Possible Stimuli For Strength and Power PDF

Possible stimuli for strength and power adaptation: Acute hormonal
responses. Sports Med. 2006;36(3):215-38
Blair Crewther1,2, Dr John Cronin1, Justin Keogh1 & Dr Christian Cook2
1
New Zealand Institute of Sport and Recreation Research, Division of Sport and
Recreation, Auckland University of Technology, Auckland 1020, New Zealand

2
Human Health and Performance Group, Bioengineering, HortResearch, Auckland, New
Zealand
 Blair Crewther
New Zealand Institute of Sport and Recreation Research
Division of Sport and Recreation,
Auckland University of Technology,
Private Bag 92006,
Auckland 1020.
New Zealand.
Phone: 649 917 9999 ext 7119
Facsimile: 649 917 9960
Email: blair.crewther@aut.ac.nz
Abstract
The acute hormonal response (e.g. testosterone – TST; growth hormone – GH; insulin,
insulin-like growth factor 1 – IGF-1, cortisol) to a single bout of resistance exercise plays
some role in mediating strength and power adaptation. Those schemes designed to
improve strength through morphological adaptation (hypertrophy schemes – moderate
loads, short rest periods, high total work) have generally been shown to elicit large
percentage increases (%) in TST, GH and cortisol levels, more so than schemes designed
to enhance strength through neural adaptation (neuronal schemes – heavy loads, long rest
periods, lower total work). Dynamic power schemes (explosive and/or ballistic
movements with light loads, moderate rest periods, low total work) have been shown to
increase both TST and cortisol. However, the hormonal response to hypertrophy schemes
has received much more attention than neuronal and dynamic power schemes. The IGF-1
and insulin response to the different loading schemes remains largely unknown. Whilst
males generally exhibit increases in TST following resistance exercise such a response is
generally not evident among females. Males also exhibit greater exercise-induced
increases in GH; however, due to much higher resting levels females still exhibit greater
circulating GH levels (absolute) than males. It would appear that the acute cortisol
response is similar between genders. Although the TST and GH response to resistance
exercise are lowered with increasing age, aging does not appear to affect the acute cortisol
response. Smaller TST and greater cortisol responses have been observed in pubescent
males compared to adult males.
Training experience influences the resistance exercise-induced TST response, as does the
type of training experience. Endurance trained males as an example show lower TST
responses to their training compared to both weight trained and untrained individuals.
Conversely, the release of GH does not appear to be sensitive to weight training
experience. Interestingly, individuals who specifically train to increase muscle mass (e.g.
bodybuilders) have shown an inhibited TST response to resistance exercise. Training
experience may only have small effects upon the release of cortisol to a single exercise
bout. Nutrition is another factor influencing acute hormonal responses. A combination of
carbohydrate (CHO) and protein (PRO), taken pre- and/or post training, has been shown to
decrease TST secretion, although this may also be due to an increase in the uptake of TST.
CHO and PRO supplementation increases the insulin response post-exercise but does not
appear to have any effect upon cortisol. The responsiveness of GH to CHO and/or PRO
supplementation appears quite variable. Again, the interactions between IGF-1 and insulin
with factors such as age, gender and training status have received little attention. Given
this equivocality of data we contend that strength and power research needs to investigate
the anabolic and catabolic hormonal responses to different loading schemes and the
interaction with other factors (e.g. age, training status, nutrition, gender, etc.), so our
understanding of how to optimise strength and power development is improved.
2
TABLE OF CONTENTS
Abstract ........................................................................................................................... 2
1. Introduction ................................................................................................................ 4
2. Acute hormonal response to resistance exercise ........................................................ 4
2.1 Testosterone ....................................................................................................... 5
2.1.1 Programme design .............................................................................................. 5
2.1.2 Gender ................................................................................................................ 9
2.1.3 Age ..................................................................................................................... 9
2.1.4 Training status .................................................................................................. 10
2.1.5 Nutrition ........................................................................................................... 10
2.2 Growth hormone .............................................................................................. 11
2.2.1 Programme design ............................................................................................ 11
2.2.2 Gender .............................................................................................................. 11
2.2.3 Age ................................................................................................................... 12
2.2.4 Training status .................................................................................................. 13
2.2.5 Nutrition ........................................................................................................... 13
2.3 Insulin-like growth factors ............................................................................... 14
2.3.2 Gender .............................................................................................................. 15
2.3.3 Nutrition ........................................................................................................... 15
2.4 Insulin .............................................................................................................. 15
2.4.2 Age ................................................................................................................... 16
2.4.3 Nutrition ........................................................................................................... 16
2.5 Cortisol............................................................................................................. 17
2.5.2 Gender .............................................................................................................. 17
2.5.3 Age ................................................................................................................... 18
2.5.4 Training status .................................................................................................. 19
2.5.5 Nutrition ........................................................................................................... 19
2.6 Limitations of research .................................................................................... 19
2.7 Implications for strength and power development .......................................... 20
3. Conclusion ................................................................................................................ 23
References .................................................................................................................... 23
3
1. Introduction
Resistance training is recognised as a major determinant of strength and power adaptation.
However, it would seem from the literature that there is no consensus regarding the
training method that best facilitates strength or power development. Although strength and
hypertrophy are traditionally associated with the use of heavy training loads (>60-70% one
repetition maximum or 1RM) [1, 2], recent research has found lighter loads (<45% 1RM)
effective in improving strength and/or hypertrophy. [3-7] The effective prescription of load
for power development is surrounded by similar controversy with both light and heavy
load training found equally effective in enhancing various measures of muscular power. [6,
8-11]
The use of different lifting techniques (e.g. ballistics, combination, traditional, etc.)
and their contribution to adaptation further confounds understanding in this area. Such
issues illustrate an apparent lack of understanding regarding the stimulus afforded by
different training methods and the adaptive response of the body to such stimuli.
The mechanical stimulus (e.g. high tension, time under tension, work, etc.) afforded by
resistance exercise has been proposed to be the most important stimuli for training-induced
adaptations to occur. [1, 2, 12] In conjunction with the various mechanical stimuli, the
endocrine responses to resistance exercise are also thought important for strength and
power development. [13, 14] The dynamic interaction between the anabolic (e.g. TST, GH)
and catabolic (e.g. cortisol) hormones are important factors regulating muscle protein
turnover and ultimately recovery and adaptation times. [15, 16] A net increase in protein
synthesis will lead to an increase in muscle cross-sectional area (CSA) and thereby
enhance the potential for force generation. However, with the majority of research
examining the acute hormonal response to hypertrophy loading schemes, much less is
known about the responses afforded by other schemes commonly used for strength and
power development. Furthermore, this analysis is generally limited to a few primary
hormones, such as TST and cortisol. Such an analysis would seem fundamental in
understanding how various training schemes affect the hormonal milieu and long-term
adaptation thereafter. The purpose of this review therefore is to discern how various
loading schemes differ in terms of their acute hormonal responses. It is hoped such a
treatise will enable better understanding of how best to integrate these stimuli, to optimise
the development of strength and/or power and as a consequence improve strength and
conditioning practice.
2. Acute hormonal response to resistance exercise

Resistance exercise is known to stimulate acute changes in blood borne hormone levels
and through these mediate the cellular processors involved in muscle tissue growth. [15, 17]
With the configuration of the various training variables (e.g. load, volume, rest periods,
etc.) determining the acute hormonal response, programme design plays an important role
mediating long-term adaptation. Examining the responsiveness of the anabolic and
catabolic hormones to different strength and power schemes should provide a better
understanding of the contribution of hormonal stimuli in developing these qualities. This
review will examine the acute hormonal responses (TST, GH, insulin-like growth factors,
insulin, cortisol) to three broad types of programmes often used within practice. That is,
hypertrophy (moderate loads, short rest periods, high total work), neuronal (heavy loads,
long rest periods, lower total work) and dynamic power (explosive and/or ballistic
movements with light loads, moderate rest periods, lower total work) schemes. The
influence of age, gender, training status and supplementation, upon acute hormone
responses to resistance exercise, will also be examined.
4
2.1 Testosterone
The majority of evidence supports the contention that testosterone (TST) has a
considerable anabolic effect, directly and indirectly, upon muscle tissue growth. [15, 16]
Secreted from the testes by way of the hypothalamic-pituitary-gonadol (HPG) axis, TST is
thought to contribute to muscle growth by increasing protein synthesis and decreasing
protein degradation. [15, 17] The secretion of TST may further enhance the hormonal
environment by stimulating the release of other anabolic hormones such as growth
hormone. Like all steroid hormones TST is derived from cholesterol and is not freely
soluble in plasma. The biologically active form of TST is in the free or unbound form,
accounting for ~2-5% of all TST, ~38% is bound to albumin, whilst the remaining 55-60%
is bound to sex hormone-binding globulin (SHBG). [18] The approximate 40% not bound
to SHBG is believed available for metabolism, the importance of which relates to the “free
hormone” hypothesis, stating that only the free component is available for cell metabolism.
The validity of the free hormone hypothesis has not yet been established. Furthermore, the
importance of the bound component may lie in the fact that the bound fraction dictates the
amount of hormone available for receptor interactions. [15, 18]
2.1.1 Programme design

