NW Spine - Library

© 1999

With puns like that found in this title, it’s a wonder that I’m still writing. Nevertheless, even worse than my puns are the feeble arguments put forth by some individuals to support their opinions on resistance exercise.

This article will be the first in a series to look at the relationship between different volumes of resistance exercise and the resultant hormonal effects. More importantly, we’ll evaluate whether any observed endocrinological differences between low- and high-volume routines have any meaningful practical significance.

A scant amount of research has directly compared the hormonal effects between two or more resistance training protocols. Perhaps the most frequently cited study on this subject is that of Gotshalk and colleagues (1997) which compared the effects of resistance training volume on growth hormone, testosterone, and cortisol. This study reported increased secretion of growth hormone and testosterone with a three-set routine versus a single-set routine for the hour following exercise. This research has been widely referred to by high-volume advocates to support the purported superiority of a multi-set approach to resistance training. For example, last summer, a good friend of mine attended a seminar instructed by body builders Chris Aceto and Laura Creavalle aboard their yacht. During the seminar, Chris expressed his opinion that he believed Arthur Jones was correct in saying that one set is all that is required to stimulate muscle growth. However, Chris elaborated that it takes a multi-set approach to create the most favorable hormonal environment for body composition changes with an emphasis on getting big and lean. Most recently, the Gotshalk study was alluded to in order to support claims by high-volume advocate Gary Lavin in a head-to-head debate with low-volume proponent Dr. James Graves (Brown, 1999).

Let’s first examine the role of growth hormone in weight training.

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. 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.

Numerous studies have demonstrated acute elevation in GH secretion with many types of exercise. This has been shown to be true of both aerobic and anaerobic activity. Of particular interest is the Gotshalk study which revealed a greater acute GH response with high-volume weight training when compared to low-volume weight training. Much has been made of this finding, as it has been used to predict that high-volume resistance exercise routines yield superior muscle growth. However, it is critical to evaluate the importance of this greater, more extended rise in GH by viewing it within the context of the vast body of data on GH.

Unfortunately, I was unable to procure the full version of the Gotshalk article for this first installment. Therefore, I am not at liberty to evaluate the experimental design or to identify confounding variables. However, I am by no means surprised that more sets result in greater transient GH levels because it is now known that lactic acid, or more specifically an increasing hydrogen ion concentration leading to more acidic blood, is a strong stimulus for GH release (Borer, 1995).

CAN A BRIEF, EXERCISE-INDUCED SURGE OF GH GREATLY INFLUENCE MUSCLE GROWTH?

To put the whole GH argument 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 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, Pakarinen, Alen, Kauhanen and Komi, 1988; Kraemer et al., 1998; McCall, Byrnes, Fleck, Dickinson, and Kraemer, 1999), with one exception which showed radically different results (Craig, Brown, and Everhart, 1989). In fact, the duration of an exercise-induced GH surge is merely a few hours (Guyton and 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 and 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.

At this time, it does not appear that any studies have evaluated the GH patterns elicited by single-set versus multi-set routines for a time period of greater than one hour post exercise.

DOES GH AFFECT MUSCLE GROWTH TO AN APPRECIABLE EXTENT?

Despite the great interest in GH release with exercise, the importance of GH for strength training adaptation is uncertain. Though supraphysiological dosages of GH have been sometimes shown to have positive effects on body composition in trained athletes, most athletes who have used GH have reported lackluster results (LeMar, 1998). In a study of elderly men engaged in resistance training at 75-90% of maximum strength, GH supplementation did not produce any significant effects on lean body mass over the course of four months (Yarasheski , Campbell, and Kohrt , 1997). 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).

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, Brasel, Barstow, Mohan, and Cooper, 1998). However, this was in contrast to a study of adolescent females which revealed a positive correlation between GH secretion and muscle mass (Eliakim, Brasel, Mohan, Barstow, Berman, and Cooper, 1996). Again, there are also several 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 and Rogol, 1997).

The fact that the evidence is clearly conflicting regarding the importance of the role of GH in 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, Isgaard, and Isaksson, 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 those such as Chris Aceto who propose that high-volume routines may 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.

