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Are Acute Post-Resistance Exercise Increases in Testosterone, Growth Hormone, and IGF-1 Necessary to Stimulate Skeletal Muscle Anabolism and Hypertrophy?

  • KITE Research Institute
Contrasting Perspectives in Exercise Science & Sports Medicine
Are Acute Post–Resistance Exercise
Increases in Testosterone, Growth Hormone,
and IGF-1 Necessary to Stimulate Skeletal
Muscle Anabolism and Hypertrophy?
Acute post–resistance exercise (RE) increases in an-
abolic hormones may not be ‘‘necessary’’ to stimulate
skeletal muscle anabolism and hypertrophy; however, as
we will support in the following discussion, post-RE
increases in these hormones are ‘‘optimal’’ for maxi-
mizing skeletal muscle anabolism and hypertrophy. For
purposes of this presentation, increases in testosterone
(T) and growth hormone (GH) will also imply increases
in insulinlike growth factor 1 (IGF-1) (22,24). Further-
more, we will limit the discussion of these adaptations to
men, while recognizing that training variables such as
training history, mode, intensity, volume, and rest inter-
val (RI) length in between sets will have compelling
influence on the hormonal responses to RE.
Studies examining the influence of acute RE-induced
T and GH responses on skeletal muscle anabolism have
included both trained and untrained young (18–30 yr)
and older (60–80 yr) men. Regardless of trained state or
age, substantial evidence indicates RE protocols and
short-term resistance training (RT) using two to four
sets, 8–15 repetition maximum (RM), e2-min RI, and
RE that activates large muscle masses (i.e., multijoint
movements) elicit the greatest acute elevations in T and
GH (1,2,6,14,21,23,24,26,27,33,35,42). Further, recent
evidence suggests strength RE protocols and short-term
RT prescribed using 1) two to eight sets, 3–6 RM, e90-s
RI, with multijoint movements (42); or 2) five sets, 3–5 RM,
3-min RI, followed by an additional set of a 25–35 RM,
after a 30-s RI (13,14) elicit significant elevations in T
and GH. Therefore, there is strong evidence that RE can
result in substantial postexercise elevations in anabolic
hormones. So the question posed is, ‘‘Do these acute RE-
induced elevations in T and GH translate into skeletal
muscle anabolism and hypertrophy?’
A pervasive view in the area of endocrine responses to
resistance exercise is that acute postexercise hormonal
responses of testosterone, growth hormone (GH), and
insulinlike growth factor 1 (IGF-1) are critical for sub-
sequent skeletal muscle anabolism. If this is the case,
then exercise regimes can be manipulated to enhance
hormonal responses and thus enhance skeletal muscle ad-
aptations such as strength and muscle mass gain. Despite
this alluring prospect, we contend that postexercise in-
creases in testosterone, GH, and IGF-1 are not necessary to
stimulate skeletal muscle anabolism and hypertrophy and
that measurement of the responses of these hormones
yields little in the way of insight into longer-term resis-
tance training-related adaptation.
Despite the prevalent view (25) that exercise-induced
hormones regulate hypertrophy, there is a surprising lack
of direct supporting evidence for this assertion. In fact,
Wilkinson et al. (48) observed significant gains in strength
and hypertrophy in the absence of any measurable changes
in free testosterone and IGF-1. More recently, we con-
ducted two studies (44,46) to directly examine whether
exercise-induced elevations in testosterone, GH, and
IGF-1 were necessary for or could enhance muscle
anabolism. We used a study design in which the elbow
flexors were exposed, postexercise, to either near-basal
hormone concentrations or high hormone concentra-
tions that were the result of an intense lower body
exercise routine. We used this ‘‘low and high’’ hormone
exposure model to examine the effects of postexercise
hormone concentrations on muscle anabolism acutely
(46) and chronically with resistance training (44). In both
studies, whey protein was provided postexercise to provide
substrate for any potential divergent anabolic responses
initiated by the low and high hormone environments
knowing that in the absence of postexercise nutrition,
positive net protein balance does not occur. In the low
hormone condition, myofibrillar protein synthesis was
elevated acutely, and gains in strength and hypertrophy
occurred after training, despite testosterone, GH, and
IGF-1 concentrations that were similar to basal levels.
Copyright Ó2013 by the American College of Sports Medicine
DOI: 10.1249/MSS.0000000000000147
Copyright © 2013 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
The following investigations incorporated dissimilar
methodologies but provide strong evidence in support of
the prevailing perspective. Three studies were selected
that used short-term RT interventions and examined the
influence of physiologically elevated acute hormonal
responses on human skeletal muscle (13,26). Two studies
were selected examining the effects of physiologically
elevated acute T on molecular mechanisms initiating skel-
etal muscle anabolism (35,49).
Kvorning et al. (26) investigated 22 recreationally
active, untrained men, 20–30 yr. The endogenous pro-
duction of T was suppressed by the use of a GnRH agonist
(goserelin) compared with a placebo group (unaltered
endogenous T levels). Both groups performed identical
8 wk of total body RT programs: 3 dIwk
training fre-
quency, sessions 1–8 (3–4 10 RM, 2-min RI), sessions
9–16 (3–4 6 RM, 3-min RI), and sessions 17–24(3–4
10 RM, 2-min RI). Two-thirds of the program was hy-
pertrophy training, designed to elicit acute elevations in
T and GH (24,27,42). Study participants in the placebo
group experienced significant acute elevations in T and
GH in response to at least 16 of the 24 total training
sessions, whereas those in the goserelin group did not
experience acute elevations of T in response to any of
the training sessions. The lean mass increases in the legs
were greater in the placebo group compared with the
goserelin group (PG0.05). Furthermore, the clinically
important increases in total body lean mass revealed a
strong trend (P= 0.07) toward statistically significant dif-
ferences between the two groups. These findings dem-
onstrate an implicit link between endogenous T, both
resting levels and the magnitude of acute responses to
RE, and the hypertrophic adaptation to short-term RT.
Goto et al. (13) evaluated 17 untrained men, 19–22 yr,
performing leg press and leg extension exercises
and compared the effects of a 4-wk periodized
combination-type RT program (5 3–5 RM; 3-min RI;
sixth set, 25–35 RM, after a 30-s RI after the fifth working
set) to a 4-wk periodized strength RT program (5 3–5
RM; 3-min RI), after a 6-wk periodized hypertrophic
RT program performed by all study participants (two rounds
of 3 10–15 RM, 30-s RI, 3-min rest in between rounds,
and 3- to 5-min rest in between exercises). Combination-
type RE induced significantly greater acute increases
in GH compared with strength RE (14). During the final
4-wk phase of training, CSA increased in response to
combination-type RT and decreased in response to
strength RT (P= 0.08 between groups). This evidence
suggests that muscle CSA may be augmented by en-
hancing the acute GH response through performance of a
single set of low-intensity, high-repetition exercise, im-
mediately after repeated sets of high-intensity, low-
repetition exercise, during short-term RT.