Those programmes designed to improve maximal strength through morphological
adaptation (i.e. hypertrophy schemes) have generally been shown to elicit large increases
in circulating TST post exercise (see Table II). In comparison those programmes designed
to enhance maximal strength through neural adaptation (i.e. neuronal schemes) have been
found to elicit smaller TST responses. For example, Kraemer et al. [19] compared the
hormonal response to eight exercises performed with either a five repetition maximum load
(5RM) for 3-5 sets per exercise and three minutes rest between sets or a 10RM load (3 sets
per exercise) with one minute rest periods. The total TST response to the hypertrophy
scheme (72%) was found to be much greater than that reported following the neuronal
scheme (27%). Similarly, Hakkinen and Pakarinen [20] reported an increase in both total
TST (24%) and free TST (22%) to a hypertrophy squat session (10 sets x 10 repetitions,
10RM). However, no significant changes in total or free TST were found after the
performance of a neuronal type squat session (20 sets x 1 repetition, 1RM). These findings
confirm the importance of programme design in modulating the acute hormonal response
to resistance exercise.
Dynamic power schemes have also been found to induce significant increases in TST (see
Table III). Mero et al. [21] examined the effect of dynamic half squat lifts (10 sets x 6
repetitions, 50% 1RM) performed with one and four minute rest periods. Both schemes
resulted in a significant increase in total TST (18-30%) post exercise. Another study
reported a similar increase in TST (15%) following the performance of a series of
explosive squat jumps (5 sets x 10 repetitions, 30% 1RM, 2 minutes rest). [22] Based upon
the studies reviewed, the average increase in TST across the dynamic power schemes
(15%) is of similar magnitude to the different hypertrophy schemes (11%). In comparison,
neuronal schemes have been found to elicit the smallest mean change in TST (8%). The
authors recognise that subtle differences in programme design (e.g. volume, exercises, etc.)
make it difficult to determine the overall response to each training regime. Gender
differences are also important in this regard (i.e. females non-responsive). Despite this,
fewer studies have reported the TST response to neuronal and dynamic power schemes.
Therefore, it is suggested that further research be conducted to examine the responsiveness
of TST to such programmes. Investigating commonly used training protocols would
improve the validity and practical significance of the findings and provide greater
understanding as to the contribution of the hormonal stimulus to a given training regime.
5
Table II. Acute hormonal response to hypertrophy schemes.
References Subjects (age) Protocols Hormone (% or fold change)

Exercise/s - sets x reps (load)
TST GH IGF-1 Insulin Cortisol
 ~10  ~80
[139]
Vanhelder et al. 5 Males - UT 1 ex - 7 x 10 (10RM) - - -
Kraemer et al. [99] 17 Males - T 10 ex - 3 x 10 (10RM) - - - -  ~46
Kraemer et al. [30] 9 Males - T 8 ex - 3 x 10 (10RM)  ~30  ~11 fold  ~26 - -
Craig et al. [135] 11 Males - UT 7 ex - 3 x 8-10 (75% 1RM) -  ~520 - - -
Kraemer et al. [19] 8 Males - T 8 ex - 3 x 10 (10RM)  ~72  ~850  ~34 - -
Kraemer et al. [19] 8 Females - T 8 ex - 3 x 10 (10RM) Nil  ~106  ~13 - -
Kraemer et al. [69] 8 Males - UT 4 ex - 3 x 10 (10RM) Nil  ~550 - Nil -
Kraemer et al. [95] 8 Males - T 8 ex - 3 x 10 (10RM) - - - -  68
Hakkinen & Pakarinen [20] 10 Males - T 1 ex - 10 x 10 (10RM) 2  24 ( 22)1  170 fold - -  149
Kraemer at al. [36] 9 Females - T 8 ex - 3 x 10 (10RM) Nil  ~110 Nil -  ~125
Chandler et al. [27] 9 Males - T 8 ex - 2 x 8-10 (75% 1RM) Control  ~20  ~700 Nil  ~20 -
8 ex - 2 x 8-10 (75% 1RM) PRO  ~12  ~900 Nil  ~230 -
8 ex - 2 x 8-10 (75% 1RM) CHO  ~20  ~820 Nil  ~560 -
8 ex - 2 x 8-10 (75% 1RM) CHO + PRO  ~20  ~900 Nil  ~650 -
McMurray et al. [24] 8 Males - T 6 ex - 3 x 6-8 (80% 1RM) 2  21  31 fold - -  21
Hakkinen & Pakarinen [44] 8 Males - UT (27yr) 1 ex - 5 x 10 (10RM) 2 9  200 fold - - Nil
8 Males - UT (47yr) 1 ex - 5 x 10 (10RM) 2  15  19 fold - -  ~80
8 Males - UT (68yr) 1 ex - 5 x 10 (10RM) 2 Nil Nil - - Nil
Hakkinen & Pakarinen [44] 8 Females - UT (25yr) 1 ex - 5 x 10 (10RM) 2 Nil  200 - - Nil
7 Females - UT (48yr) 1 ex - 5 x 10 (10RM) 2  18  20 fold - - Nil
8 Females - UT (68yr) 1 ex - 5 x 10 (10RM) 2 Nil Nil - - Nil
Mulligan et al. [66] 10 Females - T 8 ex - 1 x 10 (10RM) -  ~60 - -  ~20
8 ex - 3 x 10 (10RM) -  ~500 - -  ~175
Gotshalk et al. [32] 8 Males - T 8 ex - 1 x 10 (10RM)  ~14  ~350 - -  ~10
8 ex - 3 x 10 (10RM)  ~32  ~700 - -  ~23
Volek et al. [22] 12 Males - T 1 ex - 5 x 10 (10RM) 7 - - - Nil
McCall et al [28] 10 Males - RT 8 ex - 3 x 10 (10RM) Nil  ~38 fold Nil -  ~40
Kraemer et al. [33] 9 Males - T 4 ex - 4 x 10 (10RM)  ~20  ~430 - -  ~34
Kraemer et al. [43] 8 Males - UT (30yr) 1 ex - 4 x 10 (10RM)  ~38 ( 40)1  ~16 fold - -  ~78
8 Males - UT (62yr) 1 ex - 4 x 10 (10RM)  ~20 ( 26)1  ~230 - -  ~45
Kraemer et al. [34] 8 Males - UT (30yr) 1 ex - 4 x 10 (10RM)  ~37 ( 29)1  ~28 fold - -  ~80
9 Males - UT (62yr) 1 ex - 4 x 10 (10RM)  ~23 ( 33)1 Nil - -  ~47
Hakkinen et al. [45] 10 Males - UT (26yr) 2 ex - 4 x 10 (100% MVC) 2  ~27 ( 21)1  ~29 fold - - Nil
10 Males - UT (70yr) 2 ex - 4 x 10 (100% MVC) 2 Nil ( 17)1  ~14 fold - - Nil
Bosco et al. [57] 6 Males - T 3 ex - 12 x 8-12 (70-75% 1RM)  ~70  ~50 fold -
Hakkinen et al. [54] 10 Males - UT (40yr) 1 ex - 5 x 10 (10RM) 2  ~21  ~340 - - -
11 Males - UT (70yr) 1 ex - 5 x 10 (10RM) 2  ~14  ~150 - - -
11 Females - UT (40yr) 1 ex - 5 x 10 (10RM) 2 Nil  ~170 - - -
10 Females - UT (70yr) 1 ex - 5 x 10 (10RM) 2 Nil Nil - - -
Taylor et al. [65] 6 Females - T 7 ex - 3-4 x 10 (10RM) -  ~90 - - -
Taylor et al. [65] 6 Females - UT 7 ex - 3-4 x 10 (10RM) -  ~30 - - -
Kraemer et al. [104] 10 Males - RT 10 ex - 3 x 10 (10RM) 2, 3  ~29 - - - -
Smilios et al. [31] 11 Males - T 4 ex - 2 x 10 (75% 1RM) 2 Nil  ~400 - - Nil
4 ex - 4 x 10 (75% 1RM) 2  ~10  ~11 fold - -  ~28
4 ex - 6 x 10 (75% 1RM) 2 Nil  ~15 fold - -  ~27
Zafeiridis et al. [63] 10 Males - T 4 ex - 4 x 10 (75% 1RM) 2 -  ~13 fold - -  ~38
McGuigan et al. [96] 8 Males & 9 Females - RT 2 ex - 6 x 10 (75% 1RM) 3 - - - -  97
Thyfault et al. [88] 9 Males - T 8 ex - 3 x 10 (85-90%1RM) CHO - - -  ~160  ~67
8 ex - 3 x 10 (85-90%1RM) Placebo - - -  ~36  ~55
1
free testosterone, 2control data provided, 3salivary analysis
T = trained; UT = untrained; RT = recreationally trained; MVC = maximal voluntary contraction; TST = testosterone; GH = growth hormone;
IGF-1 = insulin growth-like factor 1; NU = non-steroid users; SU = steroid users; CHO = carbohydrate group; PRO = protein group
7
Table III . Acute hormonal response to neuronal and dynamic power schemes.
References Subjects (age) Protocols Hormone (% or fold change)

