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Testosterone Physiology in Resistance
Exercise and Training
The Up-Stream Regulatory Elements
Jakob L. Vingren,
1,2
William J. Kraemer,
2,3
Nicholas A. Ratamess,
4
Jeffrey M. Anderson,
2
Jeff S.Volek
2
and Carl M. Maresh
2,3
1 Applied Physiology Laboratories, Department of Kinesiology, Health Promotion and Recreation,
University of North Texas, Denton, Texas, USA
2 Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs,
Connecticut, USA
3 Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut, USA
4 Department of Health and Exercise Science, The College of New Jersey, Ewing, New Jersey, USA
Contents
Abstract................................................................................ 1037
1. Testosterone Production and Release. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1038
1.1 Testosterone Production . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1038
1.2 Hypothalamic-Pituitary-Gonadal Axis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1039
1.3 Stimulation and Inhibition of the Hypothalamic-Pituitary-Gonadal Axis . . . . . . . . . . . . . . . . . . . . 1039
2. The Biological Effects of Testosterone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1040
2.1 Transport of Testosterone in the Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1040
2.2 Actions on the Muscle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1040
2.2.1 Effect on Androgen Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1041
2.2.2 Importance for Normal Muscle Development and Maintenance . . . . . . . . . . . . . . . . . . . 1041
3. Testosterone Response to Resistance Exercise and Training. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1042
3.1 Men ............................................................................ 1042
3.1.1 Intensity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1043
3.1.2 Number of Sets. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1043
3.1.3 Volume . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1044
3.1.4 Choice of Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1044
3.1.5 Order of Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1045
3.1.6 Rest Period Duration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1045
3.2 Women.......................................................................... 1046
3.3 Effect of Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1047
3.4 Effect on Androgen Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1048
4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1049
Abstract Testosterone is one of the most potent naturally secreted androgenic-
anabolic hormones, and its biological effects include promotion of muscle
growth. In muscle, testosterone stimulates protein synthesis (anabolic effect)
and inhibits protein degradation (anti-catabolic effect); combined, these ef-
fects account for the promotion of muscle hypertrophy by testosterone. These
REVIEW ARTICLE Sports Med 2010; 40 (12): 1037-1053
0112-1642/10/0012-1037/$49.95/0
ª2010 Adis Data Information BV. All rights reserved.
physiological signals from testosterone are modulated through the inter-
action of testosterone with the intracellular androgen receptor (AR). Tes-
tosterone is important for the desired adaptations to resistance exercise and
training; in fact, testosterone is considered the major promoter of muscle
growth and subsequent increase in muscle strength in response to resistance
training in men. The acute endocrine response to a bout of heavy resistance
exercise generally includes increased secretion of various catabolic (break-
down-related) and anabolic (growth-related) hormones including testoster-
one. The response of testosterone and AR to resistance exercise is largely
determined by upper regulatory elements including the acute exercise pro-
gramme variable domains, sex and age. In general, testosterone concentra-
tion is elevated directly following heavy resistance exercise in men. Findings
on the testosterone response in women are equivocal with both increases and
no changes observed in response to a bout of heavy resistance exercise. Age
also significantly affects circulating testosterone concentrations. Until pub-
erty, children do not experience an acute increase in testosterone from a bout
of resistance exercise; after puberty some acute increases in testosterone from
resistance exercise can be found in boys but not in girls. Aging beyond 35–40
years is associated with a 1–3%decline per year in circulating testosterone
concentration in men; this decline eventually results in the condition known
as andropause. Similarly, aging results in a reduced acute testosterone res-
ponse to resistance exercise in men. In women, circulating testosterone con-
centration also gradually declines until menopause, after which a drastic
reduction is found. In summary, testosterone is an important modulator of
muscle mass in both men and women and acute increases in testosterone can
be induced by resistance exercise. In general, the variables within the acute
programme variable domains must be selected such that the resistance ex-
ercise session contains high volume and metabolic demand in order to induce
an acute testosterone response.
This review examines androgen endocrine
physiology (i.e. testosterone and the androgen
receptor [AR]) and its relationship to resistance
exercise and training. Knowledge of the general
testosterone physiology is important because it is
the foundation for understanding the physiolo-
gical implications of changes in testosterone and
AR concentrations. The first section provides an
overview of testosterone production and the sig-
nals for testosterone production and release. The
next section examines the biological effects of
testosterone including transport, signalling and
physiological functions with special attention gi-
ven to the importance of testosterone for normal
muscle development and maintenance. Finally, the
acute and chronic testosterone and AR responses
to resistance exercise and training is discussed
with the focus on upper regulatory elements:
acute exercise programme variable domains, sex
and age.
1. Testosterone Production and Release
1.1 Testosterone Production
Testosterone (17b-hydroxy-4-androstene-3-one)
is a 0.288 kD C
19
steroid hormone produced from
cholesterol via a series of conversions catalysed by
specific enzymes; this process takes approximately
20–30 minutes from initiation to final product.
[1]
Several of the intermediates in this process are
hormones with their own physiological actions
and include progesterone, dihydroepiandroster-
one (DHEA) and androstenedione; the former is
involved in the female reproductive cycle
[2]
and the
latter two have weak androgenic-anabolic effects.
[3]
1038 Vingren et al.
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
The primary production site of testosterone is
the Leydig cells. These cells are only found in the
testes, which largely explain the approximately
10-fold higher circulating testosterone concentra-
tions in men compared with women. Testosterone
is also produced in smaller quantities in the ovaries
and the zona reticularis of the adrenal cortex.
[4]
This testosterone formation is mainly spillover
from the production of other hormones such as
cortisol and aldosterone (in the adrenal glands)
that share some precursors with testosterone, and
estradiol (in the ovaries) for which testosterone
itself is a precursor.
