Growth Hormone and Testosterone: Practical Applications from the Laboratory to the Weight Room
by Robbie Durand

"True knowledge exists in knowing that you know nothing"
- Socrates

Just when you thought you knew it all about two of the biggest players in the game of bodybuilding, I am hoping to add a little bit more to your knowledge base of the biochemistry and training responses and adaptations of testosterone and Growth hormone (GH). It seems that both GH and testosterone have synergistic effects on creating an anabolic environment for muscle tissue anabolism. Enhancing testosterone levels directly increases GH levels and thus leads to a greater anabolic environment. Conversely, enhancing GH exerts a subtle positive effect on testosterone levels by bolstering gonadotropins, which exert their effects by producing testosterone, and suppressing cortisol (37). It has been reported that testosterone and GH have synergistic effects. When testosterone was administered to hypophysectomized rats (i.e. rats that have the area of the brain which secretes GH removed), testosterone exerted only a mild anabolic effect compared to control rats. When a combination of GH and testosterone was administered to hypophysectomized rats, tissue anabolism (i.e. increases in lean mass) was more predominant (46). In a 2002 study in JAMA, The effects of GH + testosterone on lean body mass and fat loss appeared additive, suggesting that both hormones worked by stimulating similar mechanisms or work completely independent of each other.
So every bodybuilder knows that high intensity weight lifting increases testosterone and growth hormone levels, yet scientists are still not exactly sure how testosterone levels are being increased during exercise. Normal testosterone production is influenced by an increase in leutinizing hormone (LH) production, yet there is no increase in LH production or LH may actually decrease during and immediately following exercise (25, 39). So how are testosterone levels increasing during exercise without the stimulus? These and a few other interesting topics based on testosterone and GH responses are going to be covered so read on…

Growth Hormone Secretion

GH (also called somatotropin) secretion is regulated through the anterior pituitary. Growth hormone is responsible for normal growth and development as well as metabolic effects such as a) increased mobilization of fatty acids from adipose tissue b) decreased rate of glucose utilization and c) increased rate of protein synthesis. The pulsatile secretion of GH is tightly controlled by neurotransmitters of the brain including dopamine (1), serotonin (2), acetylcholine (3), and norepinephrine (4), as well as levels of glucose (5), IGF-1 (7), and estrogens (8). The fact that women have higher circulating estrogens than men has long been hypothesized the reason women have higher resting GH levels than men. It could also be the reason that injections of testosterone increase GH levels possibly by the actions of testosterone aromatizing to estrogen. For example, Fryburg et al. (43) reported that the effects of 2 types of anabolic steroids on GH/IGF-1 release, one which could aromatize to estrogen (i.e. testosterone enanthate) and the other that would not aromatize (i.e. stanozolol). Testosterone enanthate (only 3 mg per kg per week) increased GH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had no effect on GH or IGF-1 levels. Interestingly, despite the unchanged levels in GH and IGF-1 secretion, stanozolol administration still caused potent metabolic effects which included increased urinary nitrogen balance, basal metabolic rate, and exercise-induced oxygen consumption.

The GH craze began in 1990 when Dr. Daniel Rudman and his associates at the Medical College of Wisconsin published in The New England Journal of Medicine a landmark study that glorified GH use. That study was entitled "Effects of Human Growth Hormone in Men Over Sixty Years Old." Results of the study concluded that there was a dramatic shift in the composition of body weight in the sedentary men participating in this study. There was an 8.8 % increase in lean muscle mass and a 14.4% decrease in fat tissue. Since then, many studies have failed to be able to reproduce these increases in lean muscle mass. A critical issue that seems to occur with muscle hypertrophy studies is that there are many methods for measuring muscle hypertrophy. They all rely on assumptions derived from healthy subjects, e.g. constant hydration state of lean body, constant intracellular potassium concentration, or a constant fat-free extracellular compartment. If you read the article by Dr. Dan Gwartney in August issue of Muscular Development, you would realize that GH causes a dose dependent increase in extracellular water. All these factors lead to research errors which highly affect the results of studies, when muscle hypertrophy is measured from muscle biopsies (i.e. an actual tissue sample taken from the vastus lateralis), most studies have failed to find any affect on GH and muscle hypertrophy. It seems that the greatest impact GH administration is going to have is on people who are GH deficient. Adults who are GH deficient have pronounced changes in body composition, metabolism, and function (when compared to those of normal adults) including a reduction in lean body mass, an increase in fat mass, reduced protein synthesis rates, and a reduction in maximal exercise performance (14).