Exercises/s - sets x reps (load) -
TST GH IGF-1 Insulin Cortisol
Neuronal schemes
Kraemer et al. [30] 9 Males - T 8 ex - 3/5 x 5 (5RM)  ~30  ~275  ~25 - -
Kraemer et al. [19] 8 Males - T 8 ex - 3/5 x 5 (5RM)  ~27  ~375  ~27 - -
Kraemer et al. [19] 8 Females - T 8 ex - 3/5 x 5 (5RM) Nil Nil  ~13 - -
Kraemer et al. [36] 9 Females - T 8 ex - 3/5 x 5 (5RM) Nil  70 Nil - Nil
Hakkinen & Pakarinen [20] 10 Males - T 1 ex - 20 x 1 (100% 1RM) Nil  361 - - Nil
Raastad et al. [26] 9 Males - T 3 ex - 3 x 3-6 (3-6RM) 4  ~17  ~14 fold -  ~11  ~55
Kraemer et al. [95] 8 Males - T 8 ex - 3/5 x 5 (5RM) - - - - Nil
Smilios et al. [31] 11 Males - T 4 ex - 2 x 5 (88% 1RM) 4 Nil Nil - - Nil
4 ex - 4 x 5 (88% 1RM) 4 Nil Nil - - Nil
4 ex - 6 x 5 (88% 1RM) 4 Nil  ~500 - - Nil
Zafeiridis et al. [63] 10 Males - T 4 ex - 4 x 5 (88% 1RM) 4 -  ~400 - - Nil
Dynamic power schemes
Mero et al. [21] 9 Males - T 1 ex - 10 x 6 (50% 1RM)  ~18-30 - - - -
1 ex - 2 x 30 (50% 1RM)  ~30 - - - -
Mero et al. [25] 6 Males - (24 yr) 1 ex - 10 x 6 (50% 1RM) 2  16 - - - Nil
1 ex - 10 x 6 (50% 1RM) 3  18 ( 19)1 - - - Nil
6 Males - (15 yr) 1 ex - 10 x 6 (50% 1RM) 2 Nil - - -  67
1 ex - 10 x 6 (50% 1RM) 3  13 ( 11)1 - - -  33
Bosco et al. [64] 16 Males - T 60 seconds jumping (BW)  12 ( 13)1 Nil Nil -  14
Volek et al. [22] 12 Males - T 1 ex - 5 x 10 (30% 1RM)  15 - - - Nil
1
free testosterone, 24-min rest, 31-min rest, 4control data provided
T = trained; BW = body weight; TST = testosterone; GH = growth hormones; IGF-1 = insulin growth-like factor 1.
8
2.1.2 Gender
Whilst males generally exhibit acute increases in TST following resistance exercise such a
response is not evident among females, regardless of the protocol performed (see Tables I
and II). The performance of an exercise session consisting of either 5RM and three
minutes rest or 10RM with one minutes rest, produced an increase in total TST in males
but elicited no TST response among females. [19] This may be attributed to gender
differences with regards to the production and release mechanisms of TST. In males,
luteinizing hormone (LH) and follicle-stimulating hormone (FSH) stimulates the Leydig
cells of the testes to synthesize and release large amounts of TST into the blood stream
following physical stimulation. [15, 17] For females, much smaller quantities of TST are
produced in the ovaries and the adrenal cortex, and only small amounts are released into
the blood following resistance exercise. [15, 17] Males also demonstrate much higher resting
or pre-test concentrations of TST (14-32nmol/l) [19, 20, 22-35] as compared to females (1-
2.5nmol/l) [19, 23, 35-37], which may again be related to differences in the respective
production and release mechanisms of TST. The differential responses between males and
females are not surprising given that differences in strength and hypertrophy between
genders have traditionally been attributed to the anabolic actions of this hormone. [17, 38]
2.1.3 Age
Age would appear to be another factor influencing the acute hormone response to
resistance exercise. As with mature adults, resistance exercise is known to increase
circulating TST levels among young males. [25, 39, 40] However, younger males appear to
elicit smaller hormonal responses than their older male counterparts. Pullinen et al. [23]
compared the hormonal response to a single exercise bout (5 sets x 10 knee extensions,
40% 1RM) followed by two sets to exhaustion, among men, women and pubescent boys.
Significant increases in TST (total and free) were only observed in the adult males,
although this may be partially attributed to a significant change in plasma volume. It was
of interest to note that a more pronounced diurnal rhythm was observed in the younger
males. [23] When drawn in the morning, the TST samples (total and free) of the young
males were not significantly different from men; however, by early afternoon (pre-
exercise) these samples were significantly higher among men. Mero et al. [25] also
investigated the hormonal response among boys and men, each performing a half squat
exercise session with two different rest periods. The adult males reported greater changes
in TST (total and free) in both interventions. Pre-exercise concentrations of TST (total and
free) were also much greater in the adult males. Differences in baseline and exercise-
induced hormone levels may provide adult males with a more beneficial response for
adaptation and thereby explain muscle mass and strength differences between groups.
It is generally accepted that the acute TST response to resistance exercise decreases as a
consequence of the aging process. [41, 42] A study by Kraemer et al. [43] examined the
hormonal response among two groups of males (30years and 62years), with each group
performing an identical resistance exercise session (4 sets x 10 repetitions, 10RM, 90
seconds rest). The TST response was found to be greater in the younger group for both
free TST (40% v 26%) and total TST (38% v 20%) respectively. Such a finding is
supported by other studies [34, 44], which seems to indicate a reduced TST response among
elderly males to resistance exercise. Adult males also exhibit greater resting
concentrations of total and/or free TST than elderly males. [43, 45] These differences in TST
activity may partly explain the reduction in strength and muscle mass with increasing age.
[46, 47]
Proposed mechanisms for this include, failure of the hypothalamic-pituitary axis,
changes in testicular function, an increase in SHBG levels and/or increased sensitivity of
gonadotropin secretion to androgen negative-feedback inhibition. [48] Considering the
benefits of weight training (i.e. increase exercise responses, altered basal levels), restoring
endocrine function of older adults through resistance exercise offers an attractive
hypothesis for ameliorating the age-related decline in strength and muscle mass.
2.1.4 Training status

