Possible stimuli for strength and power adaptation: acute hormonal responses

Possible stimuli for strength and power adaptation: Acute hormonal

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

Blair Crewther1,2

, Dr John Cronin1, Justin Keogh

1 & Dr Christian Cook

2

1New Zealand Institute of Sport and Recreation Research, Division of Sport and

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

2Human 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: [email protected]

2

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.

3

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

2.3.1 Programme design ............................................................................................ 14

2.3.2 Gender .............................................................................................................. 15

2.3.3 Nutrition ........................................................................................................... 15

2.4 Insulin .............................................................................................................. 15

2.4.1 Programme design ............................................................................................ 16

2.4.2 Age ................................................................................................................... 16

2.4.3 Nutrition ........................................................................................................... 16

2.5 Cortisol ............................................................................................................. 17

2.5.1 Programme design ............................................................................................ 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

4

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.

5

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.

Table II. Acute hormonal response to hypertrophy schemes.

References Subjects (age) Protocols

Exercise/s - sets x reps (load)

Hormone (% or fold change)

TST GH IGF-1 Insulin Cortisol

Vanhelder et al. [139]

5 Males - UT 1 ex - 7 x 10 (10RM) - - - ~10 ~80

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

8 ex - 2 x 8-10 (75% 1RM) PRO

8 ex - 2 x 8-10 (75% 1RM) CHO

8 ex - 2 x 8-10 (75% 1RM) CHO + PRO

~20

~12

~20

~20

~700

~900

~820

~900

Nil

Nil

Nil

Nil

~20

~230

~560

~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)

8 Males - UT (47yr)

8 Males - UT (68yr)

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

9

15

Nil

200 fold

19 fold

Nil

-

-

-

-

-

-

Nil

~80

Nil

Hakkinen & Pakarinen [44]

8 Females - UT (25yr)

7 Females - UT (48yr)

8 Females - UT (68yr)

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

Nil

18

Nil

200

20 fold

Nil

-

-

-

-

-

-

Nil

Nil

Nil

Mulligan et al. [66]

10 Females - T 8 ex - 1 x 10 (10RM)

8 ex - 3 x 10 (10RM)

-

- ~60

~500

-

-

-

- ~20

~175

Gotshalk et al. [32]

8 Males - T 8 ex - 1 x 10 (10RM)

8 ex - 3 x 10 (10RM) ~14

~32

~350

~700

-

-

-

- ~10

~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

7

Kraemer et al. [43]

8 Males - UT (30yr)

8 Males - UT (62yr)

1 ex - 4 x 10 (10RM)

1 ex - 4 x 10 (10RM) ~38 ( 40)

1

~20 ( 26)1

~16 fold

~230

-

-

-

- ~78

~45

Kraemer et al. [34]

8 Males - UT (30yr)

9 Males - UT (62yr)

1 ex - 4 x 10 (10RM)

1 ex - 4 x 10 (10RM) ~37 ( 29)

1

~23 ( 33)1

~28 fold

Nil

-

-

-

- ~80

~47

Hakkinen et al. [45]

10 Males - UT (26yr)

10 Males - UT (70yr)

2 ex - 4 x 10 (100% MVC) 2

2 ex - 4 x 10 (100% MVC) 2

~27 ( 21)1

Nil ( 17)1

~29 fold

~14 fold

-

-

-

-

Nil

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)

11 Males - UT (70yr)

11 Females - UT (40yr)

10 Females - UT (70yr)

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

1 ex - 5 x 10 (10RM) 2

~21

~14

Nil

Nil

~340

~150

~170

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

4 ex - 4 x 10 (75% 1RM) 2

4 ex - 6 x 10 (75% 1RM) 2

Nil

~10

Nil

~400

~11 fold

~15 fold

-

-

-

-

-

-

Nil

~28

~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

8 ex - 3 x 10 (85-90%1RM) Placebo

-

-

-

-

-

- ~160

~36

~67

~55 1free 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

8

Table III . Acute hormonal response to neuronal and dynamic power schemes.

