed then a delayed re-
human body. In particular, estrogens have been
sponse may be observed.
shown to reduce bone resorption
[172]
and muscle
Leptin is a critical mediator of several endocrine
damage,
[173]
which may have important ramifica-
pathways pertinent to resistance training. One such
tions for musculoskeletal adaptations to resistance
pathway regulated by leptin is testicular ster-
training. Of the estrogens, estradiol is the most ac-
oidogenesis. Leptin has been shown to directly re-
tive and has been studied most often during resis-
duce steroidogenesis by reducing enzymatic conver-
tance training. Very little is known concerning the
sion to 17-OH progesterone and through inhibition
acute responses and chronic adaptations of estradiol
of steroidogenic acute regulatory protein, cyto-
synthesis and secretion in response to resistance
chrome P450 cholesterol side-chain cleavage en-
training. Critical to examining estradiol concentra-
zyme, and steroidogenic factor 1,
[166]
while only
tions in women, is proper delineation of the men-
having small negative effects on LH and follicle
strual cycle. Studies that have examined muscle
stimulating hormone pulse amplitude.
[167]
Men who
strength, endurance and power performance in wo-
are considered obese (i.e. with high serum concen-
men during various phases of the menstrual cycle
trations of leptin) have been shown to have low
(e.g. menstruation, follicular, ovulation/mid-cycle
concentrations of total and free testosterone (i.e.
or luteal) have shown conflicting results where per-
22–45%), SHBG, and SHBG binding capacity with
formance enhancement during menstruation
[174]
and
the magnitude directly related to the level of body
ovulation
[175]
were reported; however, several stud-
fat.
[167,168]
Thus, high levels of leptin may be associ-
ies have shown no differences.
[176-178]
Thus, a lack of
ated with reduced androgen production. The impact
significant difference indicates that acute muscular
of reduced steroidogenesis on subsequent adapta-
performance is not affected by elevated concentra-
tions to resistance training requires further study but
tions of estrogens. In women, acute elevations fol-
does appear to be a potential limiting factor.
lowing resistance exercise have been report-
ed,
[144,179]
especially when women are in a hypo-
7.5 Peptide F
caloric state.
[144]
Chronically, H
¨
akkinen et al.
[50]
Peptide F is a proenkephalin fragment secreted
reported no significant changes in resting estradiol
from chromaffin cells of the adrenal medulla along
concentrations following 16 weeks of power train-
with epinephrine.
[18]
Although the physiological
ing. Thus, the role of estrogens in mediating the
function of peptide is not entirely known, it has been
acute and chronic effects of resistance training is
shown that it improves the B cell helper function of
unclear at the present time and warrants further
T lymphocytes.
[169]
Exercise has been shown to in-
investigation.
crease concentrations of peptide F.
[170]
Little is
known concerning resistance training. High-intensi-
8. Overtraining and Detraining
ty resistance exercise-induced overtraining does not
change circulating peptide F concentrations at rest Overtraining is defined as any increase in train-
or after exercise;
[171]
however, acute heavy resis- ing volume and/or intensity resulting in long-term
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
Hormones and Resistance Training 355
performance decrements.
[18]
In contrast, overreach- no change in resting concentrations of epinephrine
or norepinephrine. However, the acute catecho-
ing is a short-term increase in volume and/or intensi-
lamine response to resistance exercise was greater in
ty, which is often planned in resistance training
overtrained men. Therefore, it appears that intensi-
programmes thought to increase performance
ty-related overtraining does not alter resting hormo-
through a ‘rebound effect’ when used correct-
nal concentrations significantly with a correspond-
ly.
[121,141]
Repeated overreaching may lead to over-
ing decrease in performance, whereas volume-relat-
training and subsequent performance decrements in
ed overtraining does appear to significantly alter
addition to neuroendocrine changes. One and two
circulating hormone concentrations.
weeks of overreaching have been shown to reduce
Detraining is the cessation of resistance training
resting concentrations of testosterone and
or significant reduction of training volume, intensi-
IGF-1.
[43,59]
These decreases were significantly cor-
ty, or frequency resulting in reduced performance
related to strength decrements.
[59]
We have reported
(e.g. reduced muscle strength, power, hypertrophy,
that 4 weeks of overreaching with and without
local muscle endurance).
[2]
Alterations in hormonal
amino acid supplementation did not alter resting
activity may occur, in addition to changes in neural
concentrations of IGF-1 and cortisol (unpublished
and muscle function. It appears that the duration of
observation), although a significant elevation in cor-
the detraining period is important for the magnitude
tisol was observed in a group supplementing with
of change as well as the training status of the indi-
creatine after 1 week of high-volume overreach-
vidual. Hortobagyi et al.
[181]
reported significant ele-
ing.
[141]
However, the free androgen index (total
vations in resting concentrations of GH, testoster-
testosterone/SHBG) was reduced and this effect was
one, and the T/C ratio with a significant reduction in
more notable in the placebo group (unpublished
cortisol following 2 weeks of detraining in highly
observation). In addition, short-term overreaching
trained power lifters and football players. It was
may not result in elevated resting cortisol and may
hypothesised that this elevation in anabolic hormone
augment the acute testosterone response to resis-
concentrations was related to the body’s ability to
tance exercise when the individual has at least 1 year
combat the catabolic processes associated with de-
of weightlifting training and previous exposure to
training and suggested that short-term detraining
the overreaching stimulus.