That is, postexercise increases in testosterone, GH, and
IGF-1 were not necessary to stimulate anabolic processes
(46), as we had reported previously (48). Furthermore,
when testosterone, GH, and IGF-1 were elevated post-
exercise, there was no enhancement of myofibrillar protein
synthesis acutely or gains in strength and hypertrophy
with training. Thus, our acute mechanistic findings (46)
mirrored what we observed in a chronic training study
(44). It can be noted here that muscle protein synthesis
is measured acutely because it is the primary determinant
of enhanced muscle protein anabolism that occurs after
resistance exercise and feeding (12). According to the
proposed and validated models of protein accretion (29),
the accumulation of repeated periods of enhanced protein
balance after exercise and dietary amino acid consump-
tion result in hypertrophy.
A study that was similar in design (31) to our previ-
ous work (44) reported contrasting findings that sug-
gested that exercise-induced elevations in endogenous
hormones underpinned superior adaptations in strength
and some measures of hypertrophy. Notwithstanding
methodological considerations (30), a proposed expla-
nation for the disparate findings between studies (31,44)
was that the exercise order in our study may have masked
a ‘‘hormonal enhancement’’ effect. Specifically, because
our participants trained their arms before their legs, it was
suggested that the lower body exercised muscles may
have ‘‘stolen’’ hormone-rich blood from the arm and
therefore impaired adaptation (31). Therefore, we recently
measured brachial artery blood flow and testosterone,
GH, and determined IGF-1 concentrations to estimate
hormone delivery to the elbow flexors when they were
trained before or after leg exercise (45). We found no
differences in the hormone delivery and thus no evi-
dence that the ostensibly anabolic properties were
compromised because of the lack of hormone delivery
due to exercise order.
Other lines of evidence fail to support the thesis that
exercise-induced testosterone, GH, and IGF-1 are im-
portant regulators of muscle anabolism. Our examina-
tion of associations of exercise-induced hormones and
gains in strength and hypertrophy in a large cohort showed
that hormone responses did not account for variance in
training adaptations in strength or hypertrophy (47). Fur-
thermore, divergent gains in strength and hypertrophy by
high responders and low responders were not explained
by their hormone response. In a proof-of-concept study
(43), we demonstrated that women, who exhibited a
45-fold lower postexercise testosterone response (after
accounting for È20-fold lower baseline testosterone),
elevated myofibrillar protein synthesis to a similar ex-
tent as men. That is, despite not having the ‘‘benefit’’ of
postexercise testosterone, women were able to generate a
robust elevation in rates of myofibrillar protein synthesis,
which should have been compromised if exercise-induced
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Copyright © 2013 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
In the third study, our laboratory recently com-
pleted an investigation of 22 recreationally active men,
64–72 yr (unpublished results). Participants performed
free weight– or machine-based total body RE protocols,
with a 3 dIwk
training frequency. We compared the
effects of an 8-wk periodized strength RT program using
short RI (SS) (2–3 4–6 RM; 60-s RI) to the same 8-wk
periodized strength RT program using extended RI (SL)
(2–3 4–6 RM; 4-min RI), after a 4-wk periodized
hypertrophic RT program performed by all study partici-
pants (2–4 8–15 RM; 60-s RI). Strength RE protocols
with short RI induced significantly greater acute in-
creases in T and GH compared with strength RE pro-
tocols with extended RI. Across the final 8-wk RT phase,
total body lean mass increases were greater in response
to SS compared with SL (PG0.05). This finding sug-
gests that lean mass gains are enhanced by acute eleva-
tions in T and GH through the use of short RI within
short-term strength RT.
Willoughby and Taylor (49) examined the effects of
acute increases in T across three sequential hypertrophic
RE bouts, separated by 48 h, on skeletal muscle androgen
receptor (AR) mRNA and protein expression as well as
myofibrillar protein content in nine young men (17–21 yr).
T was elevated after all three RE bouts (PG0.05).
AR mRNA and protein were elevated 48 h after bouts
2 and 3 (PG0.05) and correlated with acute RE-induced
increases in T immediately post-RE (PG0.05). Lastly,
myofibrillar protein content was elevated 48 h after bout 3
(PG0.05). These findings suggest that repeated exposure
to RE-induced increases in T mediates upregulation in
acute AR expression and subsequent increases in myo-
fibrillar protein, possibly because of enhanced ligand-
binding capacity and via the T-AR signaling pathway.
Spiering et al. (35) investigated six men, 22–30 yr.
All study participants performed a control RE protocol
(bilateral knee extensions, 5 5 RM, 90–95% 1RM,
3-min RI) and a high-T RE protocol (upper body pro-
tocol [4 10 RM, 80% 1RM, 2-min RI], immediately
preceding the same control RE protocol). Acute T re-
sponses were significantly greater with the high-T RE
protocol compared with the control RE protocol. Muscle
tissue analysis revealed only the high-T RE protocol po-
tentiates AR responses to acute RE. RE-induced acute ele-
vations in T prevented catabolism of muscle AR content
post-RE, via enhanced AR mRNA translation and in-
creased AR half-life. This evidence suggests RE prescription
that maximally elevates T will likely optimize hypertro-
phic adaptations to RT via enhanced T–AR interactions.
Investigations in men with prostate cancer receiving
androgen deprivation therapy (castrate T levels) and
testosterone was truly necessary to the postexercise ana-
bolic response. We view these data (29,43) as providing
further support of a paradigm in which mechanisms that
are intrinsic to the muscle itself and not dependent on
systemic exercise-induced hormonal elevations, are re-
sponsible for contraction-mediated hypertrophy.
Doessing et al. (9) demonstrated that exogenous GH
administration, which produces supraphysiological sys-
temic GH and IGF-1 concentrations, does not stimu-
late myofibrillar protein synthesis but rather stimulates
synthesis of collagen proteins. It is unknown whether
exercise-induced GH/IGF-1 could also be stimulating
collagen synthesis and thus strengthening connective
tissue, which might be advantageous in supporting a
bigger stronger muscle as the result of resistance training.
From a practical standpoint, in our studies of elbow
flexor hypertrophy, the high GH/IGF-1 condition did not
result in any difference in morphological (fiber or muscle
CSA) or functional measure (1 or 10 RM or isometric
strength) that we measured versus a low (Èbasal) GH/
IGF-1 condition. Therefore, if there was some unmea-
sured difference in the composition of the connective tis-
sue between conditions, it had no benefit to strength or
hypertrophy. We do know that exercise-induced GH
does not describe the training-induced phenotype. For
example, peak GH concentration and area under the
curve (AUC) are greater after cycling at 70% V
than after resistance exercise (11). On the basis of these
observations and studies by Doessing et al. (9), it is difficult
to envision a plausible mechanism by which transient
exercise-induced increments in GH or IGF-1 concentration
stimulates hypertrophy. In contrast to GH, exogenous tes-
tosterone is unequivocal in its ability to stimulate hypertro-
phy; however, in an exercise-induced environment, what
is the real anabolic potency of testosterone?
The anabolic properties of exogenously administered
testosterone (4) are frequently and broadly cited as a
rationale for the measurement of postexercise hormonal
profiles, which are interpreted as a proxy for the anabolic
potential of skeletal muscle. However, a crucial point is
that muscle mass accretion during exogenous testosterone
analog administration is related to cumulative androgen
exposure, which is the product of both dose and duration
(4). Figure 1 illustrates this point and why the applica-
tion from exogenous to endogenous testosterone is a
flawed comparison. Basically, the transient (È30 min)
nature of exercise-induced testosterone is inconsequential
compared with the sustained increases in testosterone with
exogenous dosing which represents a markedly higher
cumulative androgen dose and that results in muscle hy-
pertrophy (4). We do not claim to have tested all the
nuances of the endocrine response to resistance exercise.