The training status of subjects appears to be an important factor influencing the acute TST
response to resistance exercise. Kraemer et al. [37] examined the effects of a nine week
training programme among a group of previously untrained males and females. The TST
response to a single exercise bout was performed before and after the nine-week
programme to ascertain the adaptive response of the endocrine system. The male subjects
reported an increase in the acute total TST after training (12%), as compared to that found
before training (nil). This is indicative of enhanced sensitivity of TST secretion among
males with weight training experience. Such a notion is supported by other research [49], as
well as evidence showing that greater training experience is accompanied by greater TST
responses to resistance exercise. [39, 50] Mechanisms accountable for this adaptation may
include the synthesis, storage and transport of hormones, hormone-receptor affinity,
receptor numbers and alterations in hormone degradation. [51] The additional influence of
age is less clear as some studies have reported enhanced secretion among elderly males [34,
52]
with others reporting no such changes. [53, 54] Still, such an adaptation would appear to
be limited to males with no changes reported among females after periods of weight
training, regardless of age. [37, 52, 54, 55] The TST response may be further sensitive to the
type of training experience. Tremblay and colleagues [56] reported a less pronounced TST
response (total and free) among endurance-trained than resistance-trained athletes. The
response of the endurance-trained athletes was also less than that of a group of untrained
males in the same study. [56] This may be explained by inter-group differences such as the
amount of lean muscle mass, muscle fibre composition and absolute strength.
Given the anabolic nature of TST, it is of interest to note that individuals who specifically
train to increase muscle mass (i.e. bodybuilders and steroid users) have shown an inhibited
TST response to resistance exercise. Bosco et al. [57] examined the TST response among
male bodybuilders performing a typical lower body workout, consisting of half squat, leg
press and leg extension exercises. This bout produced a 70% reduction in total TST
immediately post exercise. Another study examined the hormonal response among a group
of bodybuilders and power lifters who were categorised into two groups as anabolic steroid
users or non-steroid users, as determined by self-report. [58] Following an exhaustive squat
session, no significant changes in total TST were found in either group post exercise.
Rozenek et al. [59] also reported a smaller TST response among steroid lifters (10%), as
compared to non-steroid lifters (20%). Given that anabolic steroid usage is often
associated with increased strength and greater muscle mass this is somewhat surprising.
This may be due to increased binding affinity of steroids with skeletal muscle androgen
receptors [58] or the much greater circulating levels of TST seen in steroid lifters (and lower
LH levels), as compared to non-steroid lifters. [59] The responsiveness of other hormones
also needs to be considered. That is, an increase in GH [57] or a reduction in cortisol [58]
may account for the non-responsiveness of TST. These hormones will be discussed in
later sections. The relevance of these responses is limited by the fact that most studies
have examined only a single hormone sample post exercise.
2.1.5 Nutrition
It has been suggested that specific nutritional strategies, especially carbohydrate (CHO)
and protein (PRO) intake, may mediate adaptation by enhancing acute hormone responses.
[22, 27, 33, 40, 60]
Chandler and colleagues [27] compared the effect of four different treatments
10
(control, CHO, PRO, PRO and CHO) taken immediately post and two hours after a weight
training session. An initial increase in total TST in all groups (12-20%) was followed by a
reduction in TST 1-5 hours post exercise, in the supplement groups. Another study [33]
reported a similar response with PRO and CHO supplementation, taken before and after
exercise, with this response reproduced over three consecutive days. It seems that a
combination of PRO and/or CHO exaggerates the post-training decline in TST levels. The
practical significance of this response is unclear given that this may be accredited to either
a decrease in TST secretion or an increase in TST uptake. For example, the decrease in
TST reported by Chandler [27] was not associated with a decline in LH (a regulator of
TST), thereby suggesting increased clearance of TST. Kraemer [33] also found that the
TST/SHBG ratio remained unchanged after supplementation, which suggests that free
testosterone levels remain stable despite lowered total TST. Interpretation of this data is
made difficult given that supplementation also influences resting TST levels and/or SHBG
levels. [22, 33, 40] Further research is needed to differentiate the hormonal mechanisms (i.e.
secretion or clearance) determining circulating TST levels with nutrition.
2.2 Growth hormone

Growth hormone (GH) is another potent anabolic hormone influencing muscle growth.
Also known as somatotropin, this peptide hormone is synthesized and released from the
anterior segment of the pituitary gland. The release of GH is regulated by two
hypothalamic peptides, GH-releasing hormone (GHRH), which stimulates GH synthesis
and secretion, and GH-inhibiting hormone (GHIH) or somatostatin, which inhibits the
release of GH. [61] Similar to TST, this hormone is thought to contribute to muscle tissue
growth by increasing protein synthesis and reducing muscle protein degradation. [15, 17, 61]
The release of GH may further enhance the training environment by stimulating the release
of a family of polypeptides called the somatomedins from the liver [16], which are also
known for their anabolic effects upon muscle tissue. Compared to the steroid hormones,
human GH represents a family of proteins rather than a single hormone complex, with over
100 forms of GH currently identified within plasma fluid. [62] However, the function of the
different variants of GH has not yet been fully established. The most dominant form of
GH in circulation, and the most widely examined within research, is the 22kD variant.

Hypertrophy programmes have been shown to produce large increases in circulating GH
and more so than neuronal programmes (see Tables II and III). For example, the acute GH
response to a hypertrophy scheme (11-fold) was much greater than that found after a
neuronal scheme (3-fold). [30] The findings of other research [19, 20, 31, 36, 63] support the
greater GH response and confirms the importance of programme design in modulating
blood borne GH levels. On average the increase in GH in the studies reviewed was much
larger across the hypertrophy schemes (18-fold), as compared to the neuronal schemes (3-
fold). Whilst this data does confirm a much greater anabolic response to a single
hypertrophy session, fewer studies have again examined the hormonal response to a single
neuronal session. To our knowledge only one study has assessed the GH response to a
dynamic power scheme [64], with no changes in GH reported. Given the relative
importance of this anabolic hormone it is suggested that further research examine the
responsiveness of GH to neuronal and dynamic power schemes.
2.2.2 Gender
It can be observed that males generally attain greater GH responses than females to
resistance exercise (see Tables II and III). For example, increases in GH levels among
males performing a hypertrophy (850%) and neuronal (375%) protocol, were greater than
11
females performing a hypertrophy (106%) and neuronal (no change) protocol. [19] Other
research is in agreement with this finding. [23, 44, 52, 54] The hypertrophy data reviewed
provides further evidence of gender differences, with males reporting a 27-fold increase in
GH and females a 3-fold increase. It is obvious that males exhibit greater increases in GH
compared to females; however, females still exhibit greater peak GH responses (absolute
values) after a single weight-training bout. [19, 37, 54] This may be related to the estrogen
sensitisation of the somatotrophs, which are known to give an increased responsiveness to
a variety of stimuli among females. [19] These differences may be further explained by GH
concentrations at baseline, with females often exhibiting much higher pre-test
concentrations (1-8µg/l) [19, 23, 36, 37, 44, 54, 65, 66], compared to that found in males (0.1-
1.2µg/l). [28, 34, 37, 43-45, 54] Given that males still demonstrate greater changes in muscle
mass and strength, the importance of these elevated GH levels among females requires
further investigation.
2.2.3 Age
As mentioned previously, age-related differences in anabolic hormone activity may be a
contributing factor to the greater strength and muscle mass seen with adult males, as
compared to younger males. A recent study examined the endocrine responses among men
(27years) and pubescent boys (14years) to an acute exercise bout. [23] No significant
differences were found in GH levels between men and boys pre- exercise, following five
sets of knee extension and after two more sets performed to exhaustion. Even a resting
sample taken 12 hours prior to exercise showed no differences in GH levels between these
groups. It would seem that little differences exist in GH concentrations between adult
males and pubescent boys. Unfortunately, this is another area limited by a lack of
scientific reseacrh. Given that significant changes in plasma volume may have explained
the significant increases in GH after the two sets to exhaustion [23], in each group, it is
difficult to ascertain whether or not any differences would exist between the boys and men,
if a real increase in the GH response were observed. Furthermore, large individual
variability in GH concentrations in each group makes comparisons difficult. Due to the
paucity of research in this area it is recommended that further research be conducted to
elucidate any age differences in GH activity following a weight-training bout.
One of the difficulties when examining the responsiveness of the endocrine system to the
weight-training stimulus, in particular GH responses, is the fact that hormone levels often
exhibit large individual variability. For example, Raastad, Bjoro and Hallen [26] examined
the GH response of nine trained males to a weight training session consisting of three
lower limb exercises, performed at a high (3RM) and moderate (70% of 3RM) intensity. It
was reported that three subjects did not respond to either protocol, five subjects showed
moderate responses to both protocols and one subject increased his GH level to twice that
of the moderate responders, during the high and moderate schemes. Other studies are in
agreement [20, 24, 28, 34, 35, 44, 52, 53, 55, 65, 67], having found large individual variability when
examining the GH response to different resistance exercise protocols, independent of
training status, gender and age. This would suggest that even within a typically
homogenous population, there are likely to be some individual differences in the anabolic
response to a given resistance exercise bout (i.e. responders v non-responders). The
application of findings in this area must therefore be done with some caution.
Whilst the elderly are known to elicit acute increases in GH to a single bout of resistance
exercise, the aging process appears to decrease the GH response to such exercise. A study
by Hakkinen and Pakarinen [44] examined the endocrine response among three groups of
untrained males (27years, 47years, 68years) and untrained females (25years, 48years,
12
68years). Each group performed an identical weight training session, consisting of five
sets of ten repetitions with a 10RM load. For males, the 27 year old group reported the
greatest GH response (200 fold), followed by the 47 year olds (19 fold) with no changes
reported in the 68 year olds. For females, the 48 year old group were found to have a
much larger increase in GH (20 fold) than that of the 25 year olds (2 fold), with the oldest
female group being non-responsive to the exercise protocol (nil). Several other studies
have reported similar findings when examining the resistance exercise-induced GH
response across different age groups [34, 43, 45, 54, 68] These findings indicate a reduction in
the acute secretion of GH to a single resistance exercise bout, as a function of the aging
process. These findings again support suggestions that the decline in muscle mass and
strength with age may be partially attributed to changes in the function of the endocrine
system. In terms of resting or pre-test GH levels, it is difficult to determine the
importance of age. For instance, the hormonal responses reported for adult (1-8µg/l) [19, 23,
36, 37, 65, 66]
and elderly females (0.4-1.5µg/l) [52, 54, 55] does suggest some interaction with
age. Similarly, the values reported by studies examining adult (0.2-2µg/l) [19, 20, 23, 24, 26, 28,
30-34, 69]
and elderly males (0.1-1.25µg/l) [34, 44, 45, 52-54] show similar patterns, though not to
the magnitude found with females. Due to large individual variability between studies, the
effect of aging upon baseline GH should be interpreted with caution.