[5]
These shared precursors help
explain how the adrenal gland and the ovaries
can produce testosterone despite the absence of
Leydig cells in these tissues. This spillover, along
with peripheral conversion of androgens, is the
primary source of testosterone in females and
adolescent boys. The absence of functioning cells
dedicated to testosterone production and release
prevents large acute increases in circulating tes-
tosterone in females and adolescent boys in res-
ponse to exercise. Although peripheral production
(e.g. in muscle tissue) of testosterone occurs,
[6]
this production does not appear to be affected by
resistance exercise in humans.
[7]
1.2 Hypothalamic-Pituitary-Gonadal Axis
The signal for gonadal testosterone produc-
tion and release originates in the hypothalamus.
The hypothalamus is innervated by the CNS and
thus provides a direct link between the nervous
and the endocrine systems.
[8]
Specialized neurons
in the hypothalamus produce and secrete gona-
dotrophin releasing hormone (GnRH).
[8]
GnRH
travels directly to the anterior pituitary gland via
the hypothalamic-hypophyseal portal vein. This
allows for a quick delivery of the hormonal signal
from the hypothalamus to the pituitary target
cells. In the anterior pituitary, GnRH stimulates
the production and release of luteinizing hormone
(LH) and follicle-stimulating hormone (FSH) from
the gonadotrophs.
[8]
LH and FSH then enter the
circulation and are transported to the gonads. In
the gonads, LH stimulates testosterone production
in the Leydig cells of men and the theca cells of
women. LH binds to a G-protein-coupled mem-
brane receptor; the signal induced by LH acti-
vates cyclic adenosine monophosphate-dependent
protein kinases (protein kinase A),
[9,10]
which
stimulates the rate-limiting step in testosterone
synthesis.
[9]
Testosterone is a steroid hormone
and thus cannot be stored in the cells that pro-
duce it; instead, testosterone is released from the
cells following production. In women, testoster-
one is further processed to estradiol in the gran-
ulosa cells adjacent to the theca cells. FSH does
not appear to have direct effects on testosterone
production in men but is important in stimula-
tion of steroid binding protein production in the
liver. In women, FSH stimulates the production
of pregnenolone in the granulosa cells and steroid
binding protein production in the liver. The sig-
nal cascade from FSH is similar to that induced
by LH in the theca and Leydig cells; the produced
pregnenolone can leave the granulosa cells for the
theca cells where it can be further processed to
testosterone. Finally, FSH stimulates the synth-
esis of p450 aromatase, which is responsible for
the conversion of testosterone to estradiol in the
granulosa cell. This system of signalling events
from the hypothalamus to the gonads leading to
testosterone (and estradiol) production and se-
cretion is termed the ‘hypothalamic-pituitary-
gonadal axis’.
1.3 Stimulation and Inhibition of the
Hypothalamic-Pituitary-Gonadal Axis
The initiation of the hypothalamic-pituitary-
gonadal axis, which ultimately leads to increased
testosterone release, is caused either by direct
nervous stimulation of the hypothalamus by the
CNS or by reduced feedback inhibition on the
hypothalamus by testosterone. Testosterone in-
duces negative feedback on (i) the hypothalamus
to reduce GnRH release; and (ii) the gonado-
trophs in the anterior pituitary to reduce the
release of LH and FSH in response to GnRH.
The use of GnRH analogues have shown that in
the absence of a GnRH signal the gonadotrophs
in the anterior pituitary do not independently
release LH despite very low circulating testoster-
one concentrations.
[11,12]
Since the GnRH ana-
logue prevented an exercise-induced increase in
Testosterone and Resistance Exercise 1039
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
circulating LH and testosterone, it appears that
the signal for increased testosterone release with
resistance exercise is controlled at the level of the
hypothalamus.
2. The Biological Effects of Testosterone
Testosterone is one of the most potent natu-
rally secreted androgenic-anabolic hormones,
[13]
and its biological effects include promotion of
secondary male-sex characteristics, such as beard
and body hair growth, nitrogen retention and
muscle growth.
[14]
In muscle, testosterone stimu-
lates protein synthesis (anabolic effect)
[15]
and
inhibits protein degradation (anti-catabolic ef-
fect);
[16]
combined, these effects account for the
promotion of muscle hypertrophy by testoster-
one. The physiological effects of testosterone are
induced by its binding to the intracellular AR,
which then translocates to the nucleus where the
AR-testosterone complex induces transcription
of specific genes.
[17]
Recently, membrane recep-
tors for testosterone have been proposed to ex-
plain the rapid effects of testosterone on the
cell.
[18]
In addition to the anabolic effects, tes-
tosterone has anti-catabolic effects that are be-
lieved to include an inhibition of cortisol signal-
ling by blocking the glucocorticoid receptor.
[19,20]
The administration of testosterone to patients
receiving long-term glucocorticoid therapy at-
tenuates or even reverses some of the adverse
effects from glucocorticoid treatment such as re-
ductions in bone mineral density and muscle
mass.
[21]
Similarly, excess glucocorticoids can in-
terfere with testosterone signalling
[22]
and sup-
press testosterone production in the Leydig
cells.
[23]
It is mainly the anabolic effects of tes-
tosterone that are of interest to those engaged in
resistance exercise; however, the anti-catabolic
effects might also be a very important aspect be-
cause they help protect muscle protein and aid in
recovery. These anabolic effects are also primar-
ily what have led athletes from many different
sports to abuse various pharmacological forms of
testosterone. Although generally not considered
among the primary anabolic hormones in
women, testosterone has a potent effect on female
muscle tissue.
2.1 Transport of Testosterone in the Circulation
Testosterone is hydrophobic and consequently
does not readily dissolve in the blood; instead,
almost all testosterone in the circulation is bound
to binding proteins that are hydrophilic.
[24]
The
primary binding protein for testosterone is sex
hormone-binding globulin (SHBG), which binds
approximately 44–60%of total serum testoster-
one.
[25,26]
The remaining testosterone is either
loosely bound to albumin and other binding pro-
teins or free (i.e. not bound to any binding proteins);
however, only about 0.2–2%of total testosterone
is in the free form.
[26,27]
Free testosterone is the
most biologically active fraction of testosterone;
thus, the biological activity of testosterone is regu-
lated by its interaction with the different binding
proteins.