[121]
Thus, overreaching
may represent an augmented stimulus for tissue
may either not change or reduce the resting concen-
remodelling and repair. However, these increases
trations of some anabolic hormones, not change or
have only been shown during short-term detraining.
increase cortisol concentrations, and the magnitude
We have recently reported no significant changes in
may depend on the volume/intensity of the training
testosterone, GH, LH, SHBG, cortisol or ACTH
stimulus as well as nutritional supplementation.
following 6 weeks of detraining in recreationally
Overtraining, resulting from a chronic large in-
trained men.
[182]
No changes have been observed for
crease in volume, has been shown to result in elevat-
cortisol, SHBG and LH following 8 weeks of de-
ed cortisol and reductions in resting LH, total and
training in women.
[50]
Detraining periods >8 weeks
free testosterone concentrations with the free pool of
have shown significant reductions in the T/C ratio,
testosterone most sensitive to the overtraining stim-
which correlated highly to strength decrements
[48,56]
uli.
[18,71]
In addition, the exercise-induced elevation
and elevations in T
4
.
[150]
These hormonal changes
in total testosterone is attenuated during volume-
coincide with periods of muscle atrophy
[181]
and
related overtraining.
[23]
Intensity-related overtrain-
indicate a hormonal role in muscle size and strength
ing does not appear to alter resting concentrations of
reductions observed during periods of detraining.
hormones thus demonstrating a differential response
in comparison to large increases in training vol-
9. Circadian Patterns
ume.
[18]
Fry et al.
[171]
reported no changes in circu-
lating total or free testosterone, cortisol, GH, or Several hormones are secreted in various pulses
peptide F concentrations during high-intensity over- throughout the day in a circadian pattern. Salivary
training (e.g. ten 1RM lifts of the squat everyday for testosterone secretion has been shown to be secreted
2 weeks). In a similar study, Fry et al.
[180]
reported in a circadian manner with the greatest elevations
2005 Adis Data Information BV. All rights reserved. Sports Med 2005; 35 (4)
356 Kraemer & Ratamess
observed early in the morning with less throughout 10. Concurrent Strength and
Endurance Training
the rest of the waking day.
[183]
Because of circadian
patterns, it is essential that researchers examining
Several studies have indicated that there is an
resistance exercise measure hormonal concentra-
incompatibility between simultaneous high-intensi-
tions at the same time of day or use control, non-
ty strength and endurance training such that maxi-
exercised subjects for multiple sampling periods
mal strength and power appear to be limited.
[186,187]
throughout the day for circadian control. Consider-
In addition, the neuroendocrine system may or may
ing that resistance exercise stimulates acute hormo-
not be altered. Bell et al.
[187]
reported no changes in
nal elevations, it is of interest to examine whether or
resting concentrations of testosterone, GH, or
not resistance exercise alters circadian patterns.
SHBG following 12 weeks of combined strength
Kraemer et al.
[183]
reported that resistance exercise
and endurance training. However, greater urinary
did not affect circadian patterns of testosterone se-
cortisol was observed in women.
[187]
Kraemer et
cretion over a 16-hour waking period in resistance-
al.
[186]
had subjects perform a total-body, high-vol-
trained men. It has been shown that afternoon resis-
ume resistance training programme 4 days per week
tance exercise-induced elevations in testosterone are
along with 4 days per week of endurance training for
sometimes greater than that observed in the morn-
12 weeks and reported a substantial increase in
ing,
[71]
thus reflective of diurnal variations. It ap-
exercise-induced cortisol concentrations. These data
pears that regulatory mechanisms are quickly re-
indicate that the incompatibility may also be the
engaged after a resistance exercise workout such
result of overtraining which in itself may produce a
that homeostasis is maintained within 1 hour post-
catabolic hormonal environment.
exercise.
11. Conclusion
The nocturnal hormonal response following re-
sistance exercise may differ. McMurray et al.
[184]
Resistance exercise elicits a milieu of hormonal
had trained individuals perform three sets of six
responses critical to acute muscular force and power
exercises to exhaustion at 1900–2000 hours and
production as well as subsequent tissue growth and
sampled blood prior to, and at 20-minute intervals
remodelling. In general, the acute response is depen-
following from 2100 to 0700 hours. Resistance ex-
dent upon the stimulus (e.g. intensity, volume, mus-
ercise did not alter nocturnal patterns of GH and
cle mass involvement, rest intervals, frequency) and
cortisol secretion. However, testosterone secretion
may be the most critical element to tissue remodel-
was greater between 0500 and 0700 hours in the
ling. Long-term adaptations in neuroendocrine func-
resistance exercise group and nocturnal secretion of
tion appear minimal but may be related to the cur-
T
4
decreased. However, Nindl et al.
[185]
examined
rent intensity/volume of the training stimulus.
GH pulsatility at 10-minute intervals (i.e. shorter
intervals than McMurray et al.
[184]
) following high-
Acknowledgements
volume resistance exercise and reported that a dif-
No sources of funding were used to assist in the prepara-
ferential pattern during sleep such that GH was
tion of this review. The authors have no conflicts of interest
lower the first half of sleep and higher during the last
that are directly relevant to the content of this review.
half of sleep. In addition, total and free IGF-1 did
not differ overnight. However, IGFBP-2 was elevat-
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