The acute GH response to a weight-training bout does not appear to be influenced by
training experience. A group of untrained and trained males each performed a leg workout
consisting of squats, ¼ squats and unweighted vertical jumps. [70] The increase in GH in
the untrained group (41-fold) was significantly greater than that found in the trained group
(25-fold). The hypertrophy data in Table II partially support this finding, with greater GH
responses found among untrained males (31-fold) and females (6-fold), than those with
weight training experience (24-fold v 2-fold respectively). Research has also shown little
or no change in acute GH responses following periods of weight training, among
previously untrained or recreationally trained individuals. [28, 34, 37, 53, 55] This is supported
by data showing no differences in GH responses between trained and untrained athletes [49]
or as a function of training experience. [39] Thus, it appears that individuals with greater
training experience are unlikely to exhibit enhanced GH release. In contrast to these
findings, Taylor et al. [65] reported a greater GH response among trained females (90%)
compared to untrained females (30%), to the same exercise programme. This may be
partially attributed to the significantly lower resting GH values for the trained group.
Hakkinen et al. [54] also reported an increase in the GH response to a single resistance
exercise bout, after six months training among middle age males (pre-340% v post-1100%)
and females (pre-170% v post-900%). However, no such responses were found in a much
older (70years) group of males and females in the same study. This may be explained by a
reduction in pre-exercise values (although not significant) in the post training assessment.
Disparate findings in this area may be attributed to different training methodologies, as
well as differences in gender and age.
2.2.5 Nutrition
A number of studies have examined the influence of nutrition upon the acute GH response
to resistance exercise. When a combined PRO and CHO supplementation was taken 120
minutes before and immediately after resistance exercise, Kraemer et al. [33] reported a
much greater GH response (14-fold) compared to that found in a placebo group (4-fold).
This response was not repeatable over two more days of consecutive training, performing
an identical programme with the same nutritional procedures. Two nutritional supplements
(PRO and CHO, CHO) consumed immediately and 120 minutes after exercise, resulted in
13
elevated GH levels compared to a placebo treatment. [27] However, this did not occur until
six hours post exercise, which may be partially attributed to the different time course of
supplementation. In contrast, other studies have reported no differences in GH responses
to exercise with PRO and CHO [71] or PRO (amino acids) supplementation. [40, 72]
Therefore, it is difficult to determine whether or not supplementation of this nature
enhances the acute GH response to resistance exercise. Comparing the findings of these
studies is again complicated by the different administration procedures for supplementation
(e.g. timing, content, volume, etc.) and hormone sampling procedures (e.g. sampling
period). Given these inconsistencies this is yet another area in need of further research.
2.3 Insulin-like growth factors

The identification of the somatomedins, also known as insulin-like growth factors (IGF),
has added much to our understanding of the endocrine system and its contribution to
muscle growth. Whilst the anabolic role of GH is well established, more recent literature
suggests that the effects of GH may in fact be mediated by the actions of the IGF. [16, 61, 73]
The IGF represent a family of polypeptide growth factors that are produced and released
from the liver, the production and release of these factors being regulated by GH. The
most important of these factors, in the context of resistance exercise-induced adaptation, is
believed to be IGF-1 or somatomedin-C. It was traditionally believed that these factors
were released into the blood and then transported to the target tissue, as per most other
hormones. [73] However, it has been recently suggested that these factors are produced not
only within the liver, but also within the muscle itself in response to various mechanical
stimuli (e.g. tension, stretch, etc.). [74-76] The IGF’s may therefore exert their biological
actions through the blood and within the muscle itself, through autocrine (within muscle
cell) and paracrine (between adjacent muscle cells) release mechanisms. [51, 77] This
section will focus upon the IGF-1 variant of the somatomedin family.