[28]
The physiological effects of the bind-
ing proteins vary. SHBG reduces the movement
of testosterone from the blood into other bio-
compartments; whereas, albumin does not appear
to interfere with this movement.
[29,30]
Furthermore,
in contrast to free testosterone, binding proteins
cannot move across the cell membrane; as a re-
sult, association with the binding protein reduces
the likelihood for testosterone interaction with
the intra-cellular nuclear AR. Binding to SHBG
effectively prevents the biological actions of tes-
tosterone; whereas, binding to albumin appears
to still allow for a large bioavailability of testos-
terone.
[31]
In addition to facilitating the transport
of the hydrophobic testosterone in the watery
environment of the blood, binding proteins reduce
the clearance of testosterone from the blood.
[29]
Testosterone cannot be stored in the cells that
produce it, which is in contrast to most peptide
hormones, so the association with binding pro-
teins can act as storage in the circulation. The
bound testosterone can then be released to be-
come free testosterone in order to enter the cell.
2.2 Actions on the Muscle
As mentioned in section 2, testosterone is a
potent anabolic hormone that stimulates muscle
protein synthesis
[13,15]
and intramuscular amino
acid uptake,
[32]
resulting in improved net protein
balance.
[33]
1040 Vingren et al.
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
2.2.1 Effect on Androgen Receptor
Testosterone increases the AR in muscle cells
and associated myonuclei and satellite cells.
[33-36]
The precise mechanism for this upregulation is not
fully understood, but it is known that androgens
increase the half-life of AR in cell culture suggest-
ing a potential mechanism.
[37,38]
Several in vivo
studies have shown that AR content is upregulated
acutely by administration of pharmacological var-
iants of testosterone in rats
[35,36]
and humans.
[39]
AR content continues to increase for several days
after which the increased concentration of AR is
maintained. It appears that after long-term conti-
nuous high circulating concentrations of testoster-
one from exogenous use, e.g. several months, the
AR content returns to baseline in men,
[33]
whereas,
cycling on and off exogenous testosterone, as many
athletes who use anabolic steroids do, leads to a
sustained long-term AR content increase in men.
[34]
2.2.2 Importance for Normal Muscle Development
and Maintenance
Testosterone is important for the development
and maintenance of muscle mass in males. In
boys, puberty is associated with increased circu-
lating testosterone concentrations and accrual of
muscle mass.
[40]
In contrast, sarcopenia (loss of
muscle mass) has been associated with the decline
in testosterone concentrations found with aging
in men.
[41-43]
In older men, the effects of sarcope-
nia on muscle mass and function can be reversed
by testosterone administration that returns cir-
culating testosterone concentrations to within
or near the normal physiological range.
[33]
Hypo-
gonadism resulting from surgery (orchiectomy)
or pharmacological testosterone deprivation ther-
apy (the latter is commonly used with prostate
cancer) also leads to reductions in muscle mass
and function in adult males.
[44-46]
The importance
of normal circulating concentrations of testos-
terone on muscle mass in women is less clear as a
reduction in testosterone generally does not occur
independently of reductions in other hormones
such as estrogens (e.g. with menopause).
[47]
De-
spite these limitations, testosterone appears to be
important for the maintenance of muscle mass in
women. In women with muscle mass reductions
resulting from hypopituitarism, testosterone ad-
ministration that returns free testosterone to a
normal concentration increased fat-free mass and
muscle cross-sectional area.
[48]
Similarly, combined
testosterone and estrogen administration to ooph-
orectomized women resulted in increased lean
mass; whereas, estrogen administration alone had
no effect on lean mass.
[49]
In addition to these
controlled clinical trials, there is substantial, yet
anecdotal, evidence that exogenous supraphy-
siological doses of testosterone, as those used by
some women body builders, have a very potent
effect on muscle mass accretion in women.
In a series of experiments, Mauras and col-
leagues
[15,50,51]
examined the effects of testoster-
one on muscle protein synthesis and accretion
in young men and prepubertal boys. Combined,
these studies show that testosterone is vital for
the development and maintenance of muscle
mass via testosterone’s stimulation of whole body
protein synthesis and inhibition of proteolysis
resulting in a net anabolic effect. In healthy pre-
pubertal boys, acute testosterone administration
increased protein synthesis, as measured by non-
oxidative leucine disappearance as well as protein
proteolysis, with an overall improvement in leucine
and presumably protein balance.
[50]
In growth hor-
mone (GH)-deficient prepubetal boys, testoster-
one reduced protein oxidation, as measured by
leucine oxidation, but did not alter measures of
protein synthesis; however, when 22-kD GH and
testosterone were administered together, marked
increases in protein synthesis were observed.
[51]
The authors concluded that a minimum concen-
tration of GH was needed for the actions of tes-
tosterone; consequently, they suggested that GH
had a permissive or synergistic effect on testoster-
one’s promotion of protein synthesis. In accordance
with the findings on testosterone administration,
10 weeks of administration of a GnRH analogue to
young men (resulting in very low circulating testos-
terone concentrations) caused marked decreases in
the rates of whole-body protein turnover and pro-
tein synthesis.
[15]
These reductions were manifested
in decreased fat-free mass and muscle strength sup-
porting the crucial role of testosterone in the main-
tenance of muscle mass and function in men.
Testosterone also has a stimulating effect on
the production of other anabolic hormones. In
Testosterone and Resistance Exercise 1041
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
healthy, short-stature, prepubertal boys (Tanner
stage 1), testosterone administration led to in-
creases in circulating immunoreactive GH con-
centrations.
[50]
In GH-deficient prepubetal boys,
testosterone administration increased circulat-
ing insulin-like growth factor (IGF)-I, although
testosterone and 22-kD GH administered together
caused an even greater increase in IGF-I.