For instance, the numerous isoforms of GH (25) alone
may always captivate speculation until they are each
investigated, but this is a straw argument if skeletal
http://www.acsm-msse.org2046 Official Journal of the American College of Sports Medicine
Copyright © 2013 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
participating in RT programs have demonstrated signifi-
cant improvements in muscle mass and strength; how-
ever, these gains are modest at best (10). Wilkinson et al.
(48) evaluated 10 men, 21–22 yr, performing an 8-wk RT
program, 3 dIwk
training frequency, with unilateral leg
press and knee extension (three sets, 6–10 RM, 80–90%
1RM, 3-min RI). The 8-wk RT program did not elicit
significant acute changes in T, GH, or IGF-1. CT scans
revealed significant increases in muscle CSA. These
findings suggest unilateral RE that does not induce sig-
nificant acute elevations in T, GH, or IGF-I may still
stimulate muscle hypertrophy. However, it is difficult to
determine whether this anabolic response is ‘‘optimal’
because we know that both RE and T supplementation
independently stimulate skeletal muscle hypertrophy and
that the combination of RE and T supplementation re-
sults in an even greater anabolic response (3,26).
Dismissal of the role of RE-induced elevations in ana-
bolic hormones to maximally stimulate skeletal muscle
anabolism and hypertrophy appreciably understates the
importance of these hormones to the physiological mecha-
nisms responsible for hypertrophic adaptations to RT. The
aforementioned studies supporting the prevailing pers-
pective demonstrate that acute endogenous increases in
anabolic hormones, as well as their influence on skeletal
muscle receptors and resulting hypertrophic response,
are critical to optimizing RE-induced adaptations and,
thus, health and performance across the lifespan.
Post-RE elevations in anabolic hormones may not be
‘necessary’’ to promote some degree of skeletal muscle
anabolism after an RT program, and a review of recent
literature suggests that the research is inconclusive as to
whether or not the post-RE anabolic hormonal response
plays a significant role in skeletal muscle hypertrophy
(32). We maintain that these elevations are critical to
optimizing hypertrophic and strength gains as part of an
integrative response to well-designed and applicable RE
stimuli, leading to chronic functional improvements in
skeletal muscle mass and force production.
Phillips et al. have proposed a unique ‘‘low and high’
hormone exposure model to study the influence of acute
changes in T, GH, and IGF-1 after RE and chronically
with RT (43,44); however, their model includes sup-
plementation with whey protein before and/or after RE
albeit in both the low and high hormone groups. We
contend that the inclusion of a protein supplement in this
study design is a major confounding factor because it is
well known that amino acids are potent hormone secre-
tagogues that inhibit muscle protein breakdown and
muscle receptors for all these isoforms do not also exist.
Similarly, although there are hundreds of resistance ex-
ercise program permutations, all of which could affect
hormonal responses, we propose that the divergent hor-
mone models that we used gave ample opportunity for
the highly complex hormonally mediated ‘‘anabolic’’
responses to be manifest in phenotypically superior ad-
aptations. What then are the implications of a theory that
is not underpinned by exercise-induced hormones? From
an applied standpoint, it means that exercise programs
do not need to be designed based on hormonal nuances.
It means that large muscle group exercises do not need to
be paired with small exercises for the purpose of cap-
turing ‘‘anabolic effects’’ derived from the hormonal re-
sponse. From a basic sciences standpoint, hypertrophy
that occurs with resistance training is mediated by in-
tramuscular intrinsic processes which, as opposed to
measuring systemic hormonal responses as being caus-
ative or influential in hypertrophy, are an area that we
view as requiring further investigation.
We demur with Schroeder and Villanueva’s assertion
of evidence that greater hormonal responses provide an
‘optimal’’ anabolic environment; of course, we do not
disagree with their initial concession that acute postresis-
tance exercise increases in anabolic hormones may not be
necessary to stimulate hypertrophy. This admission natu-
rally means that other nonhormonal mechanisms can
clearly dictate the entire hypertrophic response.
Schroeder and Villanueva begin by stating that ‘‘for
purposes of this presentation, increases in testosterone
FIGURE 1—A comparison of the effect of exogenous testos-
terone (200 mg testosterone enanthate) (8) versus a schematic of
the diurnal variation of testosterone throughout a given week,
and the contribution of a ‘‘testosterone-spike’’ after a workout
on day 4 to cumulative testosterone (inset shows testosterone
area under the curve [AUC] on day 4 in arbitrary units [AU]).
CONTRASTING PERSPECTIVES Medicine & Science in Sports & Exercise 2047
Copyright © 2013 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
stimulate muscle protein synthesis, modulating skeletal
muscle hypertrophy (20,28,41). The anabolic implica-
tions of protein supplementation are well documented
(7,50). Dillion et al. (7) demonstrated that older women
who have negligible circulating T and were not exposed
to RE received amino acid supplementation for 3 months
and had significant increases in basal muscle protein
synthesis and increases in lean body mass, demonstrat-
ing the potent influence of amino acid supplementation
on skeletal muscle anabolism, even in the absence of RE.
In fact, Phillips et al. reported similar findings in young
women with greater gains in muscle mass and strength
when consuming fat-free milk post-RE compared with
carbohydrates (19). Furthermore, the ingestion of casein
and whey proteins 1 h after an RE bout results in greater
muscle anabolism compared with the ingestion of a
placebo after RE (40). Therefore, it could be argued that
supplementation with protein in combination with an RE
model may mask potential enhanced effects mediated by
acute increases in anabolic hormones because of the
powerful influence of amino acids on molecular tran-
scription and translation processes involved in skeletal
muscle protein synthesis.
Sex-based comparisons of myofibrillar protein syn-
thesis after RE, with or without post-RE nutrient inges-
tion, emphasize two major concerns: 1) protein synthesis
measured after an acute bout of RE (46) does not always
occur in parallel with chronic upregulation of causative
myogenic signals (5) and 2) it is not necessarily predic-
tive of long-term hypertrophic responses to RT programs
(39). In addition, circulating T levels are approximately
10-fold higher in men compared with women, and this is
believed to be the primary rationale why men display sub-
stantially greater postpubescent muscle mass (18). Lastly,
older women with low basal T levels display blunted
increases in maximal strength and hypertrophy compared
with those with higher T concentrations (15,16).
Phillips et al. previously reported that RE shortens
the duration (G28 h), for which muscle protein synthesis
is elevated after exercise (38). Yet they have designed
an RT program (44) where participants trained once
every 72 h for weeks 1–6 and once every 48 h for weeks
7–15, resulting in an average of less than two (1.87) RE
sessions per week. From an applied perspective, this
frequency of training stimuli is inadequate and likely
related to the minimal growth experienced by both
training groups. If the acute training stimulus for a hy-
pertrophic adaptation is lacking because of an inade-
quate RE scheme design, it becomes difficult to justify
the lack of RE-induced hypertrophy, let alone identify
mechanisms contributing or not contributing to the
chronic adaptive response.