As with most other hormones, resistance exercise is known to alter the concentration of
IGF-1. In the examination of six different loading protocols, Kraemer et al. [30] found that
almost all protocols resulted in increases in IGF-1 at some point during or following
exercise. However, there did not appear to be any clear interaction between the magnitude
of the IGF-1 response and the loading scheme performed. Overall, the acute effects of
resistance exercise upon circulating IGF-1 levels remain equivocal. Whilst some studies
have reported an acute increase in IGF-1 [19, 28, 30, 35] others have reported no such changes.
[27, 28, 36, 64, 78]
The inconsistency in these findings may be partly attributed to large
individual variability in these responses. Differences in circulating concentrations may be
another point to consider with active subjects (male and female) demonstrating
significantly higher levels of IGF-1 than sedentary subjects. [35] Perhaps a more valid
explanation would lie in the fact that the IGF’s are released through both systemic (blood)
and local (muscle) pathways. Consequently, the measurement of these factors in the blood
alone may not adequately reflect the responsiveness of the somatomedins to the weight-
training stimulus. It is also possible that the influence of resistance exercise upon the
secretion of this growth factor lies not in the circulating levels of IGF-1, but rather the
manner in which IGF-1 is partitioned among its family of binding proteins. [78] Further
research (in vivo and in vitro) is needed to contribute to our understanding of the
responsiveness of these growth factors to the weight training stimulus and the importance
of such responses to subsequent adaptation.
14
2.3.2 Gender
It is unclear whether or not the IGF-1 response to the weight-training stimulus is
influenced by gender. Age-matched males and females each performed two identical
exercise protocols (hypertrophy and neuronal) using the same relative loads. [19] In
response to the hypertrophy scheme, an increase in IGF-1 was observed in both males and
females; however, no differences were found between groups at any time. When
performing the neuronal scheme the males reported a significant increase in IGF-1
immediately post exercise, whilst the females demonstrated a significant increase at 60
minutes post exercise. The authors commented that the one-hour sampling period used in
this study was insufficient to adequately characterise the IGF-1 response, given that the
production of this factor may not peak until three to nine hours later [19]. In terms of
resting concentrations, the range of IGF-1 values reported within research appear
somewhat similar between males (13-27 nmol/L) [19, 26, 28, 30, 34, 79] and females (14-20
nmol/L). [19, 36, 55, 79] Unfortunately, little research has directly compared the resistance
exercise-induced response of the somatomedins between males and females. Further study
is therefore needed to clarify if any gender differences exist in the IGF-1 response to a bout
of resistance exercise.
2.3.3 Nutrition
The interaction between nutritional supplementation and the somatomedin response to
resistance exercise has received little attention. Kraemer et al. [33] found CHO and PRO
supplementation to increase pre-exercise levels of IGF-1 on days two and three, following
three consecutive days of training. However, no changes (from baseline) were found in the
acute response to exercise on any of these days. This observation is supported by the
findings of Chandler [27] when examining the effect of three different treatments (CHO,
PRO, PRO and CHO). These initial findings suggest that this type of supplementation has
little influence upon IGF-1 responses to an acute bout of resistance exercise. In spite of
this, there may be some benefits for CHO and/or PRO supplementation, as a function of
enhanced resting concentrations (pre-training) of this hormone. [33] It is interesting to note
that both of these studies found the acute IGF-1 response to be independent of GH
responses, itself a regulator for the release of the somatomedins. This may be attributed to
the time lag between GH release and subsequent stimulation of IGF-1, which is thought to
occur 16-28 hours after GH-stimulated release. [80] Such a notion is partially supported by
the data provided by Kraemer et al. [33] Still, interpretation of any data in this area is likely
to be limited by the different release mechanisms of these growth factors.
2.4 Insulin
Insulin is also known to have a strong anabolic effect upon muscle tissue [16]. Released
from the beta cells of the islets of Langerhans within the pancreas, the primary role of
insulin, in conjunction with the hormone glucagon, is to regulate blood glucose
concentrations and the metabolism of fatty acids. A secondary role of insulin is to increase
the uptake of CHO and amino acids into the muscle cell [16, 81] and in this capacity insulin
plays an important role in the accretion of muscle protein and muscle growth thereafter.
The release of insulin may further aid the physiological process of muscle growth by
suppressing the degradation of muscle protein post exercise. [81] Whilst the actions of the
other anabolic hormones would appear to directly influence cellular reactions and protein
accretion, by either binding directly inside the cell (steroid hormones) or to the cell
membrane (peptide hormones), the actions of insulin mediate the adaptive processors
involved in tissue regeneration and growth. Still, it has been suggested that the
effectiveness of insulin, as an anabolic agent, is also highly dependent upon the rate of
appearance of amino acids in the intracellular compartment of the muscle. [82]
15
Whilst insulin has been implicated in muscle growth, repair and recovery, much less data is
available concerning the response of this anabolic hormone to different loading schemes.
Taking into account the effect of different nutritional supplements, it would appear that
hypertrophy schemes have little effect upon circulating insulin levels post exercise (see
Table II). Much less data is available to characterise the insulin response to different
neuronal and power loading schemes. Therefore, it is suggested that the acute insulin
response to the different schemes be examined in order to clarify the role of this hormone
in weight-training induced adaptation, in particular muscular strength and power.
2.4.2 Age
It may be speculated that greater resting concentrations of insulin are found in older adults,
as increase in age is often associated with higher blood glucose levels (increase glucose =
increase insulin). [42, 83] The findings of Kraemer et al. [43] lend some support to such a
notion, with elderly males (62years) having greater resting concentrations of both insulin
and glucose than younger males (30years). After the performance of an acute bout of
exercise, a significant reduction in insulin (immediately post) followed by a return to
baseline levels, was observed in the older group. In contrast, the younger group did not
exhibit any significant changes in insulin across the sampling period. The practical
significance of this result, in terms of protein accretion post exercise, is unknown. In terms
of health benefits, such a response may help regulate insulin activity and support
suggestions that weight training may be used as a tool for improving insulin sensitivity for
elderly populations. [83, 84] Due to a lack of scientific data the responsiveness of this
hormone to resistance exercise and the interaction with factors such as age, training status
and gender, remains largely unknown. Examination of these interactions would also
provide greater understanding as to the contribution of this anabolic hormone to resistance-
training induced adaptation.
2.4.3 Nutrition
Nutrition plays a key role in mediating the anabolic effects of insulin. The ingestion of
CHO would result in elevated insulin levels and in the presence of PRO (increased amino
acid availability) would promote greater protein anabolism post exercise. [60, 85] A recent
study [71] examined the effect of a PRO and CHO supplement taken immediately after the
performance of three different workouts. That is, workouts characterised by low, moderate
or high training volume. Supplementation produced a mean increase of 300% in insulin
levels across these workouts (from baseline), whereas no changes were found across the
placebo groups. The findings of other studies are in agreement [27, 33, 60, 86, 87], having
observed greater levels of circulating insulin post workout with a combination of CHO and
PRO (or amino acids). Furthermore, administration of CHO and PRO pre- exercise may
elicit a greater response than post- exercise consumption. [60] In fact, the administration of
CHO alone has also been found to improve the insulin response to resistance exercise [88-90]
and produce a more favourable environment for muscle growth (i.e. reduce myofibrillar
protein breakdown). [89, 90] However, it would appear that CHO and PRO combined
produce superior results than either alone. [87] These data reveal the effectiveness of
different nutritional strategies upon the insulin response to resistance exercise, in particular
the use of CHO and PRO, and taken before exercise. Examination of long-term strategies
is now required to determine the importance of nutritional supplementation and acute
responses to adaptation, with emphasis upon target tissue effects.
16
2.5 Cortisol
Cortisol is the primary member of a family of steroid hormones called glucocorticoids.
Released from the adrenal cortex by way of the hypothalamic-pituitary-adrenal (HPA)
axis, cortisol is generally thought to inhibit muscle growth by decreasing protein synthesis
and increasing the break down of muscle protein. [38, 91] The anti-anabolic properties of
cortisol are also related to its attenuation of other anabolic hormones such as TST and GH.
[14]
Corticosterone is the other glucocorticoid of interest; however, it is generally thought
to be less potent than cortisol and believed to account for around 4-5% of total
glucocorticoid activity. [91] Thus, this section will focus upon the primary glucocorticoid,
cortisol. As increased cortisol levels are often linked to various stressors (e.g. exercise,
disease, trauma, over-training, etc.) cortisol is also considered one of the primary stress
hormones. [92, 93] For this reason cortisol is often used within research and practice as a
marker of over-training. [92, 94] As a steroid hormone cortisol is found in a number of
forms. In blood more than 90% of the glucocorticoids are bound with plasma proteins,
mainly with cortisol binding globulin (CBG) and the rest with albumin. [91] Approximately
1-2% of the circulating steroid levels make up the free hormone component. [91] Again, the
relative importance of the different fractions of cortisol has not yet been determined.