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, 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, Richter, and Kiens, 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, the authors mentioned GH only once in a chapter on lipid metabolism during exercise, and it was with regard to rat fat cells, not human fat cells, because GH is not considered a "good" or "important" stimulator of fat breakdown in humans (Turcotte, Richter, and Kiens, 1995).

IMPLICATIONS FOR THE THEORY AND PRACTICE OF RESISTANCE TRAINING

Because GH response to exercise changes with a number of variables such as rise in body temperature, physical fitness, age, gender, dietary intake, body composition, exercise duration, and intensity of exercise (Juul, 1996), to take the results of a single study such as that of Gotshalk and colleagues and to apply it to everyone who lifts weights is a gross oversimplification of the matter.

Frankly, the examination in the role of increased hormone secretion associated with various volumes of strenuous resistance exercise seems a bit "bass-ackwards" to me. The vast majority of studies have repeatedly shown that multiple-set resistance training routines do not confer any benefits to strength performance beyond single-set protocols (Carpinelli and Otto, 1998; Curto and Fisher, 1999). To the best of my knowledge, not a single study has ever shown a significant difference in lean body mass or muscle mass increases between low-volume and high-volume trainees (Carpinelli and Otto, 1998). It therefore should be obvious that the greater GH secretion observed in a high-volume resistance-training routine does not result in any meaningful increase in muscle mass.

An important question that should have been asked along the way is, "Do these increases in hormone secretion found in the Gotshalk study have any functional significance?" Given the data indicating no significant differences in muscle mass accretion between single-set and multi-set trainees, the answer should be painfully obvious. Regardless of what differences in the hormonal milieu have been observed in weight training studies between low and high-volume trainees, the differences evidently have no profound physiological impact. But, now that the pressure is on and the high-volume proponents are becoming increasingly desperate to prove the purported superiority of their method, it has become necessary to review the roles of certain hormones in resistance training.

CONCLUSION

GH at normal physiological levels has not conclusively been shown to be a necessity for exercise-induced muscle hypertrophy, and GH may not play a major role in human fat metabolism. Therefore, a training regimen’s design should not be predicated on the acute or chronic behavior of GH. For those truly concerned about losing body fat, there is a much better solution than training with multiple sets. Similar to what Dr. Ralph Carpinelli mentioned in a previous issue of Master Trainer, because single-set training is so time efficient, it would be simple to include additional steady rate exercise or interval training, the effects of which would prove superior to a reliance on multiple-set training for the purpose of fat loss. My advice is to keep exercise to a minimum with single-set training so that you may enjoy not just muscular growth, but be afforded time for personal growth as well.

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.

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Borer, K.T. (1994). Neurohumoral mediation of exercise-induced muscle growth. Medicine and Science in Sport and Exercise, 26, 741-754.

Borer, K.T. (1995). The effects of exercise on growth. Sports Medicine, 20(6), 375-397.

Brown, L.E. (1999). Point/counterpoint: Efficacy of weight training: Multiple sets versus single sets. Strength and Conditioning Journal, 21(3), 17.

Carpinelli, R.N., & Otto, R.M. (1998). Strength training: Single versus multiple sets. Sports Medicine, 26(2), 73-84.

Cooper, D.M. (1994). Evidence for and mechanisms of exercise modulation of growth--an overview. Medicine and Science in Sport and Exercise, 26, 733-744.

Craig, B.W., Brown, R., & Everhart, J. (1989). Effects of progressive reistance training on growth hormone and testosterone levels in young and elderly subjects. Mechanisms of Aging and Development, 49, 159-169.

Curto, M.A., & Fisher, M.M. (1999). The effect of single vs. multiple sets of resistance exercise on strength in trained males [Abstract]. Medicine and Science in Sport and Exercise, 31(5), S114.

Eliakim, A., Brasel, J.A., Mohan, S., Barstow, T.J., Berman, N., & Cooper, D.M. (1996). Physical fitness, endurance training, and the GH-IGF-I system in adolescent females. Journal of Clinical Endocrinology and Metabolism, 81, 3986-3992.