References Subjects (age)

Protocols

Exercises/s - sets x reps (load)

Hormone (% or fold change) -

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

4 ex - 4 x 5 (88% 1RM) 4

4 ex - 6 x 5 (88% 1RM) 4

Nil

Nil

Nil

Nil

Nil

~500

-

-

-

-

-

-

Nil

Nil

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)

1 ex - 2 x 30 (50% 1RM) ~18-30

~30

-

-

-

-

-

-

-

-

Mero et al. [25]

6 Males - (24 yr)

6 Males - (15 yr)

1 ex - 10 x 6 (50% 1RM) 2

1 ex - 10 x 6 (50% 1RM) 3

1 ex - 10 x 6 (50% 1RM) 2

1 ex - 10 x 6 (50% 1RM) 3

16

18 ( 19)1

Nil

13 ( 11)1

-

-

-

-

-

-

-

-

-

-

-

-

Nil

Nil

67

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 1free 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.

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

10

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

11

(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.

2.2.1 Programme design

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

12

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,

13

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.

2.2.4 Training status

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

14

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.

2.3.1 Programme design

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.

15

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]

16

2.4.1 Programme design

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.

17

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.

2.5.1 Programme design

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

18

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.

19

2.5.4 Training status

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.

20

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

21

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

22

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

23

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.

References 1. MacDougall JD. Hypertrophy or hyperplasia. In: Komi PV, Ed. Strength and power in

sport. Oxford: Blackwell Scientific Publications, 1992, pp. 230-8

2. McDonagh MJN, Davies CTM. Adaptive response of mammalian skeletal muscle to

exercise with high loads. Eur J Appl Physiol 1984; 52: 139-55

3. Lyttle AD, Wilson GJ, Ostrowski KJ. Enhancing performance: Maximal power versus

combined weights and plyometrics training. J Strength Con Res 1996; 10 (3): 173-9

4. Harris GR, Stone MH, O'Bryant HS, et al. Short-term performance effects of high

power, high force, or combined weight-training methods. J Strength Con Res 2000; 14

(1): 14-20

5. Moss BM, Refsnes PE, Abildgaard A, et al. Effects of maximal effort strength training

with different loads on dynamic strength, cross-sectional area, load-power and load-

velocity relationships. Eur J Appl Physiol 1997; 75 (3): 193-9

6. Schmidtbleicher D, Buehrle M. Neuronal adaptation and increase of cross-sectional

area studying different strength training methods. In International Series in

Biomechanics 10; 1987, pp. 615-20

7. Dahl HA, Aaserud R, Jensen J. Muscle hypertrophy after light and heavy resistance

training. Med Sci Sports Exerc 1992; 24 (5): S55

24

8. McBride JM, Triplett-McBride T, Davie A, et al. The effect of heavy- vs. light-load

jump squats on the development of strength, power and speed. J Strength Con Res

2002; 16 (1): 75-82

9. Fatouros IG, Jamurtas AZ, Leontsini JD, et al. Evaluation of plyometric exercise

training, weight training, and their combination on vertical jumping performance and

leg strength. J Strength Con Res 2000; 14 (4): 470-6

10. Adams K, O'Shea JP, O'Shea KL, et al. The effect of six weeks of squat, plyometric

and squat-plyometric training on power production. J Appl Sport Sci Res 1992; 6 (1):

36-41

11. Hoff J, Almasbakk B. The effects of maximum strength training on throwing velocity

and muscle strength in female team-handball players. J Strength Con Res 1995; 9 (4):

225-58

12. Komi P, Hakkinen K. Strength and Power. In: Dirix A, Knuttgen H, and Tittel K, Eds.

The Olympic book of sports medicine. Oxford: Blackwell Scientific Publications, 1988,

pp. 181-93

13. Hakkinen K. Neuromuscular and hormonal adaptations during strength and power

training. J Sports Med Phys Fit 1989; 29 (1): 9-26

14. Deschenes MR, Kraemer WJ. Performance and physiological adaptations to resistance

training. Am J Phys Med Rehab 2002; 81 (11): S3-S16

15. Kraemer W. Influence of the endocrine system on resistance training adaptations. Nat

Strength Conditioning Ass J 1992; 14 (2): 47-54

16. Deschenes MR, Kraemer WJ, Maresh CM, et al. Exercise induced hormonal changes

and their effects upon skeletal muscle tissue. Sports Med 1991; 12 (2): 80-93

17. Kraemer WJ. Endocrine responses and adaptations to strength training. In: Komi PV,

Ed. Strength and power in sport. Oxford: Blackwell Scientific Publications, 1992, pp.