Growth Hormones Affect on Muscle Protein Kinetics

Increases in whole body and muscle protein synthesis that are induced by GH cause net protein accretion. The actions of GH are thought to have an effect on muscle protein synthesis as well as reducing muscle proteolysis (i.e. being anti-catabolic) (14). Anti-catabolic effects of GH on muscle protein kinetics have been demonstrated when high doses of glucocorticoids (i.e. cortisol) were given to healthy subjects who received either a placebo or GH. Leucine oxidation (i.e. a measure of protein breakdown) increased during the placebo group but remained unchanged in the GH group demonstrating that GH has anti-catabolic effects on skeletal muscle (15).

The anabolic actions of GH are most pronounced in GH deficient men who have altered protein kinetics. Hoffman et al. (16) reported that GH deficient men have increased rates of protein breakdown and decreased protein synthesis compared to normal subjects. The use of GH replacement has acute affects on nitrogen retention (protein accretion) in GH deficient patients that are ameliorated within 1-week (17). So now that we know that GH has potent effects on muscle protein synthesis and increases in lean muscle mass with those who are GH deficient, what are the effects of GH on healthy adults? OK, here comes the big flop. GH administration does not seem to have the same physiological effects on adults with a normal pituitary axis. GH administration has been shown to have no effect on muscle growth and strength in healthy normal (20, 21) and older (22) exercising men. Yarasheski et al. (21) reported that subcutaneous GH administration (40 µg/kg/day) to experienced weight lifters significantly increased serum IGF-1 levels, but did not increase the rate of muscle protein synthesis or reduce whole body protein breakdown. Based on the literature, when GH is administered to young healthy adults, no effect on muscle protein synthesis (or indeed on muscle mass measured by other means) can been detected. Thus, at the very least, it appears that the evidence for a sustained anabolic effect of rhGH on muscle mass in normal healthy young men, trained or untrained, is extremely slim.

The direct effects of GH on skeletal muscle remains controversial but the direct effects of GH on adipose tissue are better documented. GH dramatically reduces lipogenesis (creation of new adipose calls) in adipose tissue, resulting in significant fat loss. These effects appear to be mediated by two pathways. In one case, GH decreases insulin sensitivity, resulting in down-regulation of fatty acid synthase (i.e. the rate-limiting enzyme for hepatic lipogenesis) expression in adipose tissue (18). In the second case, GH may decrease lipogenesis by affecting 2 proteins called Stat5a and 5b. The loss of Stat5a and 5b proteins in a knock-out model was recently shown to decrease fat accumulation in adipose tissue (19). So is GH responsible for its potent effects on adipose tissue lipolysis or is it being mediated by IGF-1 levels? The lipolytic (i.e. fat mobilization) effect of GH is direct, not mediated by IGF-I since mature adipocytes do not contain IGF-1 receptors (45). A interesting study in JAMA in 2000 reported that GH seems to be directly correlated with BMI in young to middle-aged adults (aged 16-43 years). In that study, those who had the highest BMI were people that had poor sleep quality and shallower, non-REM sleep (Remember: GH secretion is highest during stages 3 and 4 of non-REM sleep). Furthermore, intentional sleep deprivation almost totally abolishes GH production. Bodybuilders have known for years that getting adequate sleep is essential for training recuperation, muscle growth, and based on the JAMA study add fat loss.