[51]
Based
on these findings, testosterone and 22-kD GH
appear to have a synergistic effect on IGF-I re-
lease, although the effect of 22-kD GH alone was
not examined. In mildly hypogonadal older men,
testosterone treatment increased muscle IGF-I
protein expression,
[33]
and in young men pharma-
cological testosterone deprivation reduced IGF-I
messenger RNA (mRNA) expression (the nuclear-
derived signal for IGF-I protein production at
the ribosome) in muscle despite no changes in
circulating immunoreactive GH and IGF-I con-
centrations.
[15]
Furthermore, cell cultures incubated
with testosterone upregulate IGF-I mRNA ex-
pression in a dose-dependent manner.
[52]
Combin-
ed, these findings suggest that testosterone is re-
quired for muscle IGF-I production, and that this
is a direct effect of testosterone independent of
circulating immunoreactive growth hormone and
IGF-I concentrations. However, a synergistic effect
of testosterone and 22-kD GH on muscle IGF-I
appears to exist. The recent identification of an-
drogen response elements in the IGF-I upstream
promoter region
[52]
provides further support for
the importance of testosterone in muscle IGF-I
production. Since IGF-I is also a potent anabolic
hormone that directly increases anabolic gene
transcription via the AKT/mammalian target of
rapamycin (mTOR) pathway,
[53]
this influence of
testosterone on muscle IGF-I production provides
an additional mechanism by which testosterone can
increase muscle protein synthesis and accretion.
3. Testosterone Response to Resistance
Exercise and Training
The acute endocrine response to a bout of re-
sistance exercise includes increased secretion of
various catabolic (breakdown-related) and ana-
bolic (growth-related) hormones. One of the pri-
mary anabolic hormones released in response to
resistance exercise is testosterone; in fact, testos-
terone is believed to be the major promoter of
muscle growth and subsequent increase in muscle
strength in response to resistance training in men.
In general, total testosterone and free testosterone
are elevated directly following heavy resistance exer-
cise in men, whereas, findings on the testosterone
response to a bout of heavy resistance exercise in
women are equivocal with both increases
[54,55]
and
no changes observed.
[56-58]
The endocrine response
for the days following resistance exercise is unclear.
Ha
¨kkinen and Pakarinen
[59]
found a decrease of
both total testosterone and free testosterone in men
for the first 2 days following heavy squats (10 sets
of 10 repetitions at 70%of 1-repetition maxi-
mum [1RM] or 20 sets of 1 repetition with 100%of
1RM), whereas, Koziris and colleagues
[60]
found no
difference in total testosterone for the same time-
points following whole-body circuit resistance ex-
ercise using universal gym machines (3 circuits of
upper- and lower-body exercises with a 5RM load).
This difference in findings could be due to the dif-
ferent exercise protocols used in the two studies and
would suggest that the testosterone response for the
days following resistance exercise is also specific to
theresistanceexerciseprotocolused.Theprotocol
used by Ha
¨kkinen and Pakarinen,
[59]
especially the
10 sets of 10 repetitions, involved substantially more
volume than the protocol used by Koziris et al.
[60]
Accordingly, the extent to which testosterone is
acutely affected by resistance exercise largely de-
pends on the selection among the acute programme
variable domains for the exercise session.
Several of the acute programme variable do-
mains interact with each other, so to investigate
the effect of one variable domain on the testos-
terone response to resistance exercise other vari-
able domains must often be manipulated. To re-
duce redundancy, studies in which this occurs will
mainly be examined once and not repeated in
sections for the other variable domains.
3.1 Men
In general, circulating total testosterone and
free testosterone increase immediately after a bout
of heavy resistance exercise in men and return to,
or below, baseline within 30 minutes;
[12,27,56,61-67]
1042 Vingren et al.
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
however, the appearance and magnitude of these
testosterone increases are greatly influenced by
the selection among the ‘acute programme vari-
able domains’ (intensity, number of sets, choice
of exercise, order of exercise and rest period dura-
tion) for the exercise session.
3.1.1 Intensity
Intensity refers to the load or resistance used
for a given exercise. There appears to be a rela-
tive intensity and volume threshold (total work
performed; see section 3.1.3 below) that must be
reachedinordertoinducea testosterone response.
Comparing protocols with the same volume but
different loads (4 sets of 6 repetitions at 52.5%of
1RM vs 3 sets of 6 repetitions at 40%of 1RM
during concentric actions and 100%of 1RM dur-
ing eccentric actions) for the bench press and squat
exercises, Yarrow et al.
[68]
found that neither pro-
tocol produced an increase in testosterone. The
intensity used in that study, with the exception of
the eccentric action, was very low and this likely
explains the lack of a testosterone response.
Kraemer et al.
[61]
examined the effect of altering
the intensity while keeping total work constant and
found that when intensity was reduced, the testos-
terone response was attenuated. When the number
of repetitions is kept constant, higher intensity and
thus higher volume induces a greater testosterone
response. Raastad et al.
[69]
showed that 3 sets of 6
repetitions for three lower-body exercises at 100%of
6RM but not at 70–76%of 6RM induced a signif-
icant increase in testosterone. Similarly, 5 sets of 10
repetitions with 10RM has been found to induce a
significant testosterone increase; whereas, 5 sets of
10 repetitions with either 70%or 40%of 10RM did
not affect testosterone concentrations.
[56]
The findings on the effect of high relative in-
tensity alone on the testosterone response are
equivocal with both increases
[70]
and no changes
found post-exercise.
[59,64]
Ten sets of 1RM in re-
sistance trained men resulted in a significant acute
increase in circulating testosterone;
[70]
however,
20 sets of 1RM in elite strength athletes did not
induce an increase in testosterone.
[59]
Although
speculative, the difference in findings could be
attributed to the difference in rest periods (2 and
3 minutes, for the 10- and 20-set protocols, re-
spectively) or the training level of the participants.
In accordance with the findings by Ha
¨kkinen
and Pakarinen
[59]
high relative intensity and low-
moderate total work protocols (2, 4 or 6 sets of
5 repetitions with 80–88%of 1RM) did not induce
a testosterone response.
[64]
In general, it appears
that high relative intensity alone is not sufficient
to induce a testosterone response if the total volume
of the protocol is low; however, a relative inten-
sity minimum threshold must be met, even with a
high volume, to induce a testosterone response.