291-304

18. Loebel CC, Kraemer WJ. A brief review: Testosterone and resistance exercise in men.

J Strength Con Res 1998; 12 (1): 57-63

19. Kraemer WJ, Gordon SE, Fleck SJ, et al. Endogenous anabolic hormonal and growth

factor responses to heavy resistance exercise in males and females. Int J Sport Med

1991; 12 (2): 228-35

20. Hakkinen K, Pakarinen A. Acute hormonal responses to two different fatiguing heavy-

resistance protocols in male athletes. J Appl Physiol 1993; 74: 882-7

21. Mero A, Komi VP, Kyllonen A, et al. Acute EMG, force and hormonal responses in

male athletes to four strength exercise units. J Biomech 1991; 25 (7): 752

22. Volek J, Kraemer WJ, Bush J, et al. Testosterone and cortisol relationship to dietary

nutrients and resistance exercise. J Appl Physiol 1997; 82 (1): 49-54

23. Pullinen T, Mero A, Huttunen P, et al. Resistance exercise-induced hormonal

responses in men, women, and pubescent boys. Med Sci Sports Exerc 2002; 34 (5):

806-13

24. McMurray RG, Eubank TK, Hackney AC. Nocturnal hormonal responses to resistance

exercise. Eur J Appl Physiol 1995; 72: 121-6

25. Mero A, Pullinen T, Komi PV, et al. Biomechanical and hormonal responses to two

high intensity strength exercise units with different recovery in pubertal and adult male

athletes. In International Society of Biomechanics; 1993; Paris, France, pp. 866-7

26. Raastad T, Bjoro T, Hallen J. Hormonal responses to high- and moderate-intensity

strength exercise. Eur J Appl Physiol 2000; 82 (1/2): 121-8

27. Chandler RM, Byrne HK, Patterson JG, et al. Dietary supplements affect the anabolic

hormones after weight-training exercise. J Appl Physiol 1994; 76 (2): 839-45

25

28. McCall GE, Byrnes WC, Fleck SJ, et al. Acute and chronic hormonal responses to

resistance training designed to promote muscle hypertrophy. Can J App Physiol 1999;

24 (1): 96-107

29. Schwab R, Johnson GO, Housh TJ, et al. Acute effects of different intensities of

weight lifting on serum testosterone. Med Sci Sports Exerc 1993; 25 (12): 1381-5

30. Kraemer WJ, Marchitelli LJ, Gordon SE, et al. Hormonal and growth factor responses

to heavy resistance exercise protocols. J Appl Physiol 1990; 69: 1442-50

31. Smilios I, Pilianidis T, Karamouzis M, et al. Hormonal responses after various

resistance exercise protocols. Med Sci Sports Exerc 2003; 35 (4): 644-54

32. Gotshalk LA, Loebel CC, Nindl BC, et al. Hormonal responses of multiset versus

single-set heavy-resistance exercise protocols. Can J App Physiol 1997; 22 (3): 244-55

33. Kraemer W, Volek J, Bush J, et al. Hormonal responses to consecutive days of heavy-

resistance exercise with or without nutritional supplementation. J Appl Physiol 1998; 85

(4): 1544-55

34. Kraemer WJ, Hakkinen K, Newton RU, et al. Effects of heavy-resistance training on

hormonal response patterns in younger vs. older men. J Appl Physiol 1999; 87 (3): 982-