GH administration does have drawbacks such as being expensive as hell and some well documented side effects. The most commonly reported side effects of GH are: impaired glucose uptake (carbohydrate intolerance), increased insulin secretion, and insulin resistance, as well as increased serum triglycerides. If that is still not a kick in the ass for you, over-expression of growth hormone had been found in previous research with mice to accelerate aging and reduce lifespan (23). It’s not often that you hear about people with gigantism (i.e. pituitary disorders causes over-secretion of GH) living long lives. So now that I have given you a brief summary of how GH is needed is mildly anabolic, has potent effects on fat lipolysis and may aid in muscle hypertrophy, additional GH administration by itself does not seem to add additional gains in muscle strength or hypertrophy in normal healthy. The study by Taffee et al. (44) best describes that the best way to increase GH is thru heavy resistance training. The effects of GH administration on muscle strength was evaluated in men 65 to 82 years of age who underwent progressive strength training for 14 weeks, followed by an additional 10 weeks of strength training plus either growth hormone or placebo. Resistance exercise training increased muscle strength significantly; the addition of GH did not result in any further improvement. High intensity exercise stimulates GH secretion and is certainly cheaper than growth hormone replacement. Let’s now examine how tweaking your training routine can be the most important thing you can do to raise your GH levels.

High Intensity Exercise: A Key Component for Increasing GH

The HPA axis and the autonomic nervous system are activated in response to stressful stimuli, which can lead to a rise in circulating GH during exercise. The effects of exercise-induced GH secretion are dependent on a wide variety factors such as age (8), blood glucose levels (9), lactate levels (10), gender (11), rest period length (12) and exercise volume (13).
The duration of rest periods between sets and training volume both seem to influence the magnitude of plasma GH increases during exercise (12). Although both variables influence GH secretion, heavy resistance training protocols with shortened rest periods (< 1 minute) between sets seem to elicit greater hormonal responses than resistance training protocols with longer rest periods (> 5 minutes) (12). Low intensity exercise that does not produce significant increases in lactic acid levels above 4 mmol/L subsequently has been proven less effective in raising plasma GH. In the world of exercise physiology, 4 mmol/L is considered “lactate threshold” which is technically the point in which lactate significantly begins to increase during exercise.

There are several physiological stimulators of lactate production, which include: tissue hypoxia, increased intracellular calcium concentrations, or increased catecholamines (i.e. adrenaline). In one experimental exercise protocol, researchers wanted to see just how effective muscle hypoxia was at stimulating GH secretion. Five sets of leg extensions with 30-second rest periods performed at 20% of a 1-RM with vascular occlusion (i.e. they tied a blood pressure cuff around the person legs and pumped it up to ~220 mmHg) resulted in 290% percent increase in GH above baseline. The increased lactate resulting from tissue hypoxia elevated GH significantly although training intensity was low (27). Weltman et al. (24) reported a dose dependent response between lactate threshold (LT) and GH levels to low and high intensity treadmill running protocols. In that study, different treadmill-running intensities of varying LT were studied (0.25 LT, 0.75 LT, 1.25 LT, and 1.75 LT). GH responses to 0.25 LT were the lowest while GH responses to 1.75 LT were the highest. There was a linear increase in the mass of GH secreted per pulse with increasing exercise intensity. Additionally, Gordon et al. (75) reported that exercise-induced GH release is significantly lower when combined with alkalotic agent (i.e. large dosages of sodium bicarbonate which increase blood buffering capacity and reduces lactic acid build up) when compared to normal exercise. So is it lactate itself that is increasing GH during exercise? Research indicates it probably is not lactate by itself that increase GH as infusions of lactate at rest do not stimulate GH release (26). The physiological point in which a person reaches LT and GH begins to significantly rise may be a marker for other physiological events which stimulate GH release, e.g., intramuscular acidosis, mechano- or chemoreceptor activation, relative muscle ischemia, and increased sympathetic activity (reflected peripherally by epinephrine and norepinephrine release) associated with greater GH responses to exercise.