3.1.2 Number of Sets
This variable refers to the number of sets per-
formed for each exercise in a resistance exercise
session. When total volume is held constant,
the number of sets does not appear to influence
the acute testosterone response to resistance ex-
ercise.
[61,71]
Goto et al.
[71]
examined the effect of
adding a 30-second rest period in the middle of
each 10-repetition set. This added rest period es-
sentially produced double the number of sets with
half the repetitions but similar volume. Despite a
lower metabolic demand (i.e. attenuated lactate
response) the addition of the rest did not result in
differences in the testosterone response. When
changing the load while keeping volume constant,
(and thus changing the number of sets) Kraemer
et al.
[61]
found that no alterations in the resistance
exercise-induced testosterone concentrations oc-
curred. Similarly, 16 weeks of resistance training
with all sets to either failure or not to failure, but
the same volume and intensity (thus adding sets),
did not alter resting testosterone; however, an
increase in resting testosterone was found after
11 weeks.
[72]
It is difficult to ascertain the reason for
this transient difference on the resting testoster-
one concentration, but it does suggest that subtle
differences in adaptations can occur when sets are
manipulated while keeping load and volume con-
stant. It is possible that the high stress from per-
forming each set to failure, which prevented a
training-induced reduction in resting cortisol, led
to a state of overreaching or mild overtraining
and thus prevented a transient anabolic adaptation
manifested in elevated testosterone concentra-
tions. This possibility is supported by the finding
that IGF-I concentrations were reduced with the
Testosterone and Resistance Exercise 1043
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
sets to failure condition, although performance
did not appear to be affected in this group.
3.1.3 Volume
Volume refers to the total work performed and
is often used in the context of resistance exercise
to mean (set ·number of repetitions ·intensity).
Using this definition, volume is a function of
several different acute programme variable do-
mains and is therefore not considered an indepen-
dent acute programme variable domain. However,
manipulating volume by changing several of its
constituents can significantly affect the hormonal
response; this potent effect of volume warrants its
inclusion in this review. There appears to be a
threshold of volume or metabolic demand that
must be reached before increases in testosterone
are observed. Ratamess et al.
[66]
showed that 6 sets,
but not 1 set, of 10 repetition squats significantly
increased total testosterone post-exercise. The
metabolic demand of the 1-set protocol was rela-
tively low, manifested by an only modest increase
in lactate; whereas the 6 sets produced a large
increase in lactate, suggesting a high metabolic
demand. The requirement for a high metabolic
demand and not just high intensity for an in-
crease in testosterone post-exercise was shown by
Ha
¨kkinen and Pakarinen.
[59]
Twenty sets of 1RM
resulted in no change in testosterone, whereas
10 sets of 10RM resulted in a large increase in free
and total testosterone. The lactate response was
modest (~4 mmol/L) with the high-intensity pro-
tocol but substantially larger (~15 mmol/L) with
the high volume protocol supporting the hy-
pothesis that a large metabolic demand is needed
to induce a testosterone response. Furthermore,
an examination of various combinations of sets
and repetitions found that, in general, a higher
volume created a greater testosterone response.
[64]
In that study,
[64]
the threshold for a testoster-
one response appeared to be based more on
metabolic demand than on volume per se; how-
ever, the study did not attempt to establish this
threshold.
3.1.4 Choice of Exercise
Choice of exercise refers to the specific exercise
chosen (e.g. power clean), the equipment used
(e.g. machine or free weight), and how the ex-
ercises are performed (e.g. type of muscle action,
velocity of movement). One of the major deter-
minants for the occurrence of a testosterone in-
crease with resistance exercise is the muscle mass
used. Involvement of a small muscle mass, even
when exercised vigorously, does not elevate tes-
tosterone above resting concentrations.
[73]
Ex-
ercise selection, therefore, significantly influences
the testosterone response to a resistance exercise
session. Bilateral knee extension alone
[74]
or the
combination of unilateral knee extension and leg
press
[75]
performed with a 5–10RM load does not
induce a testosterone response. Similarly, uni-
lateral biceps curls alone do not induce a testos-
terone response, but the addition of bilateral knee
extensions and leg press to the biceps curl protocol
results in a significant testosterone response.
[76]
When resistance exercise induces an increase in
testosterone, the magnitude of that increase is
also affected by muscle mass involvement; a jump
squat protocol increases testosterone concentra-
tion more than a bench press protocol performed
by the same participants (15%vs 7%for the jump
squat and bench press, respectively).
[77]
Similarly,
exercises such as the squat
[27,66,78]
and Olympic
lifts,
[79]
that involve a large muscle mass, produce
larger elevations in testosterone compared with
smallermusclemassexercises.
[76,80,81]
Larger muscle
mass involvement allows for greater total volume,
which helps to explain the importance of muscle
mass involvement in inducing a testosterone res-
ponse to resistance exercise. As described in sec-
tion 3.1.3, the total volume of work has important
implications for the appearance and magnitude
of the testosterone response to resistance exercise.
The effect of exercise modality (free-weight or
machine exercises) on the testosterone response
does not appear to have been investigated directly,
but both modalities can produce substantial in-
creases in testosterone when a high load and
volume is used.
Only a few studies have investigated the effect
of modes of muscle contraction on the acute tes-
tosterone response to resistance exercise.
[80,82,83]
When the same relative intensity is used, there
does not appear to be a difference in the testos-
terone response between concentric and eccentric
1044 Vingren et al.
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
exercises.
[80]
Durand et al.
[82]
found that con-
centric and eccentric exercise protocols using the
same absolute intensity produced an increase in
testosterone with no difference between modes
of contraction. Despite the lack of a significant
difference between modes of contraction, the
concentric condition produced almost twice as
large an increase in testosterone compared with
the eccentric condition, suggesting that mode of
contraction can affect the testosterone response
to resistance exercise.
[82]
When the same relative
load is used, free testosterone increases similarly
following concentric and eccentric muscle action
resistance exercise.