It can be observed that the stimulus afforded by a single hypertrophy scheme generally
elicits a greater stress response, as indicated by an increase in cortisol, than that found after
a neuronal scheme (see Tables I and II). Kraemer et al. [36] compared the hormonal
response among a group of trained females to a hypertrophy scheme (3 sets x 10
repetitions, 10RM, 1 minutes rest) and a neuronal scheme (3-5 sets x 5 repetitions, 5RM, 3
minutes rest). Whilst no changes in cortisol were found after the performance of the
neuronal scheme, following the hypertrophy scheme a 125% increase in cortisol was
observed. This result is again supported by other research [20, 63, 95], indicating that
programme design can modulate the acute cortisol response to resistance exercise.
Dynamic power schemes have also been shown to elicit acute increases in cortisol,
although not to the extent of that found after the performance of a typical hypertrophy
scheme. On average the cortisol response across the hypertrophy schemes reviewed (45%)
is much greater than the dynamic power schemes (19%). Although most studies have
reported no change in circulating cortisol across the neuronal schemes, one study [26]
reported a large decrease, resulting in an overall reduction in circulating cortisol (-8%).
Whilst such a finding appears to be a novel response, this is one of the few studies that has
compared hormonal response patterns to control data and collected multiple samples.
2.5.2 Gender
Although many of the anabolic hormones are characterised by differential exercise-induced
responses as a function of gender, cortisol activity appears to be similar between males and
females. Research has generally found no gender differences in the cortisol response (%)
to a bout of resistance exercise. [23, 35, 44, 96] Kraemer and colleagues [37] also found no
significant differences in the cortisol response among males and females to a single
exercise bout, performed before and after eight weeks of heavy resistance training.
McGuigan, Egan and Foster [96] examined the salivary cortisol response to two different
protocols (6 sets x 10 repetitions with either 70% 1RM or 30% 1RM). Each protocol was
performed with a squatting exercise and a bench press exercise. No significant differences
were observed between males and females for any of the cortisol responses. The ratings of
perceived exertion (RPE) for each session also revealed no significant differences between
groups. Therefore, the stimulus afforded by this type of exercise would appear to elicit
similar stress responses for both males and females. The resting concentrations of cortisol
17
reported for males (300-600nmol/L) [22, 23, 32, 33, 35, 37, 43-45, 52, 58, 71, 79, 97] and females (260-
550nmol/L) [23, 25, 35-37, 44, 52, 66, 79] also appear similar. Given these findings it may be
speculated that gender differences relating to the accretion of muscle protein, as a function
of weight training, may lie in the differential responses of the anabolic hormones rather
than the catabolic hormones. With most studies examining women in the follicular phase
of menstruation [19, 23, 36, 37, 65, 66], the effect of resistance exercise on hormone release in
different phases of the menstrual cycle is another area warranting investigation.
2.5.3 Age
Whilst the stimulus of resistance exercise is known to elicit a stress response (increase in
cortisol) among both males and females, this response would appear to be much greater in
younger males. Mero and colleagues [25] investigated the hormonal response among
pubescent boys and men, each performing a half squat exercise session with two rest
periods (1- or 4-minutes). Whilst the boys reported significant increases in serum cortisol
to both rest periods, no changes were found in the adult males. Pullinen et al. [23] compared
the hormonal response to a single exercise bout (5 sets x 10 knee extensions, 40% 1RM)
followed by two sets to exhaustion, among men, women and pubescent boys. Only the
boys revealed an acute increase in serum cortisol post exercise. Furthermore, peak
epinephrine concentrations, another stress hormone, were found to be twice as high in this
group as compared to men and women. These data are indicative of a greater stress
response among younger males to the stimulus of weight training. This may be partly
explained by differences in endocrine function between pubertal and adult males, such as
lower resting hormone levels. [98] It has been further suggested that differences in
maturation, anxiety and adaptive capability to resistance exercise may be important factors
in this respect. [23] With younger males having a larger catabolic (cortisol) and lower
anabolic (TST) response to resistance exercise, it is not surprising that this group do not
exhibit the changes in muscle mass often seen with weight training in adult males.
Adults of any age would appear to have similar cortisol responses to resistance exercise.
No differences were found in the post exercise response between males (30years and
70years) or between females (30years, 50years and 70years) to a single exercise bout. [44]
Some of this data may however be masked by diurnal fluctuations, as indicated by data
reported on a non-exercising control day. Another study examined the endocrine response
between two groups of males (26years and 70years), each performing three exercise
treatments (lower body, upper body, lower and upper body). [45] No differences were
found between groups in the cortisol response to any of the three treatments. Irrespective
of gender, pre-test levels of cortisol reported within research also appear similar between
adults (225-580nmol/l) [20, 22-26, 28, 31-34, 36, 37, 58, 66, 70, 95, 99] and the elderly 300-550nmol/l. [34,
43-45, 97]
Although no significant differences were found between the different age groups
[44, 45]
, it is important to recognise that the interventions performed did not result in any
significant changes in cortisol. Thus, comparing gender-related stress responses with
programmes that did not sufficiently stimulate the HPA axis may be fundamentally flawed.
Some studies have reported training-related cortisol responses in adults of varying age.
Kraemer et al. [34] found no differences between two groups of untrained males (30years
and 62years) when examining acute cortisol responses. However, after ten weeks of heavy
resistance training a lowered cortisol response was found in the younger group (80% v
50% respectively) to the same exercise protocol. Changes in exercise-induced cortisol
levels after exercise, may be mediated by a reduction in adrenocorticotrophic hormone
responses to the stress of resistance exercise. [34] The combined influence of training status
and age presents other hormonal interactions that may be important to adaptation, though
beyond the scope of this review.
18
Given that stress is relative by nature determining the influence of training status upon the
acute cortisol response is difficult. For example, a similar cortisol response was reported
by resistance-trained (380%) and sedentary males (380%) to an exercise bout, although the
loads utilised were vastly different. [56] This is partially supported by the data reviewed
with similar cortisol responses reported by trained (44%) and untrained (37%) males
performing a hypertrophy session (see Table II). Similarly, other research have reported
either small or no changes in the exercise-induced cortisol responses after periods of
weight training [28, 37], or demonstrated that training experience does not influence acute
cortisol responses. [39, 49] Therefore, the cortisol response to a given weight training session
would appear independent of training experience. Other research have however reported a
greater cortisol response in untrained individuals [70], which may be due to a lesser-trained
state of untrained (e.g. strength, fatigability, etc.). The higher cortisol response may also
be the result of greater perception of stress among those with no training experience even
though they exercised at the same relative load. [70] Another study reported a lowered
exercise-induced cortisol response (after 10 weeks training) in young males but an
increased response among elderly males. [34] This may again be explained by the complex
interaction of hormonal factors with age, gender and training status. In terms of
adaptation, the importance of these acute responses is difficult to determine as a reduction
in baseline cortisol levels with weight training [28, 34, 37, 97, 100] may also prove beneficial.
2.5.5 Nutrition
Whilst nutrition appears to play an important role in regulating many of the acute anabolic
hormonal responses, it appears to be less important in determining catabolic hormone
activity post exercise. A study by Thyfault et al. [88] examined the effects of two nutritional
interventions, either a CHO or placebo supplement, taken ten minutes prior and
immediately after an exercise bout. A similar increase in cortisol was observed in both
groups with no significant differences between CHO and placebo treatments. [88] Other
studies have also reported little or no change in the cortisol response to a single exercise
bout with nutritional supplementation. [33, 40, 71] However, when comparing the hormonal
response to three consecutive days of the same programme, a diminished cortisol response
was found over days two and three with PRO and CHO supplementation. [33] The practical
significance of this is unclear as supplementation increased the cortisol response on day
one (i.e. increased protein degradation), as compared to the placebo group. The reported
changes over days two and three were not different from that reported in the placebo
groups. This information may prove beneficial for those individuals likely to suffer from
over-training or subject to a high volume of training within a short time frame.
2.6 Limitations of research

One of the difficulties in examining research in this area is the fact that a large number of
studies have performed only a single assay post exercise to determine the hormonal
response to resistance exercise. [21-23, 25, 28, 45, 53, 54, 57, 58, 99, 101, 102] Due to the continual
secretion of most hormones, frequent sampling is needed to adequately characterise the
actual dynamics of the hormonal response to the stimulus of resistance exercise. In
addition, other studies [20, 27, 44, 70, 78, 88, 103, 104] are characterised by long sampling periods
(i.e. every hour or greater) post exercise, which may also be insufficient in characterising
the exercise-induced response of the endocrine system. It is therefore suggested that
research in this area adopt a more systematic approach in the extraction and analysis (i.e.
more samples, longer sampling time, more hormones, etc.) of hormone samples when
evaluating the acute endocrine response to the stimulus of weight training. Such an
analysis would no doubt prove beneficial to researchers and practitioners alike.
19
Another difficulty in extrapolating research findings is the fact that few studies have
compared the exercise-induced hormone response to control data (see Tables I and II).
This is important as many hormones (e.g. TST, cortisol, GH) are known to exhibit a
circadian rhythm throughout a given day [61, 101, 104-108]; therefore, hormonal data that
appears to be responsive to a particular stimulus may in fact be an artefact of the normal
circadian pattern of hormone release. Such an analysis may be further confounded by the
pulsatile secretion of some hormones (e.g. GH). [61, 108] Plasma volume shifts during
exercise present others problems when interpreting data in this area. The change in plasma
volume during resistance exercise is mainly due to an accumulation of lactate and other
metabolites in the muscles. Such an alteration in the muscular environment produces an
osmotic effect, causing water to flow out of the vascular compartment. [109, 110] Previous
studies have indicated significant changes in blood borne TST concentrations after exercise
[23, 69]
; however, when accounting for a reduction in plasma volume the exercise-induced
hormone responses become non-significant. Thus, those studies that do not account for
plasma volume shifts during exercise may in fact report data that is artificially elevated.
The extraction and analysis of hormone samples from the different bodily fluids (e.g.
saliva, blood plasma, blood serum, etc.) also warrants some consideration. Saliva for
example, is a relatively new tool in the measurement of hormones within strength and
conditioning research. The measurement of steroid hormones has been validated
repeatedly in this medium. [111-123] Compared to muscle and blood sampling techniques,
saliva offers an easy compliant method that can be applied frequently and is a less stressful
mechanism for fluid collection. [124] A further benefit of salivary analysis is the fact that
only the unbound or free hormone component is thought to partition across blood into
saliva. [91] Thus, the measurement of steroid hormones in saliva reflects the biologically
active component [112, 114, 125, 126], which is advantageous as the majority of studies in this
area continue to examine total steroid concentrations in the blood (see Tables I and II).
Despite the advantages that saliva offers there are limitations. The contamination of saliva
with blood due to small lacerations would falsely increase the saliva hormone level.
Salivary protein from the mucosa may also interfere with the processing of saliva samples.
[127]
There also remains much work to be done in order to fully understand the partitioning
of hormones between blood and saliva (e.g. time lag, influence of flow rate, etc.),
particularly under exercise-induced conditions.
Some of the technical issues relating to the analysis of hormone samples have been
highlighted in other literature. [61, 127] For example, the different antibodies used by the
suppliers and the specificity of different antibodies within these kits (e.g. polyclonal v
monoclonal) may produce some cross-reactivity and elicit discrepant results when
evaluating exercise-related hormonal responses. [127] It is therefore important to note what
cross reacts with a particular assay and interpret those results accordingly. The analysis
procedures employed to assess hormone concentrations (e.g. radioactive-immunoassay,
enzyme-linked immunoassay, high performance liquid chromatography, bioassays, etc.)
also requires some careful consideration. That is, the different analysis techniques may
differ in terms of their sensitivity for hormone measurement in the various bodily fluids.
[127]
One must remain cognizant of such issues when interpreting research in this area.
2.7 Implications for strength and power development