92

35. Kostka T, Patricot MC, Mathian B, et al. Anabolic and catabolic responses to

experimental two-set low-volume resistance exercise in sendentary and active elderly

people. Aging Clinical and Experimental Research 2003; 15 (2): 123-30

36. Kraemer WJ, Fleck SJ, Dziados JE, et al. Changes in hormonal concentrations after

different heavy-resistance exercise protocols in women. J Appl Physiol 1993; 75: 594-

604

37. Kraemer WJ, Staron R, Hagerman F, et al. The effects of short-term resistance training

on endocrine function in men and women. Eur J Appl Physiol 1998; 78 (1): 69-76

38. Burger ME. Neuromuscular and hormonal adaptations to resistance training:

Implications for strength development in female athletes. Streng Cond J 2002; 24 (3):

51-9

39. Kraemer WJ, Fry AC, Warren BJ, et al. Acute hormonal responses in elite junior

weightlifters. Int J Sports Med 1992; 13 (2): 103-9

40. Fry AC, Kraemer WJ, Stone MH, et al. Endocrine and performance responses to high

volume training and amino acid supplementation in elite junior weightlifters. Int J

Sports Nutr 1993; 3: 306-22

41. Arlt W, Hewison M. Hormones and immune function: implications of aging. Aging

Cell 2004: 209-16

42. Fiatarone Singh MA. Exercise comes of age: Rationale and recommendations for a

geriatric exercise prescription. J Geront A Biol Sci Med Sci 2002; 57A (5): M262-M82

43. Kraemer WJ, Hakkinen K, Newton R, et al. Acute hormonal responses to heavy

resistance exercise in younger and older men. Eur J Appl Physiol 1998; 77 (3): 206-11

44. Hakkinen K, Pakarinen A. Acute hormonal responses to heavy resistance exercise in

men and women at different ages. Int J Sports Med 1995; 16: 507-13

45. Hakkinen K, Pakarinen A, Newton RU, et al. Acute hormone responses to heavy

resistance lower and upper extremity exercise in young versus old men. Eur J Appl

Physiol 1998; 77: 312-9

46. Hopp JF. Effects of age and resistance training on skeletal muscle: A review. Phys

Ther 1993; 73: 361-73

47. Lexell J, Taylor CC, Sjostrom M. What is the cause of the ageing atrophy? J Neuro Sci

1988; 84: 275-94

48. Vermeulen A, Rubens R, Verdonck L. Testosterone secretion and metabolism in male

senescence. J Clin Endocrinol 1972; 34: 730-5

26

49. Ahtiainen JP, Pakarinen A, Kraemer WJ, et al. Acute hormonal responses to heavy

resistance exercise in strength athletes versus nonathletes. Can J App Physiol 2004; 29

(5): 527-43

50. Hakkinen K, Pakarinen A, Alen M, et al. Neuromuscular and hormonal adaptations in

athletes to strength training in two years. J Appl Physiol 1988; 65 (6): 2406 - 12

51. Kraemer WJ. Endocrine responses to resistance exercise. In: Baechle TR and Earle

RW, Eds. Essentials of strength training and conditioning. Champaign, Illinois: Human

Kinetics, 2000

52. Hakkinen K, Kraemer WJ, Pakarinen A, et al. Effects of heavy resistance/power

training on maximal strength, muscle morphology, and hormonal response patterns in

60-75-year old men and women. Can J App Physiol 2002; 27 (3): 213-31

53. Nicklas BJ, Ryan AJ, Treuth MM, et al. Testosterone, growth hormone and IGF-1

responses to acute and chronic resistive exercise in men aged 55-70 years. Int J Sports

Med 1995; 16 (7): 445-50

54. Hakkinen K, Pakarinen A, Kraemer WJ, et al. Basal concentrations and acute

responses of serum hormones and strength development during heavy resistance

training in middle-aged and elderly men and women. J Geront A Biol Sci Med Sci

2000; 55A (2): B95-B105

55. Hakkinen K, Pakarinen A, Kraemer WJ, et al. Selective muscle hypertrophy, changes

in EMG and force, and serum hormones during strength training in older women. J

Appl Physiol 2001; 91: 569-80

56. Tremblay MS, Copeland JL, Van Helder W. Effect of training status and exercise

mode on endogenous steroid hormones in men. J Appl Physiol 2004; 96: 531-9

57. Bosco C, Colli R, Bonomi R, et al. Monitoring strength training: Neuromuscular and

hormonal profile. Med Sci Sports Exerc 2000; 32 (1): 202-8

58. Boone JB, Lambert CP, Flynn MG, et al. Resistance exercise effects on plasma

cortisol, testosterone and creatine kinase activity in anabolic-androgenic steroid users.