Eliakim, A., Brasel, J.A., Barstow, T.J., Mohan, S., & Cooper, D.M. (1998). Peak oxygen uptake, muscle volume, and the growth hormone-insulin-like growth factor-I axis in adolescent males. Medicine and Science in Sport and Exercise, 30(4), 512-517.

Gotshalk, L.A., Loebel, C.C., Nindl, B.C., Putukian, M., Sebastianelli, W.J., Newton, R.U., Häkkinen, K., & Kraemer, W.J. (1997). Hormonal responses of multiset versus single-set heavy-resistance exercise protocols. Canadian Journal of Applied Physiology, 22(3), 244-255.

Guyton, A.C. & Hall, J.E. (1996). Textbook of medical physiology (9th edition). Philadelphia, PA: W.B. Saunders.

Hakkinen, K., Pakarinen, A., Alen, M., Kauhanen, H., & Komi, P. (1988). Daily hormonal and neuromuscular responses to intense strength training in one week. International Journal of Sports Medicine, 9, 422-428.

Jennishe, E., Isgaard, J. & Isaksson, O.G.P. (1992). Local expression of insulin-like growth factors during tissue growth and regeneration. In: P.N. Schofield (Ed.), The insulin-like growth factors: Structure and biological functions (pp. 221-239). New York, NY: Oxford University Press.

Juul, A. (1996). Adult growth hormone (GH) deficiency and effects of GH treatment on muscle strength, cardiac function and exercise performance. In: A. Juul, J.O.L. Jorgensen, & A. Juull (Eds.), Growth hormone in adults: Physiological and clinical aspects (pp. 234-245). Cambridge, UK: Cambridge University Press.

Kraemer, W.J., Staron, R.S., Hagerman, F.C., Hikida, R.S., Fry, A.C., Gordon, S.E., Nindll, B.C., Gothshalk, L.A., Volek, J.S., Marx, J.O., Newton, R.U., & Hakkinen, K. (1998). The effects of short-term resistance training training on endocrine function in men and women. European Journal of Applied Physiology and Occupational Physiology, 78(1), 69-76.

LeMar, H.J. (1998). Growth hormone use and abuse. In: M.T. McDermott (Ed.), Endocrine secrets (2nd edition, pp. 172-174). Philadelphia, PA: Hanley & Belfus.

McCall, G.E., Byrnes, W.C., Fleck, S.J., Dickinson, A., & Kraemer, W.J. (1999). Acute and chronic hormonal responses to resistance training designed to promote muscle hypertrophy. Canadian Journal of Applied Physiology, 24(1), 96-107.

Roemmich, J.M. & Rogol, A.D. (1997). Exercise and growth hormone: Does one affect the other? Journal of Pediatrics, 131, S75-S80.

Samuels, M.H. (1998). Growth hormone-secreting pituitary tumors. In: M.T. McDermott (Ed.), Endocrine secrets, (2nd edition, pp. 129-133). Philadelphia, PA: Hanley & Belfus.

Thompson, J.L., Butterfield, G.E., Gylfadottir, U.K., Yesavage, J., Marcus, R., Hintz, R.L., Pearman, A., & Hoffman, A.R. (1998). Effects of human growth hormone, insulin-like growth factor I, and diet and exercise on body composition of obese postmenopausal women. Journal of Clinical Endocrinology and Metabolism, 83(5), 1477-84.

Turcotte, L.P., Richter, E.A., & Kiens, B. (1995). Lipid metabolism during exercise. In: M. Hargreaves (Ed.), Exercise metabolism (pp. 99-128). Champaign, IL: Human Kinetics.

Vance, M.L. (1999). Growth hormone-secreting adenomas. In: A. Krisht and G. Tindal (Eds.), Pituitary disorders: Comprehensive management (pp. 235-242). Baltimore, MD: Lippincott Williams and Wilkins.

Yarasheski, K.E., Campbell, J.A., & Kohrt, W.M. (1997). Effect of resistance exercise and growth hormone on bone density in older men. Clinical Endocrinology, 47(2),223-229.

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