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Every once in a while, I like to play devil’s advocate. In this article, I use my pitchfork to sift through some data that allow for an alternative interpretation growth hormone’s role in physique augmentation.

GROWTH HORMONE (AKA SOMATOTROPIN)

Growth hormone (GH) is a polypeptide hormone (191 amino acids long, for the truly curious) secreted by the anterior portion of the pituitary gland that dangles under the brain by a little stalk. GH is released in direct response to growth hormone-releasing hormone (GHRH) from the hypothalamus, a part of the brain capable of producing hormones. It is secreted at a rate of 0.4-1.0mg/day in men, and is secreted at a greater rate in teens and women (Reents, 2000). GH has been shown to exert anabolic actions on a number of tissues, including bone, connective tissue, and muscle. GH also influences fuel mobilization and utilization.

GH has—for as long as I can recall—been an endocrinological and pharmacological focal point for many in the body building community. The effects of GH are widely touted, and a number of strategies have been proposed to increase GH secretion. (For example, I refer readers to detailed contributions by Dr. Michael Diamond and soon-to-be Dr. Tom Incledon on the subject of GH in other issues of ASMJ. Dr. Jeff Stout, another top sports nutritionist and personal friend, is a believer in GH’s role in health, fitness, and anti-aging (2000).) Those interested in maximizing their circulating GH levels in the name of physique enhancement have tried higher-volume resistance exercise routines, afternoon naps, GH secretagogues, and, of course, exogenous GH injections. In fact, some professional body builders are reported to spend up to $30,000 annually to purchase synthetic GH (Reents, 2000)! Despite this intense interest in GH, somewhere along the way we forgot to ask a fundamental question: does GH play a significant role in physique enhancement?

To put the whole GH issue into perspective, it will be helpful to look at some medical observations.

More important than the magnitude of the peak concentration of hormone is the duration of the elevation and the total area under the curve (i.e., total amount secreted over the course of a day). For example, at certain points in time, daily GH secretion in a healthy person has been shown to match or even exceed those levels in a patient with acromegaly, a disfiguring disease caused by very prolonged hypersecretion of GH (Vance, 1999). Thus, these normal peaks, regardless of how great, do not appear to have the same effect as chronic GH elevation. Likewise, most patients with acromegaly display only slightly elevated GH concentrations when compared to the levels in healthy subjects (Samuels, 1998). Again, the key element for GH-induced soft tissue growth, including muscle tissue, appears to be the sustained increase in GH over a long period of time.

At the other extreme of GH-related disorders are GH-deficient patients. For GH-deficient patients receiving GH therapy, it has been shown that equivalent weekly dosages of exogenous GH are most effective if administered daily as opposed to twice or thrice each week (LeMar, 1998). This further points to the importance of sustained levels of GH since large spikes in GH fail to yield the same results when compared to the smaller injections leading to evenly elevated levels.

Given the above medical scenarios that serve to elucidate the time course for the action of GH, does resistance exercise—regardless of volume—result in GH surges of sufficient duration to meaningfully affect protein synthesis in muscle? It has been reported that daily bouts of exercise do not result in chronic elevation of baseline GH concentration (Hakkinen et al., 1988; Kraemer et al., 1998; McCallet al., 1999), with one exception which showed radically different results (Craig et al., 1989). In fact, the duration of an exercise-induced GH surge is merely a few hours (Guyton & Hall, 1996, p. 939). Furthermore, in their standard medical physiology text, Guyton and Hall (1996, p. 937) explain that GH can stimulate protein synthesis within minutes of its release, but for GH to markedly affect protein synthesis through increased transcription of nuclear DNA to RNA, GH must be elevated for "prolonged periods (24-48 hours)..." The authors go on to say, "In the long run, this perhaps is the most important of all the functions of growth hormone."

Although a few authors still speculate that the exercise-induced GH bursts may play a role in tissue repair and synthesis (Cooper, 1994; Roemmich & Rogol, 1997), the evidence seems to indicate the short bursts of GH associated with exercise do not meet the time duration requirement consistent with long-term adaptation in the form of increased muscle protein.