So now you realize that GH increases in response to high intensity exercise, does not mean that you can just load up the squat bar with 135 and crank out 15 reps with 30 second rest periods thinking you are going to get huge increases in GH? HELL NO!! Pyka et al. (30) reported that young men who performed a circuit training routine consisting of thirteen stations with 30 sec rest periods had minimal GH responses at 60 % of 1 RM, while GH increased progressively using the same protocol at 70 and 85% of 1 RM. Minimal GH responses from the 60% protocol were attributed to the lack of training intensity. Additionally, Van Helder et al. (28) used two intermittent weight lifting exercises of equal total external work output and duration (20 min) and identical work-rest intervals but different load and frequency of movements. Subjects performed 7 sets of leg press at 85% of a 7 RM and a week later they performed seven sets of the same exercise 33% of a 7 RM for 21 reps. The 85% workload produced significant increases in GH while the low intensity 33% workload produced no changes in serum GH.
In addition to using adequate training intensity, using multiple sets seems to produce greater GH responses than single set protocols. Gotshalk et al. (29) reported that subjects who performed a heavy resistance training protocol which consisted of eight exercises with a training volume of 3 sets at 10 RM produced greater GH secretion than the same exercises with 1 set at 10 RM. Results of the study demonstrated that higher volumes of total work produced significantly greater increases in circulating GH during exercise and upon recovery of exercise. The results of using multiple sets for increased GH secretion may be a good reason to steer clear of HIT (High Intensity Training) type protocols which advocate 1-set to failure is all that is needed for muscular hypertrophy. So I hope you get that point that a combination of high intensity exercise (i.e. rest periods less than a minute) with sufficient training volume (70-85% of a 1-RM), and multiple sets per body part seem to be the key to raising GH levels during exercise. In addition to GH, resistance exercise has been shown to elevate other anabolic hormones such as testosterone.

Testosterone Physiology
Testosterone (T) is loosely bound to sex hormone binding globulin (SHBG) after excretion from the testis and circulates in the blood for about 30 minutes to 1-hour. Approximately 5 to 6 mg of testosterone is secreted into plasma daily in men. In men, LH and testosterone are secreted in a pulsatile manner every 60 to 90 minutes in a diurnal rhythm, with peak levels occurring in the morning.
T has many functions in the body which include: development of adult primary and secondary sexual characteristics, bone growth, increased calcium retention, red blood cell production, muscular development, fat lipolysis, and protein synthesis.

Testosterone and Protein Synthesis

A number of studies have documented the effects of testosterone on protein synthesis. Testosterone transcriptional activation by androgens leads to the production of specific mRNA’s and subsequently increased protein synthesis (31). Growth factors (e.g. IGF-1) are an important class of proteins, which are secreted by cells upon stimulation by testosterone. The mechanism by which testosterone increases protein synthesis is not completely understood. It is debated whether testosterone increases protein synthesis through the androgen receptor, or whether the effects of testosterone on protein synthesis are mediated through the GH/ IGF-1 axis or other systems. Testosterone effects on protein synthesis can cause anabolic actions on skeletal muscle. Testosterone administration has been reported to be increase skeletal muscle protein synthesis and strength in the elderly as well as increasing mixed protein synthesis rates normal subjects. The protein accretion from testosterone can result in muscle hypertrophy. Mauras et al. (48) administered Lupron (a drug that suppresses natural testosterone production) to six 23 year old healthy men which reduced circulating testosterone levels to those of prepubertal boys and found that testosterone deficiency caused marked changes in whole body protein metabolism, including decreased rates of whole body protein turnover and protein synthesis, decreased fat free muscle, decreased strength, and increased adiposity. Interestingly, there were no decreases in GH and IGF-1 production but there was a decrease in gene expression for IGF-1 in muscle.
Additionally, Urban et al (49) reported that testosterone increases muscle protein synthesis by stimulation of serum IGF-1 and a down regulation of its binding protein IGFBP-4. Testosterone influences muscle hypertrophy through a variety of mechanisms such as: increases satellite cell activation, increases protein synthesis rates, enhanced growth factor activity (e.g. GH, IGF-1, etc.), enhanced myonuclear number, and new myofiber formation. Satellite cell activation seems to be a necessary for hypertrophy, without satellite cell activation, hypertrophy will not occur (50). Satellite cells are located between the sarcolemma and the basal lamina of the myofibers. In vivo rat studies have reported that at the onset of puberty the increase in testosterone production causes hypertrophy with an increase in muscle cell diameter, a transient increase in satellite cell number and a increase in myonuclear number. Testosterone is thought to be the predominant factor that produces greater hypertrophy in men than women when placed on identical training regimens.