Lastly, the selection of elbow flexor musculature
should be challenged (44,46). How relevant is elbow
flexor hypertrophy? How much additional growth can be
(T) and growth hormone (GH) will also imply increases
in IGF-1’’ (22, 24). This is problematic because exercise-
induced GH responses are robust and related to large
muscle masses employed, whereas IGF-1 responses are
equivocal. This problem is highlighted by merely ex-
amining the two studies (22,24) that the authors cite as
justification for the ‘‘implied’’ IGF-1 response:
‘SM-C [IGF-1] demonstrated random significant in-
creases above rest in both males and females in response
to both HREPs IThe more anaerobic P-2 HREP pro-
duced a clear and sustained elevation of hGHI’’ (22).
‘The pattern of SM-C did not consistently follow hGH
changes IFurthermore, whereas an exercise protocol
consisting of 10 repetitions and 1 min rest produced a
greater GH AUC than other protocols, IGF-1 AUC was
no different’’ (24).
Therefore, clearly changes in postexercise IGF-1 cannot
be implied by changes in postexercise GH. More to the
point, there is little evidence that exercise-induced GH me-
diates gains in strength and hypertrophy at all, through
IGF-1 or otherwise as evidenced by numerous studies that
are not citable here due to word limits; however, most
notably, GH does not enhance myofibrillar protein syn-
thesis (9) or hypertrophy (37).
The authors state, ‘‘Furthermore, we will limit the
discussion of these adaptations to menI’ This limita-
tion is perplexing but we suspect that the reason that
women are left out is that they do not conveniently fit the
authors’’ ‘‘optimal hormonal’’ paradigm? For example,
despite a 45-fold lower exercise-induced testosterone
response than men (43), women show similar MPS (43)
and hypertrophy (36) responses compared with men.
Schroeder and Villanueva continue, ‘‘Three studies were
selected that utilized short-term RT interventions and
examined the influence of physiologically elevated acute
hormonal responses on human skeletal muscle’’ (13,26).
First, Schroeder and Villanueva overstate the original
viewpoint of Goto et al. (13) who were far more cautious
in concluding, ‘‘However, this interpretation [of a partial
role in hypertrophy] of the circulating of GH needs much
precaution [emphasis added]I’ Second, reference 26
describes a study in which testosterone was pharmaco-
logically ablated to concentrations that were chronically
near castrate levels. We disagree with the viewpoint that
this is an experimental paradigm that is reflective of the
effect of physiological acute exercise-induced hormone
responses on hypertrophy (discussed further in the fol-
lowing sections). Finally, the third study is an unpublished
study by Schroeder and Villanueva’s laboratory and thus
cannot be scrutinized.
Schroeder and Villanueva rely on more research of
questionable relevance to the exercise-induced question,
citing a resistance training study in cancer patients un-
dergoing ADT (again, this treatment reduces testosterone
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experienced by such a small muscle mass in response to
RT? We contend that the majority of RE protocols rel-
evant to applied professions inevitably induce transient
elevations in anabolic hormones, specifically training
multiple compound movements before isolation move-
ments within a single RE bout (at least 4–6 movements
total), using moderate to high volumes, moderate to high
training loads, and short rest interval lengths in between
sets. We believe that investigations of adaptations elic-
ited by RE protocols that are not of value to clinicians or
strength and conditioning professionals considerably limits
the meaningfulness, applicability, and clinical relevance
of the findings.
The anabolic hormonal milieu is necessary to maxi-
mize functional adaptations to RT. Although post-RE
elevations in anabolic hormones may not be necessary to
acutely stimulate muscle protein synthesis or promote
hypertrophy of small muscle masses, these elevations in
anabolic hormones are ideal to optimize functional per-
formance gains in whole body skeletal muscle mass and
strength in men and women across the lifespan.
E. Todd Schroeder
Matthew Villanueva
University of Southern California
Division of Biokinesiology &
Physical Therapy
Los Angeles, CA
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to near castrate levels 24 h a day). Notwithstanding
limited relevance, it is interesting (and encouraging for
those undergoing ADT) that robust gains in strength and
hypertrophy, that are similar to gains in healthy in-
dividuals, can still be achieved by using high intensity
resistance exercise protocols even despite undergoing
ADT (17). Further references cited by Schroeder and
Villanueva continue to have limitations as to the insight
they provide. For example, Willoughby and Taylor (49)
compared resistance exercise to a nonexercised control.
Spiering et al. (35) showed divergence in androgen re-
ceptor content at one of two time points postexercise
but because androgen receptor content was the lone out-
come measure in that study, it is impossible to determine
whether these findings have implications for hypertro-
phy. To summarize, we view Schroeder and Villanueva’s
interpretation of the studies cited to be lacking in support
for the original question posed in some cases and incor-
rectly interpreted as being supportive in others.
Schroeder and Villanueva draw their perspective to
a close by citing two interesting studies (4,26). Al-
though seminal, in our view, these studies (4,26)
have little to do with whether or not physiological
postexercise testosteronemia mediates hypertrophy with
resistance exercise. That is, testosterone ablation to
hypogonadal levels (26) or exogenous testosterone ad-
ministration to create supraphysiological testosteronemia
(4) are not models that come close to mimicking exercise-
induced androgen exposure. There are several reasons
FIGURE 2—Fold changes in cumulative testosterone (from
basal rested) versus hypertrophy curve. Data points 6 and
7 show postexercise testosterone (low vs high respectively)
within a physiological range having a negligible effect on cu-
mulative androgen exposure andtherefore hypertrophy. REx,
resistance exercise; ADT, androgen deprivation therapy; TE,
testosterone enanthate. Points with No REx: 1, from Smith
et al. (34); 2, Reference point at position (0,0) representing
young men no resistance exercise (REx); 3, from Bhasin et al.
(3). Points with REx: 4, from Kvorning et al. (26); 5, from
Hanson et al. (17); 6, average of low hormone condition
from West et al. (44) and Ronnestad (31); 7, average of high
hormone condition from West et al. and Ronnestad; 8, Bhasin
et al. (3). Further research is required to determine the exact
shape of the curve between data points (estimated).
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why pharmacologic elevations or ablation of testoster-
one cannot be used to ‘‘imply’’ relevance to transient
postexercise testosteronemia. First, elevations in postex-
ercise hormonal concentrations are fleeting compared
with the long-lasting hypo- or hyperandrogenemia seen
in pharmacological interventions (see Fig. 1). Second,
pharmacological-induced hormone concentrations are
far greater than those that occur in normal diurnal vari-
ation and transiently postexercise. Finally, pharmacologi-
cal hyperandrogenemia is accomplished by administering
testosterone derivatives that have different chemical
structures, excretion kinetics and half-lives, and receptor
affinities versus endogenous androgens and so do not
appropriately mimic normal transient hormonal changes
occurring postexercise.