Higher-volume exercise routines have been demonstrated to result in greater GH secretion when compared to lower-volume routines (Gotshalk et al., 1997). Given a constant workout intensity level, more exercise sets should equate to greater lactic acid production. In turn, greater lactic acid should result in greater GH release (Borer, 1995). If this amount of GH release is meaningful, then trainees who train at higher volumes should exhibit greater increases in lean body mass. There are about ten published studies comparing single-set versus multiple-set resistance exercise programs which examined the differential effect of number of exercise sets on muscle mass measurements. You may be surprised to learn that despite widespread belief to the contrary, multiple sets (greater than one set) have never been scientifically shown to be superior to single sets in stimulating muscle mass increases in studies lasting up to 6 months in trained and previously untrained subjects (Carpinelli & Otto, 1998; Curto & Fisher, 1999; Sanborn et al., 2000). An exception is one author’s work comparing different exercises, different sets, different repetition ranges, and different frequencies between training groups, which makes it tough to say that what led to greater body mass differences in higher-volume trainees (Kraemer, 1997). I don’t wish to open up a can of worms here because arguments about proper exercise volume can become quite heated; I’m donning my white lab coat and simply stating what the sum of the scientific evidence has shown. Given what the preponderance of evidence suggests to date, augmented GH concentration due to increased volume of resistance exercise does not appear to have a significant impact on lean mass accretion.

The same argument regarding the brevity of GH peaks may also be applied to peaks created by naps and supplements. Is the duration of exposure to GH sufficient to increase tissue anabolism? Probably not.

Despite the great interest in GH, the importance of GH for strength training adaptation is uncertain. Though supraphysiological dosages of GH have been occasionally shown to have positive effects on body composition in trained athletes, most athletes who have used GH have reported lackluster results (LeMar, 1998).

One team of researchers who examined the relationship of growth hormone to adolescent muscle growth in males found "no statistically significant correlations between thigh muscle volume and mean GH levels or GH pulsatility patterns" (Eliakim et al., 1998). However, this was in contrast to a study of adolescent females which revealed a positive correlation between GH secretion and muscle mass (Eliakim, et al., 1996). Again, there are a few studies showing increased muscle mass with GH administration, but one review on the subject concluded, "The data to date do not indicate that the augmented secretion of endogenous GH or the injection of biosynthetic GH has major salutory effects on athletic performance" (Roemmich & Rogol, 1997).

Let’s look at a different population. In a study of post-menopausal women engaged in a weight loss program consisting of a 500 kcal dietary restriction, walking, and strength training, GH supplementation did not show any significant benefit on lean body mass or strength (Thompson et al., 1998).

Some studies using GH in young men and experienced weightlifters do not suggest a benefit to concurrent weight training and GH administration. In the first study (Yarasheski et al., 1992) of young men who resistance trained, GH was given in the amount of 40 micrograms per kilogram body weight over the course of 12 weeks. Because whole-body protein increased but muscle protein synthesis did not, the researchers suspected that the lean body mass increase occurred in a tissue other than muscle. They concluded: "resistance training supplemented with GH did not further enhance muscle anabolism." An increase in non-muscle protein content would account for the many distended tummies that have allegedly resulted from GH use secondary to internal organ growth.

In a follow-up study (Yarasheski et al., 1993) of experienced weight lifters, the same dosage of GH was used for 2 weeks. The rate of muscle protein synthesis was not increased by the addition of GH, and the rate of protein catabolism was not decreased (i.e., not anticatabolic). The study’s authors concluded, "These findings suggest that short-term GH treatment does not increase the rate of muscle protein synthesis or reduce the rate of whole body protein breakdown, metabolic alterations that would promote muscle protein anabolism in experienced weight lifters attempting to further increase muscle mass."

One earlier study did suggest that GH administration leads to enhanced body composition in healthy, resistance-trained individuals with 6.5 years of training experience. The investigators used 8 mg of GH divided into 3 weekly doses over the course of 6 weeks. They noted significantly greater increases in fat-free mass in the GH group as compared to a placebo condition at the study’s conclusion (Crist et al., 1988).

In older persons over the age of 60 who are known to have diminished GH levels, GH interventions have been relatively consistent in showing increased lean body mass. However, the origin of the increased lean body mass is unclear because most studies have failed to report changes in indices that would reflect muscle growth. For example, GH plus exercise was not found to increase muscle protein synthesis more profoundly than exercise alone (Zachwieja & Yarasheski, 1999). As accomplished GH researchers explain, "It appears doubtful… that the increments in lean body mass are occurring in the skeletal muscle, specifically the skeletal muscle contractile proteins… It is likely that a large portion of the reported gain in lean body mass associated with [GH] administration in elderly individuals is simply fluid retention" (Zachwieja & Yarasheski, 1999).

The fact that the evidence is clearly conflicting regarding the importance of the role of GH in muscle growth should prevent anyone from concluding that GH is a critical factor in exercise-induced muscle growth. Indeed, in her 1994 analysis of the role of GH in strength training, Borer concluded, "Hypertrophic growth does not depend on anabolic action of GH..." She further stated, "...overloading alone is sufficient to elicit the hypertrophic responses." The following year, Borer explained, "Hypertrophic response produces the same relative increases in muscle mass in the absence of GH ...as it does in hormonally intact ...animals" (1995). These findings are explained by the activity of identified local anabolic hormones in muscles that carry on without regard for the input of GH (Jennishe et al., 1992).