[83]
It seems likely that the po-
tential difference in the testosterone response
between modes of contraction using the same
absolute load, as presented by Durand and col-
leagues,
[82]
might be because the maximal force
capability is higher for eccentric muscle actions
than for concentric muscle actions
[84]
and as a con-
sequence, the relative intensity was lower during
the eccentric exercises.
In recent years, whole-body vibration (WBV)
has resurfaced as an alternative mode of resis-
tance training. The hormonal response to WBV
has been examined by a few studies with both no
effects
[85-87]
and elevations found for testoster-
one.
[88]
Ten sets of 1-minute isometric half squats
during WBV did not affect salivary testosterone
concentrations;
[85]
similarly, neither 25 minutes
of standing WBV
[87]
nor 6 sets of 8 repetitions of
unloaded squat (30-second per set) during WBV
affected circulating testosterone concentra-
tions.
[86]
Adding WBV to a protocol consisting
of 6 sets of 8RM squats did not affect the post-
exercise increase in testosterone compared with
the squat protocol alone; furthermore, this res-
ponse was not altered by 9 weeks of training using
WBV and squats.
[86]
In contrast to these findings,
Bosco and colleagues
[88]
found that 10 sets of
1-minute isometric squats during WBV signif-
icantly increased circulating testosterone, al-
though the increase was only modest (1.6 nmol/L,
equal to ~7%). It appears that WBV has no or
only a limited effect on testosterone. More re-
search is needed to firmly establish the effects
of WBV on the acute testosterone response to
exercise.
3.1.5 Order of Exercise
The order of exercise refers to the sequence of
exercises within an exercise session; this order
affects the power output and the number of repeti-
tions that can be completed for each exercise.
[89]
The order of exercise can also affect the timing
of the hormonal response to resistance exercise.
Large muscle mass exercises are needed to acutely
increase circulating testosterone concentrations
and as a result when large muscle mass exercises
are performed in the beginning of an exercise ses-
sion, the muscle used during subsequent exercises
will be perfused with an elevated testosterone con-
centration. The importance of elevated anabolic
hormones including testosterone was shown by
the finding that when the biceps is trained after
4 sets of leg press, it hypertrophied significantly
more compared with training of the biceps alone.
[76]
It remains to be determined if altering the order
of exercises while keeping the load and repeti-
tions constant, affects the post-exercise testos-
terone response.
3.1.6 Rest Period Duration
The duration of rest periods refers to the time
(minutes or seconds) between each set and each
exercise. Rest period duration can substantially
affect the metabolic demand of a bout of resistance
exercise as evident by the lactate response
[61]
and
the average oxygen consumption
[90]
for the ses-
sion. It is well established that increased meta-
bolic demands augment the response of certain
other hormones, such as immunoreactive GH,
[61]
yet this effect has not been shown for testoster-
one. Only a single study appears to have isolated
the effect of rest period duration on the testos-
terone response to resistance exercise. That study
observed that only in the context of moderate
loads (10RM) with high volume (~60 000 J) did
short rest (1 minute) result in a significantly larger
testosterone response compared with longer rest
(3 minutes).
[61]
Ahtiainen and colleagues
[91]
reported
no effect of rest period duration (2 vs 5 minutes)
on the testosterone response to resistance ex-
ercise; however, the protocols used for each rest
period duration condition differed slightly in the
load and sets used making direct comparisons dif-
ficult. It appears that with different combinations
Testosterone and Resistance Exercise 1045
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
of load and volume, rest period can affect the
acute resistance exercise-induced testosterone
response. Synergistic integration among resis-
tance, rest and volume therefore likely exists, but
the magnitude of each required for the different
testosterone response patterns remains to be de-
termined.
3.2 Women
The biological mechanisms for a potential ex-
ercise-induced increase in testosterone might be
different in women compared with men. Women
do not have Leydig cells and Kvorning et al.
[12]
have shown that the Leydig cells are likely in-
volved in the acute resistance exercise-induced
increase in testosterone in men. An increase in
free or total testosterone for women has been
found in some studies
[54,55,62,92]
but not all stud-
ies.
[56,58,93]
One might speculate that such equi-
vocal findings are due to differences in the selections
within each acute programme variable domain;
however, this has not been substantiated.
Only a few studies have directly examined the
effect of specific acute programme variable do-
mains on the testosterone response to resistance ex-
ercise in women; however, these studies have found
no acute elevation in testosterone post-exercise.
Linnamo et al.
[56]
demonstrated no changes in
total testosterone following 5 sets of 10 repeti-
tions each of sit-ups, bench press and leg press
using three different loading conditions: maximal
(10RM), submaximal (70%of 10RM) and explosive
(40%of 10RM). In men, the same maximal load
condition led to a significant increase in total
testosterone.
[56]
Similarly, Kraemer et al.
[58]
showed
that with heavy resistance exercise altering rest
period duration or load while keeping total volume
constant did not result in post-exercise testoster-
one concentrations above baseline in women.
Although no acute changes following exercise
were found, the simultaneous manipulation within
several of the acute programme variable domains
has been shown to affect resting total testosterone
following long-term resistance training in women.
[93]
A low-volume, single-set circuit programme pro-
duced only a modest increase in resting testos-
terone after 12 weeks, but resting testosterone
returned to baseline at 24 weeks of training. In
contrast, a periodized high-volume, multiple-set
programme produced a large increase in resting
testosterone at 12 weeks and an even larger in-
crease at 24 weeks of training. Thus, the train-
ing programme design significantly affected the
magnitude and sustainability of the increase in
resting testosterone concentration.
It has been reported that in men a GnRH
analogue (goserelin), which suppresses circulat-
ing LH and thus Leydig cell function resulting in
castrate concentrations of testosterone, prevents
an acute resistance exercise-induced increase in
total and free testosterone.