Int J Sport Med 1990; 11 (4): 293-7

59. Rozenek R, Rahe CH, Kohl HH, et al. Physiological responses to resistance-exercise

in athletes self-administering anabolic steroids. J Sports Med Phys Fit 1990; 30 (4):

354-60

60. Tipton KD, Rasmussen BB, Miller SL, et al. Timing of amino acid-carbohydrate

ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol

Endocrinol Metab 2001; 281: E197-E206

61. Widerman L, Weltman JY, Hartman ML, et al. Growth hormone release during acute

and chronic aerobic and resistance exercise. Sports Med 2002; 32 (15): 987-1004

62. Baumann G. Growth hormone heterogeneity: genes, isohormones, variants, and

binding proteins. Endocr Rev 1991; 12 (4): 424-49

63. Zafeiridis A, Smilios I, Considine RV, et al. Serum leptin responses after acute

resistance exercise protocols. J Appl Physiol 2003; 94: 591-7

64. Bosco C, Tihanyi J, Rivalta L, et al. Hormonal responses in strenuous jumping effort.

Jpn J Physiol 1996; 46: 93-8

65. Taylor JM, Thompson HS, Clarkson PM, et al. Growth hormone response to an acute

bout of resistance exercise in weight-trained and non-weight-trained women. J Strength

Con Res 2000; 14 (2): 220-7

66. Mulligan SE, Fleck SJ, Gordon SE, et al. Influence of resistance exercise volume on

serum growth hormone and cortisol concentrations in women. J Strength Con Res 1996;

10 (4): 256-62

67. Tsolakis C, Vagenas G, Dessypris A. Growth and anabolic hormones, leptin, and

neuromuscular performance in moderately trained prepubescent athletes and untrained

boys. J Strength Con Res 2003; 17 (1): 40-6

27

68. Pyka G, Wiswell RA, Marcus R. Age-dependent effect of resistance exercise on

growth hormone secretion in people. J Clin Endocrinol Metab 1992; 75 (2): 404-7

69. Kraemer RR, Kilgore JL, Kraemer GR, et al. Growth hormone, IGF-1, and

testosterone responses to resistive exercise. Med Sci Sports Exerc 1992; 24 (12): 1346-

52

70. McMillan JL, Stone MH, Sartin J, et al. 20-hour physiological responses to a single

weight-training session. J Strength Con Res 1993; 7 (1): 9-21

71. Williams AG, Ismail AN, Sharma A, et al. Effects of resistance exercise volume and

nutritional supplementation on anabolic and catabolic hormones. Eur J Appl Physiol

2002; 86 (4): 315-21

72. Suminski RR, Robertson RJ, Goss FL, et al. Acute effect of amino acid ingestion and

resistance exercise on plasma growth hormone concentrations in young men. Int J

Sports Nutr 1997; 7 (1): 48-60

73. Le Roith D, Bondy C, Yakar S, et al. The somatomedin hypothesis: 2001. Endocr Rev

2001; 22 (1): 53-74

74. Goldspink G. Skeletal muscle as an artificial endocrine tissue. Best Prac Res Clin

Endocrinol Metab 2003; 17 (2): 211-22

75. Goldspink G, Harridge SDR. Growth factors and muscle ageing. Exp Gerontol 2004;

39 (10): 1433-8

76. Goldspink G. Changes in muscle mass and phenotype and the expression of autocrine

and systemic growth factors by muscle in response to stretch and overload. J Anatomy

1999; 194 (3): 323-34

77. Kraemer WJ, Mazzetti SA. Hormonal mechanisms related to the expression of

muscular strength and power. In: Komi PV, Ed. Strength and power in sport. Boston:

Blackwell Scientific Publishing, 2003, pp. 73-95

78. Nindl BC, Kraemer WJ, Marx JO, et al. Overnight responses of the circulating IGF-1

system after acute, heavy-resistance exercise. J Appl Physiol 2001; 90: 1319-26

79. Kostka T, Arsac L, Patricot MC, et al. Leg extensor power and

dehydroepiandrosterone sulfate, insulin-like growth factor-1 and testosterone in healthy

active elderly people. Eur J Appl Physiol 2000; 82: 83-90

80. Copeland JL, Underwood LE, Van Wyk JJ. Induction of immunoreactive

somatomedin-C in human serum by growth hormone: dose response relationships and

effect on chromatographic profiles. J Clin Endocrinol Metab 1980; 50: 690-7

81. Biolo G, Williams BD, Fleming DRY, et al. Insulin action on muscle protein kinetics

and amino acid transport during recovery after resistance exercise. Diabetes 1999; 48:

949-57

82. Sheffield-Moore M, Urban RJ. An overview of the endocrinology of skeletal muscle.

Trends Endocrinol Metab 2004; 15 (3): 110-5

83. Willey KA, Fiatarone Singh MA. Battling insulin resistance in elderly obese people

with type 2 diabetes. Diabetes Care 2003; 26 (5): 1580-8

84. Winett RA, Carpinelli RN. Potential health-related benefits of resistance training.

Prevent Med 2001; 33: 503-13

85. Volek J. Influence of nutrition on responses to resistance training. Med Sci Sports

Exerc 2004; 36 (4): 689-96

86. Rasmussen BB, Tipton KD, Miller SL, et al. An oral essential amino acid-

carbohydrate supplement enhances muscle protein anabolism after resistance exercise. J

Appl Physiol 2000; 88 (2): 386-92

87. Miller SL, Tipton KD, Chinkes DL, et al. Independent and combined effects of amino

acids and glucose after resistance exercise. Med Sci Sports Exerc 2003; 35 (3): 449-55

28

88. Thyfault JP, Carper MJ, Richmond S, et al. Effects of liquid carbohydrate ingestion on

markers of anabolism following high-intensity resistance exercise. J Strength Con Res

2004; 18 (1): 174-9

89. Roy BD, Tarnopolsky MA, MacDougall JD, et al. Effect of glucose supplement timing

on protein metabolism after resistance training. J Appl Physiol 1997; 82 (6): 1882-8

90. Borsheim E, Cree MG, Tipton KD, et al. Effect of carbohydrate intake on net muscle

protein synthesis during recovery from resistance exercise. J Appl Physiol 2004; 96 (2):

674-8

91. Viru A, Viru M. Hormones as tools for training monitoring. Biochemical monitoring

of sport training. Champaign, Illinois: Human Kinetics, 2001, pp. 73-112

92. Urhausen A, Kindermann W. Diagnosis of overtraining: What tools do we have?

Sports Med 2002; 32 (2): 95-102

93. Sapolsky RM, Romero ML, Munck AU. How do glucocorticoids influence stress

responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

Endocr Rev 2000; 21 (1): 55-89

94. Urhausen A, Gabriel H, Kindermann W. Blood hormones as markers of training stress

and overtraining. Sports Med 1995; 20 (4): 251-76

95. Kraemer WJ, Dziados JE, Marchitelli LJ, et al. Effects of different heavy-resistance

exercise protocols on plasma beta-endorphin concentrations. J Appl Physiol 1993; 74:

450-9

96. McGuigan MR, Egan AD, Foster C. Salivary cortisol responses and perceived exertion

during high intensity and low intensity bouts of resistance exercise. J Sports Sci Med

2004; 3: 8-15

97. Izquierdo M, Hakkinen K, Ibanez J, et al. Effects of strength training on muscle power

and serum hormones in middle-aged and older men. J Appl Physiol 2001; 90: 1497-507