We constructed Figure 2, using published data, to illus-
trate how changes in cumulative androgen exposure im-
pact hypertrophy. According to Figure 2, atrophy occurs
during hypotestosteronemia, but resistance training can
provoke partial (26) or potentially full (17) hypertrophy
responses. At top center, elevations in testosterone
postexercise have a negligible effect on cumulative an-
drogen exposure (data points 6 and 7 are nearly overlaid)
and hypertrophy. Exogenously induced hyperandroge-
nemia enhances muscle mass; resistance training further
enhances the gain in muscle mass. In summary, hyper- or
hypoandrogenemic states bear little resemblance to short-
lived (È30 min) exercise-induced hormonal changes;
therefore, we fail to see the relevance of arguments that
invoke these states as being supportive of the original
topical question that was posed. Overall, a hypothesis
that is based on cumulative androgen exposure explains
why transient exercise-induced elevations in testosterone
do not have a significant effect on hypertrophy.
It is time to write the requiem for studies that measure
only postexercise hormonal responses and infer a po-
tential effect on hypertrophy. We find that the evidence
for such an assertion lacking and causal interpretation
unwarranted given the lack of evidence that exercise-
induced hormones are important in regulating hypertro-
phy after resistance exercise. Moreover, pharmacologic
ablation and exogenous androgen administration are
not appropriate models from which to draw conclu-
sions about the effect of exercised-induced changes in
hormonal concentrations on hypertrophy.
Daniel W. D. West
Stuart M. Phillips
McMaster University
Department of Kinesiology
Exercise Metabolism Research Group
Hamilton, Ontario, CANADA
http://www.acsm-msse.org2050 Official Journal of the American College of Sports Medicine
Copyright © 2013 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
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CONTRASTING PERSPECTIVES Medicine & Science in Sports & Exercise 2051
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... The influence of GH and IGF-1 on the development of muscle mass after strength training also is unclear as its direct involvement in muscle hypertrophy seems negligible (73,81). Nonetheless, others have found that the effects of GH and circulating IGF-1 might be complementary in maximizing muscle anabolism, thereby optimizing the adaptations (45,80). For example, GH might increase the net muscle protein synthesis indirectly by facilitating amino acid transport and availability via both endocrine and locally produced IGF-1/MGF (82) or by inducing muscle growth through satellite cell activation, proliferation, and differentiation ( Fig. 1) (see [15,45,50]). ...
... Another issue that needs more attention is the role of anabolic hormones in training-induced adaptations (see [14,50,80,135,136]). Many studies have reported a transient increase in the levels of hormones in the blood (testosterone, GH, and IGF-1), and their relative concentrations seem to depend on several exercise variables, such as type of exercise (mono-vs multiarticular), workout volume, interset interval (72,118), and whether or not the exercise is performed under BFR (13). ...
... Many studies have reported a transient increase in the levels of hormones in the blood (testosterone, GH, and IGF-1), and their relative concentrations seem to depend on several exercise variables, such as type of exercise (mono-vs multiarticular), workout volume, interset interval (72,118), and whether or not the exercise is performed under BFR (13). Although mechanistic studies suggest that these hormones do not play a direct role in muscle protein synthesis (15,16,73), they may have an indirect influence by promoting satellite cell activation and fusion (45,50,80). As exercise-related increases in the levels of these hormones are relatively modest compared with their exogenous administration, it would be useful to determine their dose-dependent effects in both women and men and the influence of various training protocols. ...
Training with low-load exercise performed under blood-flow restriction can augment muscle hypertrophy and maximal strength to a similar extent as the classical high-load strength training method. However, the blood-flow restriction method elicits only minor neural adaptations. In an attempt to maximize training-related gains, we propose using other protocols that combine high voluntary activation, mechanical tension and metabolic stress.
... Also, administration of testosterone adjuvant to RET promoted muscle mass increase in older adults who have lower baseline levels of endogenous testosterone (85). RE endogenously increases the systemic concentration of testosterone by 2-4 times above baseline for~15-30 min in healthy young men (86). Contrary to exogenous testosterone administration, this transient~30 min spike in serum testosterone has a minimum impact on daily testosterone physiological fluctuation, and it is far lower (4-to 6-fold) than the concentrations reached by exogenous administrations of testosterone (Fig. 4) (86). ...
... RE endogenously increases the systemic concentration of testosterone by 2-4 times above baseline for~15-30 min in healthy young men (86). Contrary to exogenous testosterone administration, this transient~30 min spike in serum testosterone has a minimum impact on daily testosterone physiological fluctuation, and it is far lower (4-to 6-fold) than the concentrations reached by exogenous administrations of testosterone (Fig. 4) (86). Furthermore, we have repeatedly shown no association between changes in systemic testosterone concentrations and skeletal muscle hypertrophy response to RET (73,75). ...
... B, Cumulative AUC of serum testosterone over the first 7 d comparing 1) DV changes, 2) DV + 1 bouts of RE, and 3) 200 mg T enanthate. The schematic is adapted (with permission) from Schroeder et al.(86). AUC, area under the curve; DV, diurnal variation; T, testosterone. ...
Full-text available
Skeletal muscle plays a critical role in physical function and metabolic health. Muscle is a highly adaptable tissue that responds to resistance exercise (RE; loading) by hypertrophying or, during muscle disuse, RE mitigates muscle loss. Resistance exercise training (RET)-induced skeletal muscle hypertrophy is a product of external (e.g., resistance exercise programming, diet, some supplements) and internal variables (e.g., mechano-transduction, ribosomes, gene expression, satellite cells activity). Resistance exercise is undeniably the most potent non-pharmacological external variable to stimulate the activation/suppression of internal variables linked to muscular hypertrophy or countering disuse-induced muscle loss. Here, we posit that despite considerable research on the impact of external variables on RET and hypertrophy, internal variables (i.e., inherent skeletal muscle biology) are dominant in regulating the extent of hypertrophy in response to external stimuli. Thus, identifying the key internal skeletal muscle-derived variables that mediate the translation of external resistance exercise variables will be pivotal to determining the most effective strategies for skeletal muscle hypertrophy in healthy persons. Such work will aid in enhancing function in clinical populations, slowing functional decline, and promoting physical mobility. We provide up-to-date, evidence-based perspectives of the mechanisms regulating RET-induced skeletal muscle hypertrophy.
... Significant gains in strength and hypertrophy, without changes in testosterone and insulin-like growth factor 1 (IGF-1), have been previously observed [40], corroborating our results in respect of MCL and gastrocnemius CSA data, and testosterone concentrations. Some authors believe that the increase in performance and hypertrophy are not dependent on testosterone, GH or IGF-1 [40,41]. Schroeder et al. [41] argue that acute levels of anabolic hormones may not be necessary to stimulate protein synthesis A study by Linbdlim et al. reported no alterations in the androgenic receptor in the hypothalamus and in the adrenal gland following DECA administration, but these results could be explained by the low concentration used [42]. ...
... Some authors believe that the increase in performance and hypertrophy are not dependent on testosterone, GH or IGF-1 [40,41]. Schroeder et al. [41] argue that acute levels of anabolic hormones may not be necessary to stimulate protein synthesis A study by Linbdlim et al. reported no alterations in the androgenic receptor in the hypothalamus and in the adrenal gland following DECA administration, but these results could be explained by the low concentration used [42]. ...