[12]
Thus, it appears
that the Leydig cells are responsible for acute
increases in testosterone following resistance ex-
ercise, and this would explain the lack of con-
sistent findings for the testosterone response to
resistance exercise in women. The acute increase
in testosterone, especially free testosterone, fol-
lowing resistance exercise reported in some stud-
ies could originate as a byproduct of cortisol
production. Adrenocorticotropic hormone, which
stimulates production and release of cortisol, also
causes release of testosterone from the adrenal
cortex.
[94]
Adrenocorticotropic hormone concen-
trations increase in response to heavy resistance
exercise,
[95]
which could lead to a greater adrenal
production and release of testosterone. Con-
sidering that free testosterone is a very small part
of total testosterone (0.5–2%), a small increase in
free testosterone might not be detectable in total
testosterone concentration analysed using standard
enzymatic procedures. None of the studies that
showed an increase in testosterone included mea-
surements of the adrenocorticotropic hormone
response to resistance exercise, and only one study
included measurements of cortisol; Copeland
et al.
[55]
found that both testosterone and cortisol
were elevated compared with control following
resistance exercise. Alternatively, the resistance
exercise-induced increases in testosterone could
simply be due to a reduction in plasma volume,
which could cause an increase in circulating tes-
tosterone concentration without a change in the
amount of testosterone in the circulation. It is
also possible that statistical limitations due to the
relatively low number of subjects in some of these
1046 Vingren et al.
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
studies might negate findings of significant in-
creases due to the potential variance involved in
women’s response patterns.
3.3 Effect of Age
Age significantly affects circulating testosterone
concentration. Children have low concentrations
of testosterone until puberty when testosterone
increases markedly in boys and to a minor extent
in girls.
[96]
Aging beyond 35–40 years is asso-
ciated with a 1–3%decline per year in circulating
testosterone concentration (1.6%in total and
2–3%in bioavailable testosterone) in men.
[97]
This reduction can eventually lead to very low
resting concentrations of circulating testosterone,
a condition that has been termed andropause.
[98]
In women, circulating testosterone concentrations
also gradually decline until menopause after which a
60%reduction is found within 2–5 years.
[47]
The testosterone response to resistance exercise
is also greatly affected by age. Boys do not ex-
perience an acute increase in testosterone in res-
ponse to resistance exercise; even after the onset
of puberty when resting testosterone is increased
in boys, they appear to experience no or only a minor
resistance exercise-induced increase in testoster-
one.
[63,99]
Following the same resistance exercise
session, testosterone increased in college-aged men
but not in high school-aged young men.
[100]
Sim-
ilarly, Pullinen et al.
[63,99]
showed that in con-
trast to resistance-trained men, there was no or
only a minor increase in testosterone following
resistance exercise in 14- and 15-year-old boys,
respectively, who had been engaged in resistance
training for at least 1 year. This lack of exercise-
induced increase in testosterone in boys existed
even though there was no difference in resting
testosterone concentrations between the men and
boys.
[63,99]
Although speculative, the reason for
this limited testosterone response to resistance
exercise in teenage boys might be due to an in-
ability of the testis to quickly increase testoster-
one release or a lack of sufficient metabolic
stimulus (volume) from the exercise session based
on the relatively low maximal strength in this pop-
ulation. This notion is supported by the finding
that junior weightlifters (14–18 years of age) with
more than 2 years of weight-lifting experience
produce a greater acute testosterone response
than those with less than 2 years of experience.
[79]
In older (‡59 years)
[27,62,78,101]
and middle-aged
(38–53 years)
[62,81,101]
men a bout of resistance
exercise can elicit a significant elevation in cir-
culating total and free testosterone, but the mag-
nitude of this elevation is generally smaller
compared with that in younger (20–30 years)
men.
[27,78,81,101]
This attenuated exercise-induced
increase is especially apparent for free testoster-
one. The discrepancy between findings for free
testosterone and total testosterone could be due
to the increased concentrations of SHBG and
reduced concentrations of albumin found with
aging.
[102,103]
The findings for training effects on
the acute testosterone response to resistance exer-
cise in older men are equivocal with both no ef-
fects and augmented responses found. A 10-week
periodized strength-power training programme
led to increased pre-exercise free testosterone
and post-exercise total testosterone concentra-
tions in ~60-year-old men with no changes found
for ~30-year-old men undergoing the same train-
ing programme.
[78]
In contrast, Ha
¨kkinen and
colleagues
[62]
found no changes in the acute pre-
or post-resistance exercise testosterone response
following 6 months of strength training in older
(~70 years old) and middle-aged (~40 years old)
men. Both studies,
[62,78]
however, found that there
were no changes in testosterone concentrations
of older men at rest (i.e. not immediately pre-
exercise) after the resistance training period. It is
difficult to speculate on the cause of the dis-
crepancy in the findings for the acute testosterone
response to resistance exercise, but it is possible
that an anticipatory response was present fol-
lowing training in the study by Kraemer et al.
[78]
In middle-aged (~40-year-old) and older (~60-
to 70-year-old) women who are untrained, total
and free testosterone do not change acutely
in response to a high (5 sets of 10RM in the
leg press)
[62,104]
or moderate (1 set of 13 exer-
cises at 80%of 1RM)
[105]
volume resistance ex-
ercise session. Long-term strength training does
not appear to change resting total and free testos-
terone
[62,104-107]
or post-exercise total testoster-
one concentrations in response to high
[62,104]
or
Testosterone and Resistance Exercise 1047
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
moderate volume.
[105]
One study, however, found
that in recreationally trained 19- to 69-year-old
women, total testosterone increased acutely fol-
lowing a high-volume (3 sets of 8 exercise at
10RM and 1 minute rest between sets) resistance
exercise session and that this increase was not
affected by age.
[55]
Findings on the effect of train-
ing on the acute free testosterone response to re-
sistance exercise in aging women are equivocal.
In both middle-aged and older women, an acute
increase in free testosterone following resistance
exercise (5 sets of 10RM in the leg press) after
6 months of resistance training has been observ-
ed.
[62]
A different study by the same authors
[104]
using similar older female populations and the
almost identical acute resistance exercise protocol,
(2 minutes instead of 3 minutes of rest between
sets) found that 21 weeks of strength training did
not change the acute free testosterone concen-
trations following a bout of resistance exercise.