98. Fry AC, Schilling BK. Weightlifting training and hormonal responses in adolescent

males: Implications for program design. Streng Cond J 2002; 24 (5): 7-12

99. Kraemer WJ, Noble BJ, Clark MJ, et al. Physiologic responses to heavy-resistance

exercise with very short rest periods. Int J Sport Med 1987; 8 (4): 247-52

100. Staron RS, Karapondo DL, Kraemer WJ, et al. Skeletal muscle adaptations during

early phase of heavy-resistance training in men and women. J Appl Physiol 1994; 76

(3): 1247-55

101. Deschenes MR, Kraemer WJ, Bush JA, et al. Biorhythmic influences on functional

capacity of human muscle and physiological responses. Med Sci Sports Exerc 1998; 30

(9): 1399-407

102. Fry AC, Kraemer WJ, Ramsey LT. Pituitary-adrenal-gonadal responses to high-

intensity resistance exercise overtraining. J Appl Physiol 1998; 85 (6): 2352-9

103. Fry RW, Morton AR, Garcia-Webb P, et al. Monitoring exercise stress by changes in

metabolic and hormonal responses over a 24-h period. Eur J Appl Physiol 1991; 63:

228-34

104. Kraemer WJ, Loebel CC, Volek JS, et al. The effect of heavy resistance exercise on

the circadian rhythm of salivary testosterone in men. Eur J Appl Physiol 2001; 84: 13-8

105. Dimitriou L, Sharp NC, Doherty M. Circadian effects on the acute responses of

salivary cortisol and IgA in well trained swimmers. Br J Sports Med 2003; 36 (4): 260-4

106. Gooren LJ, Harmsen-Louman W, Van Kessel H, et al. Basal and LHRH-stimulated

gonadotropin levels and the circadian rhythm of testosterone and the effects of

exogenous testosterone thereon. Andrologia 1984; 16 (3): 249-55

107. Thuma JR, Gilders RM, Verdun M, et al. Circadian rhythm of cortisol confounds

cortisol responses to exercise: implications for future research. J Appl Physiol 1995; 78

(5): 1657-64

29

108. Nindl BC, Hymer WC, Deaver DR, et al. Growth hormone pulsatility profile

characteristics following acute heavy resistance exercise. J Appl Physiol 2001; 91: 163-

72

109. Durand RJ, Kraemer RR, Hollander AP, et al. Different effects of concentric and

eccentric mucsle actions on plasma volume. J Strength Con Res 2003; 17 (3): 541-8

110. Wallace BM, Moffatt RJ, Hancock LA. The delayed effects of heavy resistance

exercise on plasma volume shifts. J Strength Con Res 1990; 4 (4): 154-9

111. Wang C, Plymate S, Nieschlag E, et al. Salivary testosterone in men: Further

evidence of a direct correlation with free serum testosterone. J Endocrinol Met 1981; 53

(5): 1021-4

112. Sannika E, Terho P, Suominen J, et al. Testosterone concentrations in human seminal

plasma and saliva and its correlation with non-protein-bound and total testosterone

levels in serum. Int J Androl 1983; 6: 319-30

113. Khan-Dawood FS, Choe JK, Dawood MY. Salivary and plasma bound and "free"

testosterone in men and women. Am J Obstet Gynecol 1984; 148 (4): 441-5

114. Vittek J, L'Hommedieu DG, Gordon GG, et al. Direct radioimmunoassay (RIA) of

salivary testosterone: correlation with free and total serum testosterone. Life Sci. 1985;

37 (8): 711-6

115. Magrini G, Chiodoni G, Rey F, et al. Further evidence for the usefulness of the

salivary testosterone radioimmunoassay in the assessment of androgenicity in man in

basal and stimulated conditions. Horm Res 1986; 23 (2): 65-73

116. Ohzeki T, Manella B, Gubelin-De Campo C, et al. Salivary testosterone

concentrations in repubertal and pubertal males: comparison with total and free plasma

testosterone. Horm Res 1991; 36 (5-6): 235-7

117. Granger DA, Schwartz EB, Booth A, et al. Salivary testosterone determination in

studies of child health development. Horm Behav 1999; 35 (1): 18-27

118. Walker RF, Riad-Fahmy D, Read GF. Adrenal status assessed by direct

radioimmunoassay of cortisol whole saliva or parotid saliva. Clin Chem 1978; 24 (9):