Our aim was to evaluate the independent and associated effects of nandrolone decanoate (DECA) and resistance exercise (REx) on central and peripheral hormones and neuropeptides related to energy balance in male rats. The experimental protocol was performed for eight weeks and comprised four groups: control (C) – exposed to vehicle 3x/wk; trained (T) – REx 5x/wk and vehicle 3x/wk; decanoate (D) – exposed to DECA (5 mg/kg) 3x/wk, and REx with DECA (TD) – submitted to REx 5x/wk and DECA (5 mg/kg) 3x/wk. Cross-sectional area analysis of the gastrocnemius muscle was higher in the T and TD groups compared to the C group. Biometrical analyses showed a decrease in body weight only in the TD compared to the C group, however, a reduction in total fat mass was observed in both the T and TD when compared to the C group. In respect of hypothalamic mRNA expression, there was an increase in prepro-orexin in the T compared to the C group. In mesenteric fat there was a decrease in leptin expression in the T and TD compared to the C group. Plasma evaluations showed reduced leptin concentrations in D, T and TD compared to C, and an increase in orexin-A in the D group compared to the C and T groups. Our data showed that REx was related to central and peripheral changes in energy metabolism, while DECA changed only peripheral components. REx associated with DECA promoted peripheral changes in energy metabolism and decreased body and fat weights.
... On the other hand, Ozaki et al. (2017) observed increases in GH in both BFR and control groups, whereas muscle hypertrophy had previously been observed only in the BFR walk group (Ozaki et al., 2011b). Additionally, there is an intense debate on the contributions of anabolic hormones to the exercise-induced hypertrophic response (Schroeder et al., 2013). It has also been speculated that a potential exercise-induced metabolic response during aerobic exercise with BFR could facilitate the recruitment of the more prone to hypertrophy type II muscle fibers. ...
Full-text available
The use of blood flow restricted (BFR) exercise has become an accepted alternative approach to improve skeletal muscle mass and function and improve cardiovascular function in individuals that are not able to or do not wish to use traditional exercise protocols that rely on heavy loads and high training volumes. BFR exercise involves the reduction of blood flow to working skeletal muscle by applying a flexible cuff to the most proximal portions of a person’s arms or legs that results in decreased arterial flow to the exercising muscle and occluded venous return back to the central circulation. Safety concerns, especially related to the cardiovascular system, have not been consistently reported with a few exceptions; however, most researchers agree that BFR exercise can be a relatively safe technique for most people that are free from serious cardiovascular disease, as well as those with coronary artery disease, and also for people suffering from chronic conditions, such as multiple sclerosis, Parkinson’s, and osteoarthritis. Potential mechanisms to explain the benefits of BFR exercise are still mostly speculative and may require more invasive studies or the use of animal models to fully explore mechanisms of adaptation. The setting of absolute resistive pressures has evolved, from being based on an individual’s systolic blood pressure to a relative measure that is based on various percentages of the pressures needed to totally occlude blood flow in the exercising limb. However, since several other issues remain unresolved, such as the actual external loads used in combination with BFR, the type of cuff used to induce the blood flow restriction, and whether the restriction is continuous or intermittent, this paper will attempt to address these additional concerns.
... Conversely, high-intensity, low-volume programs utilizing long rest intervals primarily target muscle strength increases with secondary improvements in muscle hypertrophy (Baechle et al. 2008;Ratamess et al. 2009). However, it has been hypothesized that muscle hypertrophy may increase substantially across a larger spectrum of intensity and volume combinations (Schroeder et al. 2013). ...
... While the fundamental roles of hormones in muscle development and their decline in aging are well-established, the impact of physiological fluctuations (e.g., due to circadian rhythms or transient increases following bouts of RE) in hormones remains unclear (Schroeder et al., 2013). RE induces marked anabolic hormone responses, in particular those involving testosterone, growth hormone (GH) and IGF-1 (Spiering et al., 2008). ...
Full-text available
Maintenance of skeletal muscle mass throughout the life course is key for the regulation of health, with physical activity a critical component of this, in part, due to its influence upon key hormones such as testosterone, estrogen, growth hormone (GH), and insulin-like growth factor (IGF). Despite the importance of these hormones for the regulation of skeletal muscle mass in response to different types of exercise, their interaction with the processes controlling muscle mass remain unclear. This review presents evidence on the importance of these hormones in the regulation of skeletal muscle mass and their responses, and involvement in muscle adaptation to resistance exercise. Highlighting the key role testosterone plays as a primary anabolic hormone in muscle adaptation following exercise training, through its interaction with anabolic signaling pathways and other hormones via the androgen receptor (AR), this review also describes the potential importance of fluctuations in other hormones such as GH and IGF-1 in concert with dietary amino acid availability; and the role of estrogen, under the influence of the menstrual cycle and menopause, being especially important in adaptive exercise responses in women. Finally, the downstream mechanisms by which these hormones impact regulation of muscle protein turnover (synthesis and breakdown), and thus muscle mass are discussed. Advances in our understanding of hormones that impact protein turnover throughout life offers great relevance, not just for athletes, but also for the general and clinical populations alike.
... In this perspective, resistance training has shown to increase the release of testosterone associated with reduced catabolic hormones like cortisol, which leads to an improvement in muscle size and strength in older subjects ( Figure 2) [118]. The differences in hormone response may also lie in types of exercise performed, considering that larger muscle groups can elicit a higher release of anabolic hormones [119]. However, other authors, despite an acute spike in anabolic hormones after a single bout of exercise, demonstrated that this acute increase was not determinant in the process of muscle hypertrophy with chronic exposure to resistance training [120]. ...
Full-text available
As elite athletes demonstrate through the Olympic motto ‘citius, altius, fortius’, new performance records are driven forward by favourable skeletal muscle bioenergetics, cardiorespiratory, and endocrine system adaptations. At a recreational level, regular physical activity is an effective non‐pharmacological therapy in the treatment of many endocrine conditions. However, the impact of physical exercise on endocrine function and how best to incorporate exercise therapy into clinical care are not well understood. Beyond the pursuit of an Olympic medal, elite athletes may therefore serve as role models for showcasing how exercise can help in the management of endocrine disorders and improve metabolic dysfunction. This review summarises research evidence for clinicians who wish to understand endocrine changes in athletes who already perform high levels of activity as well as to encourage patients to exercise more safely. Herein, we detail the upper limits of athleticism to showcase the adaptability of human endocrine‐metabolic‐physiological systems. Then, we describe the growing research base that advocates the importance of understanding maladaptation to physical training and nutrition in males and females; especially the young. Finally, we explore the impact of physical activity in improving some endocrine disorders with guidance on how lessons can be taken from athletes training and incorporated into strategies to move more people more often. This article is protected by copyright. All rights reserved.
