NW Spine - Library

© 1999

In this second installment comparing the endocrinological effects of low- and high-volume resistance training programs, we will turn our attention to a class of hormones that are frequently mentioned in the strength training literature.

INSULIN-LIKE GROWTH FACTORS (AKA SOMATOMEDINS)

I alluded to insulin-like growth factors (IGFs) in the previous 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 and 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, Reijneveld, Wokke, Jacobs, and Bootsma, 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). (For a thorough review of muscle growth mechanisms including the role of satellite cells, read the book Rational Strength Training available at www.i-a-r-t.com.)

(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. As I explained in Part I, exercise-induced GH spikes are probably too transient to have a meaningful effect on muscle protein synthesis, not to mention that GH has not been conclusively demonstrated to play a role in exercise-induced muscle growth anyway. 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. For simplicity, let’s assume that circulating IGF-1 is just as effective as locally secreted IGF-1. A study that revealed circulating IGF-1 to be elevated more with multiple-set resistance training would provide some evidence (and a physiological mechanism) that multiple-set training could hypothetically result in slightly greater muscle hypertrophy over extended periods of training (>25 weeks since no significant growth differences have been found even with 25 weeks of single vs. multi-set exercise (Pollock, Abe, De Hoyos, Garzarella, Hass, and Werber, 1998)). Now, the question is, does there exist any exercise study demonstrating a volume-dependent increase in IGF-1?

In the first study to examine the effects of heavy resistance exercise on plasma IGF-1, Kraemer and colleagues recruited nine men with recreational weight-training experience to participate in six workout protocols (1990). Each subject randomly completed each of the six protocols, which were spaced one week apart. The six workouts were grouped into two "series" with each series consisting of three workouts. The study was designed so that Series 1 performed significantly less total work than Series 2 with Series 1 performing 82% of the total work of Series 2. Both series required the performance of 3-5 sets of the subjects’ 5 or 10-RM for eight exercises. Different volume between series was chiefly achieved by Series 1 consisting of two workouts with 5-RM and one workout with 10-RM and Series 2 consisting of two workouts with 10-RM and one workout with 5-RM. Although both series showed an increase in IGF-1 above resting levels, statistical analysis revealed no significant difference in total plasma IGF-1 (integrated area under the curve) between the high and even-higher volume groups over the course of two hours post-exercise. Certainly the "low-volume" series implemented in the study is much, much higher than what most proponents of abbreviated, single-set training would advocate. However, the study does demonstrate that an 18% increase in total work does not result in a further increase in total circulating IGF-1.

In a 25-week study comparing two resistance exercise routines of different volumes, Borst and coworkers tracked the circulating IGF-1 levels in 22 subjects performing single-set or multi-set exercise (1998). Both groups of eleven subjects showed significant increases in IGF-1 by 13 weeks, and maintained those increases until the completion of the study at 25 weeks at which time the single-set group showed an increase of 34% and the three-set group showed an increase of 30%. There was no significant difference between the groups. Interestingly, there was no significant difference between the IGF-1 levels at 13 and 25 weeks, showing that levels of this hormone had already plateaued.

DOES CIRCULATING IGF-1 REALLY HAVE A SUBSTANTIAL EFFECT ON MUSCLE HYPERTROPHY?

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 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, Isgaard, and Isaksson, 1992). As Gregory Adams, PhD explains, "significant increases in skeletal muscle IGF-1 expression (=50 fold) are not reflected by an increase in plasma IGF-1 concentration" (Adams, 1998). In fact, measuring circulating IGF-1 in resistance trainees is fallacious. "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."

CONCLUSIONS

After reading this installment, it should become even more clear that GH is not important for exercise-induced muscle hypertrophy. Since GH does not directly exert effects on anabolic processes, the anabolic effects must be mediated via circulating IGF-1. But, two studies have shown no significant difference in plasma (circulating) IGF-1 between resistance exercise routines of different volumes. Furthermore, plasma IGF-1 doesn’t appear to exert a strong influence in skeletal muscle adaptation to loading.

IGF-1 research is hardly obscure. I didn’t even have to leave my apartment to obtain most of this information--it was right on my bookshelf. Because of the immense body of literature showing little to no effect of GH and/or circulating IGF-1 on load adaptation in muscle, I would question the utility in continuing to measure exercise-induced alterations in GH and plasma IGF-1 in exercise science studies. I certainly would question anyone who tries to justify using a high-volume routine based on the behavior of these hormones! Measuring autocrine and paracrine IGF-1 expression in exercised muscle seems like a better place for physiologists to focus their attention, but no research will negate the numerous studies that have demonstrated no differences between low- and high-volume resistance exercise routines.

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.

Back to Library Main Page

References

Adams, G. (1998). Role of insulin-like growth factor-I in the regulation of skeletal muscle adaptation to increased loading. In: J. O. Holloszy (Ed.), Exercise and sport sciences reviews (pp. 31-60). Baltimore, MD: Williams and Wilkins.

Bar, P., Reijneveld, J., Wokke, J., Jacobs, S., and Bootsma, A. (1997). Muscle damage induced by exercise: nature, prevention and repair. In: S. Salmons (Ed.), Muscle damage (pp. 1-27). New York, NY: Oxford University Press.

Borst, S., De Hoyos, D., Lowenthal, D., Vincent, K., Garzarella, L., Pollock, B., & Pollock, M. (1998). Six months of high- or low-volume resistance training increases circulating insulin-like growth factor [Abstract]. Medicine and Science in Sport and Exercise, 30(5), S274.

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

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.

Kraemer, W., Marchitelli, L., Gordon, S., Harman, E., Dziados, J., Mello, R., Frykman, P., McCurry, D., & Fleck, S. (1990). Hormonal and growth factor responses to heavy resistance exercise protocols. Journal of Applied Physiology, 69(4), 1442-50.

Pollock, M., Abe, T., De Hoyos, D., Garzarella, L., Hass, C., & Werber, G. (1998). Muscular hypertrophy responses to 6 months of high- or low-volume resistance training [Abstract]. Medicine and Science in Sport and Exercise, 30(5), S116.

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.

Greg Bradley-Popovich holds a Master of Science in Exercise Physiology from the School of Medicine at West Virginia University, and a second M.S. in Human Nutrition, also from WVU. He is currently a Doctor of Physical Therapy scholar at Creighton University in Omaha, Nebraska where his area of focus is myoplasticity in resistance training. He welcomes your feedback and can be contacted at gregebp@aol.com.

Back to Library Main Page