1460-3

119. Vining RF, McGinley RA, Maksvytis JJ, et al. Salivary cortisol: a better measure of

adrenal cortical function than serum cortisol. Ann Clin Biochem 1983; 20: 329-35

120. Stupnicki R, Obminski Z. Glucocorticoid response to exercise as measured by serum

and salivary cortisol. Eur J Appl Physiol 1992; 65 (6): 546-9

121. Aardal-Eriksson E, Karlberg BE, Holm AC. Salivary cortisol-an alternative to serum

cortisol determination in dynamic function tests. Clin Chem Lab Med 1998; 36 (4):

215-22

122. Duclos M, Corcuff JB, Arsac L, et al. Corticotroph axis sensitivity after exercise in

endurance-trained athletes. Clin Endocrinol 1998; 48: 493-501

123. Neary JP, Malbon L, McKenzie DC. Relationship between serum, saliva and urinary

cortisol and implication during recovery from training. J Sci Med Sport 2002; 5 (2):

108-14

124. Cook CJ. Rapid non-invasive measurement of hormones in transdermal exudate and

saliva. Physiol Behav 2002; 75: 169-81

125. Johnson SG, Joplin GF, Burrin JM. Direct assay for testosterone in saliva:

relationship with a direct serum free testosterone assay. Clin Chim Acta 1987; 163 (3):

309-18

126. Umeda T, Hiramatsu R, Iwaoka T, et al. Use of saliva for monitoring unbound free

cortisol levels in serum. Clin Chim Acta 1981; 110 (2-3): 245-53

127. Tremblay MS, Chu SY, Mureika R. Methodological and statistical considerations for

exercise-related hormone evaluations. Sports Med 1995; 20 (2): 90-108

30

128. Goldspink G. Cellular and molecular aspects of adaptation in skeletal muscle. In:

Komi P, Ed. Strength and power in sport. Boston: Blackwell Scientific Publications,

1992, pp. 211-29

129. Goldspink G. Gene expression in muscle in response to exercise. J Muscle Res Cell

Motil 2003; 24: 121-6

130. Bloomer RJ, Ives JC. Varying neural and hypertrophic influences on a strength

program. Nat Strength Conditioning Ass J 2000; 22 (2): 30-5

131. Tesch PA, Larsson L. Muscle hypertrophy in bodybuilders. Eur J Appl Physiol 1982;

49: 301-6

132. Alway SE, Grumbt WH, Stray-Gundersen J, et al. Effects of resistance training on

elbow flexors of highly competitive bodybuilders. J Appl Physiol 1992; 72: 1512-21

133. Tesch PA, Colliander EB, Kaiser P. Muscle metabolism during intense, heavy-

resistance exercise. Eur J Appl Physiol 1986; 55: 362 - 6

134. Tesch P. Acute and long-term metabolic changes consequent to heavy resistance

exercise. Med Sport Sci 1987; 26: 67-89

135. Craig BW, Lucas J, Pohlman R, et al. The effects of running, weightlifting and a

combination of both on growth hormone release. J Appl Sport Sci Res 1991; 5 (4): 198-

203

136. O'Conner PJ, Corrigan DL. Influence of short-term cycling on salivary cortisol

levels. Med Sci Sports Exerc 1987; 19 (3): 224-8

137. Kindermann W, Schnabel A, Schmitt WM, et al. Catecholamines, growth hormone,

cortisol, insulin and sex hormones in anaerobic and aerobic exercise. Eur J Appl Physiol

1982; 49: 389-99

138. Consitt LA, Copeland JL, Tremblay MS. Hormone responses to resistance vs.

endurance exercise in premenopausal females. Can J App Physiol 2001; 26 (6): 574-87

139. Vanhelder WP, Radomski MW, Goode RC, et al. Hormonal and metabolic response

to three types of exercise of equal duration and external work output. Eur J Appl

Physiol 1985; 54: 337-42