Testosterone and Muscle Tissue Hypertrophy

The importance of testosterone on muscle tissue hypertrophy can be demonstrated in a study of hypogonadal men (i.e. men with low testosterone levels) who were sedentary and received testosterone replacement for 10 weeks. The men gained an average of 5.7kg of bodyweight and strength increased in both the bench press and parallel bar squat. The amazing aspect of this study was that the men were not exercising during the 10-week study yet strength and lean body mass were improved (47). Testosterone has been shown to increase circulating levels of both GH and IGF-1 concentrations (32). Kadi et al. (33) measured the effects of anabolic steroids for nine months on muscle tissue hypertrophy in 5 elite trained powerlifters and compared steroid users to drug-free powerlifters who were the same weight and trained the same amount of years. Testosterone injections in the steroid group induced a significant increase in muscle size by both hypertrophy and the formation of new muscle fibers via satellite cell activation. The anabolic steroid group had increased DNA content, which likely facilitated an increase in muscle protein synthesis and greater muscle tissue hypertrophy than the non-steroid group.

How Does Testosterone levels increase during Exercise?

Testosterone levels are positively correlated with fitness levels and levels of fatigue in weightlifters (34). Resistance training has also been shown to increase circulating testosterone concentration in men during exercise. Testosterone responses to exercise are stimulated to varying degrees depending upon many factors including, the rest periods between sets, volume of training, age, and amount of muscle mass activated. So here is the million dollar question researchers are asking: What is the mechanism or how does intense exercise stimulate testosterone production? Testosterone levels under resting conditions are influenced by leutinizing hormone (LH), which stimulates Leydig cells to secrete testosterone, however during brief intense resistance exercise testosterone levels have been reported to increase despite no increases in LH (39). Nindl et al. (25) had subjects perform a high volume resistance training protocol which consisted of 50 total sets of upper and lower body exercise with repetitions of 5 and 10 RM loads with 90-second rest periods between sets. The suspected research hypothesis would be that there would be huge increases in testosterone with such a high intensity, high volume training protocol mediated by some increases in LH. The high volume resistance training protocol resulted in just the opposite of what was expected. There was no change in testosterone and LH during exercise and immediately after exercise; shockingly there was a concomitant lower LH secretion and suppressed total and free testosterone for up to 13 hours after exercise.

The results of this study can be extrapolated to the bodybuilder who thinks spending hours in the gym performing countless sets is the key to stimulating anabolic hormones is a sure means to overtraining. In another study which documented what excessive training volume can do to your testosterone levels, Hakkinen et. al (51) monitored elite Olympic lifters testosterone concentrations to twice daily training for 1 week. Elite Olympic weightlifters trained twice a day using similar volume (> 90% of a 1-RM) but different exercises. The morning session (9:00 a.m. to 11:00 a.m.) consisted of Olympic snatches, clean & jerks, and front squats, while the afternoon session (3:00 p.m. to 5:00 p.m.) consisted of power snatches, power cleans, and back squats. Testosterone started to decrease after the first training day and continued to systematically decrease over the course of the training period. When the training stress was reduced to one training session a day, serum testosterone concentrations started to increase, and after 1 full day of rest, values returned to the pre-training level. Strength levels of the elite athletes did not decline over the course of the week despite a decline in testosterone concentrations.