So what may be the physiological purpose of the acute spike of GH associated with intense exercise if it is not involved in muscle growth? One possible role is in sweating (Juul, 1996), but its primary function likely deals with energy substrate availability and utilization (Borer, 1994). The utilization of energy substrates is influenced by acute elevations in GH. For example, GH surges increase blood glucose concentration, inhibit glucose uptake by cells, and mobilize free fatty acids from storage in fat cells (Borer, 1995). This fact fuels the arguments put forth by some GH proponents who propose that increased GH levels lead to greater body fat losses. However, it has been shown that GH’s fatty acid-mobilizing effect is "not strongly-dose dependent" (Borer, 1994). Therefore no one can state with confidence that modestly more GH leads to more fatty acid mobilization.

Interestingly, use of female oral contraceptives (i.e., birth control pills) have been demonstrated to enhance exercise-induced GH secretion (Reents, 2000, p. 152). Come on now… Have you ever known of any woman using birth control that actually felt it helped her lose body fat? Are post-exercise spikes in GH that critical for fat loss? I doubt it, but they may be helpful.

You may be surprised to learn that GH use in a 6-week study of resistance-trained power athletes resulted in a significant decline in thyroxine levels (Reents, 2000, p. 155). Since thyroxine is the hormone that stokes the body’s metabolic furnace, wouldn’t a decrease in thyroxine eventually sabotage— rather than enhance—fat-loss efforts? Perhaps this could be avoided by cycling the use of GH or other tactics that increase GH levels.

Another consideration in the fat burning argument is the 1-2 hour delay in fatty acid mobilization from the time that GH levels rise (Borer, 1994). Clearly, in an exercise-induced context, this delayed mobilization is typically by the end of a trainee’s workout when most trainees consume a recovery carbohydrate/protein supplement or meal, which will nix any additional fat burning due to the ensuing surge of the potent antilipolytic insulin (Turcotte et al., 1995).

Some studies have shown that an infusion of GH does have lipolytic effects in healthy humans, while others do not support these findings (Juul, 1996). Also, in the preceding reference, Juul and colleagues mentioned GH only once in an entire chapter on lipid metabolism during exercise, and it was with regard to rat fat cells, not human fat cells. Also, experts on metabolism have downplayed the role of GH in lipolysis because GH is not considered a "good" or "important" stimulator of fat breakdown in humans (Turcotteet al., 1995).

A very recent study does, however, support the lipolytic properties of GH in which GH was shown to play the most important role in fatty acid utilization during a 3.5 hour recovery period following high-intensity treadmill exercise (Pritzlaff, 2000). Also in support of GH’s role in fat loss is the previously mentioned study of experienced weight trained subjects by Crist et al. (1988) that did report significantly greater decreases in percent body fat when GH was supplied exogenously. As well, several GH-intervention studies of elderly patients have noted decreased fat mass (Zachwieja & Yarasheski, 1999). In healthy resistance-trained subjects, I personally find the evidence linking GH use and decreased body fat far more compelling than GH use and muscle growth.

This is probably the least controversial point in this article because the scientific literature is in pretty good agreement on this subject, as pharmacist Dr. Stan Reents explains. Take it, Stan: "When non-GH deficient subjects are studied, regardless of their level of fitness, the combination of GH plus weight training does not produce further improvements in muscle strength over weight training alone. This has been documented in male power athletes and healthy [previously] untrained males. When elderly subjects were studied, GH was shown to improve muscle strength regardless of whether GH and weight training began simultaneously or if, instead, GH was added after several months of weight training had already occurred. Even when GH was given to elderly subjects in the absence of weight training, no improvements in muscle strength were seen" (Reents, 2000, p. 155). Stan the man also states, "GH does not appear to be ergogenic in subjects who are not GH deficient" and "data obtained in GH-deficient subjects should not be extrapolated to subjects who are not GH-deficient" (Reents, 2000, p. 155).

INSULIN-LIKE GROWTH FACTORS (AKA SOMATOMEDINS)

I alluded to insulin-like growth factors (IGFs) earlier in the article as "local anabolic hormones in muscles that carry on without regard for the input of GH." IGFs are a class of peptide hormones having insulin-like effects on growth. There are at least four subtypes, but the best described and most influential is IGF-1, also known as somatomedin-C (Guyton & Hall, 1996, p. 938). IGF-1, 70 amino acids in length, is synthesized in the liver and other tissues, including skeletal muscle and its satellite cells (Adams, 1998; Bar et al., 1997). Depending upon the particular site of synthesis, IGF-1 can act in the following ways: endocrine (throughout the body), paracrine (on nearby cells), or autocrine (on the same cell that secreted it) (Adams, 1998).