Based on these findings, it appears that the tes-
tosterone response to resistance exercise and train-
ing in aging women is similar to that for younger
women. In both younger and older women, re-
sistance exercise can induce an acute increase in
circulating testosterone; however, the selection
among the acute programme variable domains
required for this increase to occur has not yet
been fully determined.
3.4 Effect on Androgen Receptor
Only a limited number of studies have exam-
ined the acute AR response to a bout of resistance
exercise in men;
[12,65-67,74,92,108]
only one study
appears to have been conducted in women.
[92]
From the studies in men combined with the
findings from animal research,
[109,110]
it appears
that the AR concentration is initially reduced
acutely following a bout of resistance exercise,
but that AR is upregulated during the later stages
(several hours after exercise) of recovery from
resistance exercise. The timeline for this AR
down- and upregulation has not been fully eluci-
dated. Ratamess et al.
[66]
and Vingren et al.
[92]
found that in young resistance-trained men 6
sets of 10 repetitions in the squat exercise with
2 minutes of rest between sets resulted in a sig-
nificant decline in AR 1-hour post-exercise. Sim-
ilarly, Lee et al.,
[35]
using a male rat model, found
that overload ablation caused a decrease in AR
24-hours post-overload introduction. In contrast
to these findings, Kraemer and colleagues,
[67]
using a similar population to Ratamess et al.
[66]
and Vingren et al.
[92]
but a slightly different re-
sistance exercise protocol (4 sets of 10 repetitions
of squat, bench press and shoulder press and row
with 2 minutes of rest between sets), found that
AR increased 1-hour post-exercise when subjects
ingested either water or a carbohydrate-protein
drink immediately after exercise. The increase in
AR was much greater with the carbohydrate-
protein drink compared with the water ingestion
condition suggesting a potent effect of nutrition
on the AR response to resistance exercise.
[67]
The
differences in AR expression between the studies
in the fasted conditions (water) were observed
despite similar testosterone responses and involve-
ment of the muscle sampled for AR. This indicates
that other variables such as time from onset of
exercise or testosterone exposure might affect the
AR response. Finally, Spiering et al.
[74]
recently
found that in untrained men, AR was upregulated
3 hours post-resistance exercise only when the
exercise bout produced an increase in circulating
testosterone. Although not considered resistance
exercise, it is also worth noting that strenuous
swimming has been shown to upregulate AR
acutely (within hours) following exercise.
[111]
Combined, these studies suggest that after an in-
itial reduction in AR following exercise, an acute
upregulation of AR in the hours following a bout
of resistance exercise in men occur, although the
timeline for the events in this response is uncertain.
The only finding for women suggest that the AR
response is similar among men and women ex-
cept that the initial reduction in AR is present
10-minutes post-exercise and AR returns to base-
line by 70-minutes post-exercise.
[92]
Findings for AR during the later stages of re-
covery from resistance exercise are more consistent.
Forty eight hours following a bout of resistance
training AR mRNA is upregulated.
[65,108]
How-
ever, Willoughby and Taylor
[65]
did not find an
increase in AR protein content until 48 hours
after two consecutive resistance exercise sessions
1048 Vingren et al.
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
separated by 48 hours. In animal models, elec-
trical stimulation
[110,112]
and overload ablation
[109]
result in an acute upregulation of AR during the
later stages of recovery (several days after the initial
overload stimulus). Collectively, these studies
suggest that the acute AR response to resistance
exercise includes a stabilization phase followed
by an acute initial downregulation after which an
upregulation of AR to above baseline concentra-
tions occur. Despite the few studies on the acute
AR response to resistance exercise, it appears
that factors such as exercise volume and nutrient
intake affect this response. Ratamess et al.
[66]
showed that a single set of 10 repetitions in the
squat exercise did not alter AR 1-hour post-exercise.
This was mirrored by limited changes in circu-
lating lactate and hormonal concentrations sug-
gesting that a minimum of volume is needed to
induce AR changes in response to resistance ex-
ercise. Post-exercise ingestion of a drink contain-
ing protein and carbohydrate led to an increase in
AR 1-hour post-exercise with or without L-carnitine
supplementation.
[67]
Interestingly, it has also
been demonstrated that when a protein and/or
carbohydrate drink is ingested before or after
resistance exercise, the increase in testosterone
is attenuated during exercise, and the reduc-
tion in testosterone during recovery is augmented
compared with a placebo condition.
[67,113,114]
The
authors of these studies suggested that increased
testosterone uptake by the AR might account for
this attenuated testosterone response.
4. Conclusions
As a hormone, circulating testosterone sig-
nalling resides within a multivariate system of
anabolic signals for many different target tissues
through the body, and the exact role of testos-
terone in the temporal timeframes of a resistance
training programme are hard to pinpoint. Yet,
dismissal of its anabolic role in the human body
due to a lack of a simple correlation or compar-
ison of punctual circulating testosterone con-
centrations with variables that have accumulated
over time with training (e.g. muscle size, strength)
is over-simplistic at best and understates the im-
portance of this hormone to the physiology of
adaptational mechanisms in the human body to
exercise stressors. The interaction of testosterone
with a host of receptors on different tissues and
the resulting signalling processes are vital to human
health and performance. The increase in testos-
terone found in men is important for the resis-
tance exercise-induced adaptations. The importance
of testosterone for adaptations to resistance ex-
ercise in women has not been substantially
examined, but it appears that testosterone plays
only a minor role.
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this review. The authors have no potential conflicts of
interest that are directly relevant to the content of this review.
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Correspondence: Dr William J. Kraemer, Human Perfor-
mance Laboratory, Department of Kinesiology, 2095
Hillside Road, Unit-1110, University of Connecticut,
Storrs, CT 06269-1110, USA.
E-mail: william.kraemer@uconn.edu
Testosterone and Resistance Exercise 1053
ª2010 Adis Data Information BV. All rights reserved. Sports Med 2010; 40 (12)