The absent response of LH to an acute bout of resistance exercise despite an increase in testosterone has led researchers to speculate other mediators are influencing testosterone production. Possible mechanisms for increasing testosterone levels during high intensity exercise are due to increased circulating lactic acid levels that are being produced from anaerobic glycolysis. Lactic acid has been shown to stimulate testosterone release in vitro (i.e. which means in the test tube) (35). So this is one of those research studies you don’t think your job is that bad after all, at least you are not in a lab removing rat testicles all day long. Researchers exposed the testosterone producing portion of the cell (i.e. Leydig cells) to lactic acid and found that administration of lactate at 5-20 mM dose-dependently increased the basal testosterone production by 63-187%. Remember, that anaerobic threshold is 4 mM and its not uncommon for high intensity weight training sessions to exceed 15mM, but remember this was done with rat testes so lets not jump to conclusions to fast. More research needs to be conducted, so before you start injecting lactic acid into your “family jewels” wait till more research is available on the subject. A second mechanism that has been proposed for increased testosterone levels during exercise is what is called a plasma volume shifts (36), which concludes that during high intensity resistance exercise as you muscles become engorged with blood, water or plasma is displaced from your circulatory system, as a result your blood becomes more concentrated with active metabolites (in this case testosterone). Kraemer et al. (36) reported that after a resistance training protocol of three sets of bench press, lat-pulldowns, leg extension, and leg curls performed at a 10-RM load for 10 repetitions or until muscular failure resulted in a significant increase in testosterone levels, but when he corrected for the plasma volume shifts or the amount of fluid lost from blood and found that there was no change in testosterone. Interesting!! The training induced rise in testosterone has also been thought to be stimulated by catecholamines (i.e. adrenaline). Schwab et al. (7) investigated the effect of heavy weight lifting and moderate weight lifting on concentrations of serum testosterone in males. The heavy weight lifting consisted of four sets of six squats at 90-95% of a six-repetition maximum (RM), while the moderate weight lifting consisted of four sets of 9 or 10 repetitions at 60-65% of a 1-RM. The weight and number of repetitions were manipulated such that the total weight lifted for the two sessions were equal. Testosterone levels were measured after each set to determine when a rise in testosterone occurs. Testosterone levels did not rise until the fourth set for both the groups. Schwab hypothesized because the exercise bout was brief, possibly epinephrine and nor-epinephrine, which have been shown to increase during exercise to the magnitude of the intensity of the exercise, could have significantly increased testosterone levels in response to the exercise bout. Regardless of which mechanism is causing these acute increases in testosterone during exercise, androgen skeletal muscle receptors are actively binding to a higher concentration of testosterone.

Testosterone and Resistance Training Intensity

Resistance training routines, that incorporate short rest periods between sets, produce higher testosterone concentrations than training protocols that use the same workload and prolonged rest periods. Hakkinen et al. (38) subjected ten male strength athletes to two different training intensities while maintaining similar rest periods (3 minutes). The first session consisted of maximal loads (20 sets x 1 RM x 100 %), while one week later they performed sub-maximal training (10 sets x 10 RM x 70%). Testosterone levels with maximal training (20 sets x 1 RM) did not change immediately and 1-hour post exercise, however testosterone and cortisol responses to submaximal training (10 sets x 10 RM) increased significantly after and 1 hour post-exercise with the submaximal training loads. Hakkinen concluded that heavy resistance exercises can stimulate varying endocrine responses of anabolic hormones, which differ in duration, and magnitude depending on the degree of stress of the exercise protocol. W.J. Kraemer (52) compared bodybuilders and powerlifters of the same age, size, and experience to an intense resistance training protocol, which shorted rest periods. The experimental sessions consisted of 3 sets of 10 repetitions for 10 exercises with 10-second rest periods between sets and 30 to 60 second rest periods between exercises. There was no significant difference between the groups as peak plasma lactate levels 5 min post-exercise was 21 mmol/L( talk about high intensity training session! Remember lactate threshold starts to increase at 4 mmol/L) for both groups. Testosterone increased significantly for both groups, but regardless of previous training experience, both bodybuilders and powerlifters had similar increases in testosterone concentrations.