It is generally agreed that GH does not act directly on tissues but instead relies on IGF-1 to exert its actions (Samuels, 1998). It was once thought that IGF-1 simply did the bidding of the almighty growth hormone, but research has since emancipated IGF-1 by recently recognizing that it can operate independently of GH by paracrine and autocrine mechanisms. In fact, load-induced muscle growth processes (satellite cell recruitment and general muscle anabolism) are thought to rely substantially on IGF-1 (Adams, 1998; Jennishe, Isgaard, and Isaksson, 1992).

(As an interesting side note, African Pygmies have an inability to synthesize IGF-1 despite having normal to high GH levels (Guyton and Hall, 1996, p. 938). Thus, a lack of IGF-1 is responsible for their small stature. Isn’t that neat?)

In the blood, IGF-1 has a half-life of 20 hours, compared to a GH half-life of just 20 minutes (Guyton and Hall, 1996, p. 939). The prolonged presence of IGF-1 is more consistent with the duration required to effect changes in protein synthetic machinery. Again, GH has not been conclusively demonstrated to play a role in exercise-induced muscle growth. On the contrary, IGF-1 (unlike GH) has been shown with certainty to exert meaningful influences on overloaded skeletal muscle, at least when it is secreted locally.

Above, we rationalized why IGF-1 may be of greater interest than GH with respect to exercise-induced muscle growth. However, there is much more to the story.

The premise that circulating IGF-1 in the blood greatly influences muscle growth is flawed because circulating IGF-1 does not indicate the level of IGF-1 where it really counts—in skeletal muscle (Jennishe et al., 1992). As Dr. Gregory Adams explains, "significant increases in skeletal muscle IGF-1 expression (=50 fold) are not reflected by an increase in plasma IGF-1 concentration" (1998).

In fact, measuring circulating IGF-1 in resistance trainees is fallacious, as indicated by Dr. Adams. "When carefully examined, the data from the majority of animal studies using animal models indicate a general failure of systemic GH or IGF-1 treatment to produce a functionally significant enhancement of... skeletal muscle." Dr. Adams continues, "...several reviewers conclude that circulating (endocrine) IGF-1 at best plays a minor role in the modulation of the mass of specific skeletal muscles during adaptation to changes in loading. In the context of skeletal muscle adaptation to altered loading, and assuming that the primary relevant effect of GH treatment is to increase circulating IGF-1, these collective results raise questions as to the relative importance of circulating IGF-1 in functional adaptations of skeletal muscle (i.e., functionally significant increases in strength or mass). Taken together, the majority of the literature from both human and animal studies suggests that circulating IGF-1 levels are of minimal importance in the adaptation of specific muscles to changes in loading."

CONCLUDING REMARKS

GH at normal physiological levels has not conclusively been shown to be a necessity for exercise-induced muscle hypertrophy, but it may assist in fat loss. Indeed, the effects of GH on body composition changes, particularly lean body mass accretion, have been overstated.

Apparently, GH is not important for exercise-induced muscle hypertrophy. Since GH does not directly exert effects on anabolic processes, it has been proposed that the anabolic effects must be mediated via IGF-1. But, plasma (circulating) IGF-1 secondary to GH secretion doesn’t appear to exert a strong influence in skeletal muscle adaptation to loading. Therefore, using GH to increase circulating IGF-1 is an error in judgment. It seems more likely that autocrine IGF-1, which is produced within the muscle itself, is where we should be focusing our attention in our quest to maximize muscle mass.

For those who maintain a desire to pursue optimizing their GH levels, careful attention should be paid to strategies that allow a sustained elevation of GH concentration. Because natural GH normally has a half-life of only 20 minutes, supplements to enhance GH output would need to be taken on a very frequent basis throughout the day. Such an approach, however, would likely be inconvenient and cost-prohibitive with many supplements.

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ABOUT THE AUTHOR

Dr. Greg Bradley-Popovich holds dual master's degrees in Exercise Physiology and Human Nutrition from West Virginia University as well as a doctorate in Physical Therapy from Creighton University. He is the Director of Clinical Research at Northwest Spine Management, Rehabilitation, and Sports Conditioning in Portland, Oregon. Greg is a contributor to the textbook Sports Supplements. Greg also serves on the editorial board of scholarly publications such as the Journal of Sports Chiropractic and Rehabilitation and the Journal of Performance Enhancement.

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