The endocrine response to resistance exercise plays an important role in facilitating
changes in maximal strength and power through morphological adaptation. In conjunction
with various mechanical stimuli (e.g. high forces, time under tension, stretch, etc.) the
interaction of the anabolic and catabolic hormones assist in the remodelling of muscle
20
tissue (i.e. protein synthesis and degradation) post exercise. Over time a net increase in
protein synthesis would result in an increase in muscle fibre area and thereby lead to
greater CSA of the gross muscle. Given that force generation is a function of muscle CSA,
such an adaptation (i.e. increase muscle CSA) would enable a muscle to exhibit greater
potential for muscular strength and power. The stimulus of resistance exercise is also
known to modulate the “quality” of muscle protein synthesized [128, 129]. However, less is
known about such changes and their contribution to the expression of maximal strength
and power.
Resistive exercise programmes that are typically used for hypertrophy elicit hormonal
responses that would appear important for morphological adaptation to occur. The
anabolic environment (increase in TST and GH) afforded by hypertrophy schemes appears
conducive to the accretion of protein post exercise. In particular, the increase in GH is
much greater than the other loading schemes. Although training in this manner appears to
have little effect upon insulin and IGF-1, relatively little is known about their acute
response to resistance exercise. Interestingly, programmes designed to induce muscle
growth also elicit the largest cortisol or catabolic responses. Such a response would
contribute to greater protein degradation post exercise and thereby inhibit muscle growth.
However, in breaking down muscle protein the catabolic actions of the glucocorticoids
may also create an increased pool of amino acids for protein synthesis to occur or increase
protein turnover rate in previously active muscles during the recovery period. [91] Thus, an
elevation in circulating cortisol may in fact aid the remodelling of muscle tissue. Although
the actions of cortisol have yet to be fully elucidated, the much larger anabolic responses
found with this type of training may still account for any catabolic effects of cortisol and
lead to greater protein synthesis post exercise.
Table I. Summary of research on acute anabolic and catabolic hormone responses to

hypertrophy, neuronal and dynamic power schemes.
Hypertrophy Neuronal Dynamic power

Testosterone   
GH   
IGF-1   
Insulin   
Cortisol   
 indicates increase;  indicates decrease,  indicates no change or equivocal results
The number of arrows indicates the magnitude of each hormone response (relative across
schemes). GH = growth hormone; IGF-1 = insulin growth-like factor 1
The heavy load-neuronal type schemes generally resulted in much smaller anabolic
responses (TST and GH) than the hypertrophy schemes. This was accompanied by much
smaller cortisol responses, collectively suggesting that those processors involved in the
remodelling of muscle tissue are less likely to occur. Again, the IGF and insulin response
to such schemes remains largely unknown. Given the relatively small hormonal responses
it may be speculated that training in such a manner (i.e. heavy loads, long rest periods, low
total work) is less likely to result in substantial protein accretion compared to hypertrophy
21
type schemes. This supports the notion that neuronal type training is thought to contribute
to maximal strength through neural rather than morphological adaptation. [130] Such a
notion is also evident in the fact that different strength athletes (i.e. bodybuilders and
powerlifters/Olympic lifters) are characterised by different morphological profiles [131-134],
which may be partially attributed to the different type of training regimes performed and
the associated hormonal responses.
The dynamic power loading schemes revealed a slightly greater TST response than the
hypertrophy schemes. This suggests some possible contribution of androgen activity to
subsequent adaptation. However, determining the responsiveness of the other anabolic
hormones (i.e. GH, IGF-1 and insulin) was hindered by the lack of data in this area.
Cortisol is responsive to these types of programmes. A larger stress response was found in
comparison to the neuronal schemes, although not to the extent found in the hypertrophy
schemes. With the information at hand it is difficult to determine the importance of the
hormonal stimulus for such training methods. Still, it may be that other mechanical factors
(e.g. forces, time under tension, etc.) are of greater importance in determining whether
morphological adaptation will occur. For instance, endurance exercise is known to
produce significant increases in circulating hormone levels and of similar magnitude to
hypertrophy schemes [107, 135-138]; however, this type of exercise does not generally result in
any substantial changes in muscle size. This may be due to the mechanical stress afforded
by a given loading scheme (e.g. forces, work, etc.), which may be the major determinant
for morphological adaptation to occur. These are likely to be quite different between the
hypertrophy and dynamic power loading schemes, in spite of the similar TST responses.
The contribution of the hormonal stimulus is based upon the premise that an increase in
blood borne hormone levels increases the likelihood of cellular reactions [15, 17] and
adaptation (protein accretion) thereafter. Still, the endocrine system is highly complex and
many issues remain unresolved with regards to skeletal muscle and mechanisms for
adaptation. These not only involve release mechanisms, which are the focus for most
investigations, but include many other factors such as hormone clearance rates, changes in
binding proteins, fluid shifts, hormone degradation and hormone-receptor interactions. [15,
17, 51]
The biological actions of the hormone-receptor complex will itself be determined by
several factors such as the receptor domain, number of receptors and receptor binding
sensitivity. [51, 77] Consequently, the level of circulating hormones is only one of many
factors mediating morphological adaptation. The different adaptive mechanisms may
explain the non-responsiveness of those athletes who specifically train to increase muscle
mass or are likely to elicit greater muscle size (i.e. body builders and steroids users).
Although an understanding of the mechanisms for adaptation is important for researchers
and conditioners, it is beyond the scope of this review. This information may be sourced
elsewhere. [51, 77] Whilst the various hormones reviewed are important, other hormones
(e.g. catecholamines, thyroid hormones, etc.) may also influence the maintenance of
normal body function and potentially, in the adaptive responses to resistance training.
It is evident that programme design plays an important role in determining the acute
hormonal response to a single bout of resistance exercise. Still, other factors such as
training status, type of training experience, gender, age, nutrition and genetic
predisposition, may further influence the hormonal responses to a single training session.
Whether or not these differential responses contribute to, or otherwise, inhibit muscular
adaptation is not yet known. It would therefore appear that those processors involved in
muscle tissue growth are a complex function of not only programme design, but also other
lifestyle, nutritional and genetic factors. Such is the nature of weight training where a
22
multitude of adaptive strategies exist for the development of muscle growth. It is also
recognised that the practical significance of the hormone responses to the different
schemes (peak as a % from baseline) provides only a discreet value for interpretation. The
importance of these values compared to absolute circulating levels, temporal changes or
area under curve responses, warrants further investigation. As intimated throughout this
review there are also a number of other areas in need of further research and interactions to
be addressed. It is further suggested that research adopt a more systematic approach in the
extraction and analysis of hormone samples. Such an analysis would enhance
understanding in this area and improve the prescription of resistance exercise for strength
and power development.
3. Conclusion
It is apparent that the contribution of the endocrine stimulus to strength and power has not
yet been fully elucidated. The configuration of the various loading schemes (i.e.
hypertrophy, neuronal or dynamic power) imposed a specific activation pattern and
resulted in different acute hormonal responses. However, understanding in this area is still
limited by the lack of scientific data, particularly in the examination of the hormonal
responses to neuronal and dynamic power schemes. Data regarding insulin and IGF-1
responses to resistance exercise are largely non-existent, across all schemes. The
interaction of acute hormone responses with factors such as age, gender, nutrition and
training status, requires further investigation. It is also suggested that research adopt a
more systematic approach (i.e. more samples, longer sampling time, etc.) when evaluating
hormonal changes, in order to adequately characterise the endocrine response to exercise.
Unresolved issues with regards to skeletal muscle and mechanisms for adaptation also
make interpretation of research difficult. Collectively, such information would provide
better understanding as to the importance of the endocrine system to adaptation and
thereafter, enable resistance exercise to be prescribed more effectively for inducing
changes in strength and power.
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Possible stimuli for strength and power adaptation: Acute hormonal

responses. Sports Med. 2006;36(3):215-38

Blair Crewther1,2, Dr John Cronin1, Justin Keogh1 & Dr Christian Cook2

Recreation, Auckland University of Technology, Auckland 1020, New Zealand

New Zealand Institute of Sport and Recreation Research

Division of Sport and Recreation,

Auckland University of Technology,

Private Bag 92006,

Phone: 649 917 9999 ext 7119

Facsimile: 649 917 9960

2. Acute hormonal response to resistance exercise

2.1.1 Programme design

References Subjects (age) Protocols Hormone (% or fold change)

References Subjects (age) Protocols Hormone (% or fold change)

2.1.4 Training status

2.2 Growth hormone

2.2.1 Programme design

2.2.4 Training status

2.3 Insulin-like growth factors

2.3.1 Programme design

2.5.1 Programme design

2.6 Limitations of research

2.7 Implications for strength and power development

Table I. Summary of research on acute anabolic and catabolic hormone responses to

Hypertrophy Neuronal Dynamic power

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