Testosterone responses to resistance training in men are less with low intensity resistance training protocols than those that use high intensity. Raastad et al. (39) compared testosterone responses to two protocols, which utilized different intensities of squats, front squats, and leg extensions yet workload remained constant. One protocol was a moderate intensity (70% of a 1-RM) and the other protocol was a high intensity workload (100% of a 6-RM). Rest periods between sets were 4-6 min for both workouts. Testosterone responses were higher during and one hour after the 70% protocol compared to the 100% protocol. So now you are understand that training intensity should be at least 70% or more to stimulate sufficient rises in testosterone production. So now that you understand that powerlifting type protocols which incorporate high training % (90> and above) and long rest periods are not conducive for increasing GH and testosterone during exercise, however using high training % should be incorporated into your routines for increasing muscular strength.
Testosterone levels are also influenced by the amount of muscle mass activated in response to exercise. Craig et al. (40) reported that testosterone levels did not increase from pre to post exercise for younger and older men to upper and lower body isolation-type resistance exercise on a Nautilus machine consisting of 3 sets of 10-repetitions. Contrary to these finding, W.J. Kraemer (41) reported significant increases in testosterone responses of older and younger men in response to a high intensity squat protocol. Kraemer speculated the greater testosterone produced in his study compared to the study by Craig et al. (38) was due to his protocol used large muscle mass and higher training intensity. Fahey et al. (56) reported significant increases in testosterone after deadlifts in college age men; however, maximal and submaximal efforts in the bench press resulted in no increases in testosterone in experienced weightlifters (8). The disparities in results between the studies is probably due to large amount of muscle groups activated during the deadlift (i.e. legs, back, arms, abdominals) ,whereas a much smaller amount of muscle mass is activated during the bench press (i.e. pectoralis major, triceps brachii, and anterior deltoid)

Effects of Training Experience on Testosterone Levels

Training experience could also influence the degree in which testosterone in produced in response to an intense resistance training protocol. W.J. Kraemer (42) investigated adolescent Olympic weightlifters (17-18 yrs. old) testosterone concentrations in response to an a intense weightlifting session that consisted of 10 maximal effort vertical jumps and high intensity, low volume resistance training with the Olympic snatch and snatch pull. Subjects were separated into two experimental groups: < 2 years lifting experience and > 2 years lifting experience. Exercise induced increases in testosterone occurred only in the weightlifters who trained for > 2 years, while weightlifters with less than 2 years experience did not experience a significant exercise induced increase in testosterone. W.J. Kraemer hypothesized that the experienced weightlifters had enhanced hypopituitary-gonadal axis (HPG) from training and testicular function that was remodeled to promote enhanced release of testosterone. A most intriguing aspect of study was that lactate levels were similar in both groups post-exercise; these data suggest that in adolescent boys, blood lactate is not a strong activator of the HPG axis.

In conclusion, GH and testosterone have synergistic effects on muscle and leads to increases in intramuscular growth factors that may work on similar molecular pathways or may work completely independent of each other. GH has potent effects on fat lipolysis, yet GH effects on muscle hypertrophy are less well documented and are mild at best. Testosterone has potent effects on increasing muscular hypertrophy and is a potent stimulator of satellite cell activation which is essential for muscle hypertrophy. High intensity exercise with short rest periods seems to lead to dual rises in both GH and testosterone though a one or possibly many mechanisms.


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