IntroductionThis study aimed to examine the effect of high-load resistance training (HLRT) on bone mineral density (BMD) in patients with osteoporosis and osteopenia using a meta-analysis.Materials and methodsWe searched for randomized controlled trials (RCTs) on HLRT in patients with osteoporosis and osteopenia from medical databases. Our meta-analysis was performed with the primary endpoints being the standardized mean difference (SMD) of the change in BMD of the lumbar spine (LS), femoral neck (FN), and total hip (TH). The robustness of the results was assessed by subgroup analysis. Heterogeneity factors were examined by meta-regression. Publication bias was evaluated using a funnel plot.ResultsWe selected nine RCTs, with 259 patients in the HLRT group (women, 55.2%) and 236 patients in the control group (women, 62.7%). The HLRT group showed a significant increase in BMD in the LS [SMD = 1.40, 95% confidence interval (CI) = 0.68–2.12, p < 0.001, I2 = 90%], the FN (SMD = 0.86, 95% CI = 0.05–1.67, p = 0.04, I2 = 92%), and the TH (SMD = 1.26, 95% CI = 0.45–2.08, p = 0.002, I2 = 91%). Subgroup analysis confirmed the robustness of the results only in LS. Total sessions and a high risk of bias were identified as the factors of heterogeneity in FN and TH (p < 0.05). The funnel plot showed asymmetry in all measurement sites.Conclusion This study suggested that HLRT can be effective in increasing BMD, mainly of LS, in patients with osteoporosis and osteopenia. However, due to high heterogeneity and publication bias, additional studies with a low risk of bias should be conducted to generalize our findings.
Teixeira, EL, Ugrinowitsch, C, de Salles Painelli, V, Silva-Batista, C, Aihara, AY, Cardoso, FN, Roschel, H, and Tricoli, V. Blood flow restriction does not promote additional effects on muscle adaptations when combined with high-load resistance training regardless of blood flow restriction protocol. J Strength Cond Res 35(5): 1194-1200, 2021-The aim of this study was to investigate, during high-load resistance training (HL-RT), the effect of blood flow restriction (BFR) applied during rest intervals (BFR-I) and muscle contractions (BFR-C) compared with HL-RT alone (no BFR), on maximum voluntary isometric contraction (MVIC), maximum dynamic strength (one repetition maximum [1RM]), quadriceps cross-sectional area (QCSA), blood lactate concentration ([La]), and root mean square of the surface electromyography (RMS-EMG) responses. Forty-nine healthy and untrained men (25 ± 6.2 years, 178.1 ± 5.3 cm and 78.8 ± 11.6 kg) trained twice per week, for 8 weeks. One leg of each subject performed HL-RT without BFR (HL-RT), whereas the contralateral leg was randomly allocated to 1 of 2 unilateral knee extension protocols: BFR-I or BFR-C (for all protocols, 3 × 8 repetitions, 70% 1RM). Maximum voluntary isometric contraction, 1RM, QCSA, and acute changes in [La] and RMS-EMG were assessed before and after training. The measurement of [La] and RMS-EMG was performed during the control sessions with the same relative load obtained after the 1RM test, before and after training. Similar increases in MVIC, 1RM, and QCSA were demonstrated among all conditions, with no significant difference between them. [La] increased for all protocols in pre-training and post-training, but it was higher for BFR-I compared with the remaining protocols. Increases in RMS-EMG occurred for all protocols in pre-training and post-training, with no significant difference between them. In conclusion, despite of a greater metabolic stress, BFR inclusion to HL-RT during rest intervals or muscle contraction did not promote any additive effect on muscle strength and hypertrophy.
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Effects of strength training (ST) for 21 wk were examined in 10 older women (64 ± 3 yr). Electromyogram, maximal isometric force, one-repetition maximum strength, and rate of force development of the leg extensors, muscle cross-sectional area (CSA) of the quadriceps femoris (QF) and of vastus lateralis (VL), medialis (VM), intermedius (VI) and rectus femoris (RF) throughout the lengths of 3/12–12/15 (Lf) of the femur, muscle fiber proportion and areas of types I, IIa, and IIb of the VL were evaluated. Serum hormone concentrations of testosterone, growth hormone (GH), cortisol, and IGF-I were analyzed for the resting, preexercise, and postexercise conditions. After the 21-wk ST, maximal force increased by 37% ( P < 0.001) and 1-RM by 29% ( P < 0.001), accompanied by an increase ( P < 0.01) in rate of force development. The integrated electromyograms of the vastus muscles increased ( P < 0.05). The CSA of the total QF increased ( P < 0.05) throughout the length of the femur by 5–9%. The increases were significant ( P< 0.05) at 7/15–12/15 Lf for VL and at 3/15–8/15 Lf for VM, at 5/15–9/15 for VI and at 9/15 ( P < 0.05) for RF. The fiber areas of type I ( P < 0.05), IIa ( P < 0.001), and IIb ( P < 0.001) increased by 22–36%. No changes occurred during ST in serum basal concentrations of the hormones examined, but the level of testosterone correlated with the changes in the CSA of the QF ( r = 0.64, P < 0.05). An acute increase of GH ( P < 0.05), remaining elevated up to 30 min ( P < 0.05) postloading, was observed only at posttraining. Both neural adaptations and the capacity of skeletal muscle to undergo training-induced hypertrophy even in older women explain the strength gains. The increases in the CSA of the QF occurred throughout its length but differed selectively between the individual muscles. The serum concentrations of hormones remained unaltered, but a low level of testosterone may be a limiting factor in training-induced muscle hypertrophy. The magnitude and time duration of the acute GH response may be important physiological indicators of anabolic adaptations during strength training even in older women.
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It has been well-documented in the literature that resistance training can promote marked increases in skeletal muscle mass. Post-exercise hypertrophic adaptations are mediated by a complex enzymatic cascade whereby mechanical tension is molecularly transduced into anabolic and catabolic signals that ultimately leads to a compensatory response, shifting muscle protein balance to favor synthesis over degradation.Myocellular signaling is influenced, in part, by the endocrine system. Various hormones have been shown to alter the dynamic balance between anabolic and catabolic stimuli in muscle, helping to mediate an increase or decrease in muscle protein accretion.Resistance training can have an acute impact on the post-exercise secretion of several of these hormones including insulin-like growth factor (IGF)-1, testosterone, and growth hormone (GH). Studies show that hormonal spikes are magnified following hypertrophy-type exercise that involves training at moderate intensities with shortened rest intervals as compared to high-intensity strength-oriented training. The observed positive relationship between anabolic hormones and hypertrophy-type training has led to the hormone hypothesis, which postulates that acute post-exercise hormonal secretions mediate increases muscle size. Several researchers have suggested that these transient hormonal elevations may be more critical to hypertrophic adaptations than chronic changes in resting hormonal concentrations. Theoretically, high levels of circulating hormones increase the likelihood of interaction with receptors, which may have particular hypertrophic importance in the post-workout period when muscles are primed for anabolism. Moreover, hormonal spikes may enhance intracellular signaling so that post-exercise protein breakdown is rapidly attenuated and anabolic processes are heightened, thereby leading to a greater supercompensatory response. While the hormone hypothesis has received considerable support in the literature, however, several researchers have questioned its veracity, with some speculating that the purpose of post-exercise hormonal elevations is to mobilize fuel stores rather than promote tissue anabolism. Therefore, the purpose of this paper will be to critically and objectively review the current literature, and then draw relevant conclusions as to the potential role of acute systemic factors on muscle protein accretion.
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Does resistance exercise order affect hormone availability? Participants performed arm exercise before and after leg exercise. Hormone delivery was estimated by multiplying brachial artery blood flow and hormone concentrations. Blood flow increased after arm (276%) and leg (193%; both p < 0.001) exercise. Testosterone, growth hormone, and insulin-like growth factor 1 showed with distinct delivery patterns between conditions; however (interactions all p < 0.001), net exposure was similar. The anabolic potential of postexercise hormones was not affected by exercise order.
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Background: Androgen deprivation therapy (ADT) for prostate cancer (PCa) is associated with weakness, fatigue, sarcopenia, and reduced quality of life (QoL). Black men have a higher incidence and mortality from PCa than Caucasians. We hypothesized that despite ADT, strength training (ST) would increase muscle power and size, thereby improving body composition, physical function, fatigue levels, and QoL in older black men with PCa. Methods: Muscle mass, power, strength, endurance, physical function, fatigue perception, and QoL were measured in 17 black men with PCa on ADT before and after 12 weeks of ST. Within-group differences were determined using t tests and regression models. Results: ST significantly increased total body muscle mass (2.7%), thigh muscle volume (6.4%), power (17%), and strength (28%). There were significant increases in functional performance (20%), muscle endurance (110%), and QoL scores (7%) and decreases in fatigue perception (38%). Improved muscle function was associated with higher functional performance (R (2) = 0.54) and lower fatigue perception (R (2) = 0.37), and both were associated with improved QoL (R (2) = 0.45), whereas fatigue perception tended to be associated with muscle endurance (R (2) = 0.37). Conclusions: ST elicits muscle hypertrophy even in the absence of testosterone and is effective in counteracting the adverse functional consequences of ADT in older black men with PCa. These improvements are associated with reduced fatigue perception, enhanced physical performance, and improved QoL. Thus, ST may be a safe and well-tolerated therapy to prevent the loss of muscle mass, strength, and power commonly observed during ADT.
Vastus lateralis muscle samples were obtained by needle biopsy from 18 healthy elderly men (65-82 yr) participating in a double blind, placebo (PL)-controlled trial of recombinant human GH (rhGH) and exercise and assessed for muscle morphology and skeletal muscle tissue expression of GH and insulin-like growth factors (IGFs). Subjects initially underwent progressive resistance training for 14 weeks and were then randomized to receive either rhGH (0.02 mg/kg, sc) or PL while undertaking a further 10 weeks of training. Muscle samples were obtained at baseline and at 14 and 24 weeks. The mean (+/- SEM) cross-sectional areas of type I and II fibers were similar (type I, 3891 +/- 167 microns2; type II, 3985 +/- 200 microns2) at baseline and increased (P < 0.01) by 16.2 +/- 4.1% and 11.8 +/- 3.8%, respectively, after the initial 14-week training period. After treatment (weeks 14-24), two-way repeated measures ANOVA revealed a main effect of time for type I (P < 0.01) and type II fibers (P < 0.05), but no...
Conference Paper
High-performance physical activity and postexercise recovery lead to significant changes in amino acid and protein metabolism in skeletal muscle. Central to these changes is an increase in the metabolism of the BCAA leucine. During exercise, muscle protein synthesis decreases together with a net increase in protein degradation and stimulation of BCAA oxidation. The decrease in protein synthesis is associated with inhibition of translation initiation factors 4E and 4G and ribosomal protein S6 under regulatory controls of intracellular insulin signaling and leucine concentrations. BCAA oxidation increases through activation of the branched-chain a-keto acid dehydrogenase (BCKDH). BCKDH activity increases with exercise, reducing plasma and intracellular leucine concentrations. After exercise, recovery of muscle protein synthesis requires dietary protein or BCAA to increase tissue levels of leucine in order to release the inhibition of the initiation factor 4 complex through activation of the protein kinase mammalian target of rapamycin (mTOR). Leucine's effect on mTOR is synergistic with insulin via the phosphoinositol 3-kinase signaling pathway. Together, insulin and leucine allow skeletal muscle to coordinate protein synthesis with physiclogical state and dietary intake.
The determination of whether increased dietary protein can positively affect health outcomes is hindered by the absence of prospective, randomized trials directly addressing this issue in which all pertinent variables are controlled. Consequently, we can only address the question deductively by considering the support for the rationale underlying the notion of a beneficial effect of increased dietary protein intake. With regard to health outcomes, we have focused on older individuals. Muscle mass and function are progressively lost with aging, so that by the age of 60 many individuals have reached a threshold where function begins to be affected. An association between reduced muscle mass and strength and unfavourable health outcomes is more likely to be revealed in individuals who have significant decrements in muscle mass and strength. In this article support for the rationale underlying the notion of a beneficial effect of increased dietary protein intake is considered. Dietary protein intake, and the resulting increased availability of plasma amino acids, stimulates muscle protein synthesis. If all other variables are controlled, increased muscle protein synthesis leads to improved muscle mass, strength and function over time. Increased muscle mass, strength and function are related to improved health outcomes in older individuals. Since adverse effects of reasonable increases in protein intake above the recommended dietary allowance (RDA) of 0·8 g protein/kg/day have not been reported, it is reasonable to conclude that the optimal protein intake for an older individual is greater than the RDA.
Villanueva, MG, Villanueva, MG, Lane, CJ, and Schroeder, ET. Influence of rest interval length on acute testosterone and cortisol responses to volume-load-equated total body hypertrophic and strength protocols. J Strength Cond Res 26(10):2755-2764, 2012-We hypothesized that total body strength (S) and hypertrophic (H) resistance training (RT) protocols using relatively short rest interval (RI) lengths between sets will elicit significant acute increases in total testosterone (TT) and cortisol (C) in healthy young men. Six men, 26 (±2.4) years, completed 4 randomized RT sessions, after a control session (R). The S and H protocols were equated for volume load (sets × repetitions × load); S: 8 sets × 3 repetitions at 85% 1RM, H: 3 sets × 10 repetitions at 70% 1RM, for all exercises. The RI used 60 seconds (S60, H60) and 90 seconds (S90, H90). Blood was drawn preexercise (PRE), immediately postexercise (POST), 15 minutes postexercise (15 MIN), and 30 minutes postexercise (30 MIN). The H60 elicited significant increases in TT from PRE (7.32 ± 1.85 ng·ml) to POST (8.87 ± 1.83 ng·ml) (p < 0.01), 15 MIN (8.58 ± 2.15 ng·ml) (p < 0.01), and 30 MIN (8.28 ± 2.16 ng·ml) (p < 0.05). The H90 also elicited significant increases in TT from PRE (8.37 ± 1.93 ng·ml) to POST (9.90 ± 1.25 ng·ml) (p < 0.01) and 15 MIN (9.46 ± 1.27 ng·ml) (p < 0.05). The S60 elicited significant increases in TT from PRE (7.73 ± 1.88 ng·ml) to 15 MIN (8.35 ± 1.64 ng·ml) (p < 0.05), and S90 showed a notable (p < 0.10) difference in TT from PRE (7.96 ± 2.29 ng·ml) to POST (8.75 ± 2.45 ng·ml). All the protocols did not significantly increase C (p > 0.05). Using relatively short RI between RT sets augments the acute TT response to hypertrophic and strength schemes. Shortening RI within high-intensity strength RT may lead to concomitant enhancements in muscle strength and size over a longer period of training.