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Hypertrophy and Load



by Anoop Balachandran

Needless to say, resistance training induced hypertrophy is inextricably linked to its participating variables, such as frequency, load, rest intervals, and the number of sets. As is true for adaptations like endurance and strength, the severity of the response is dependent on the manipulation of these variables. Although the role of these variables has been extensively studied and well documented, the optimum ”value” of these variables for maximum hypertrophy is still under considerate debate.

Among these variables, load seems to be the most dominant variable dictating these muscular adaptations, and hence will assume the lead role in this article. Load, typically advertised in terms of repetition maximum (RM), can be equated to the number of repetitions performed in a set. The generally accepted repetition bracket for hypertrophy is 67 – 85% 1RM, which can be equated to 6–12 repetitions, and 85-100% 1RM (1-6 repetition) for strength (7, 21).

Though the load recommendations for strength and hypertrophy seem to differ, except for existential evidence, there is hardly any scientific data to support this differential rep continuum. Interestingly, in contrast to the above said guidelines, the couple of studies which directly compared low rep and high rep protocols demonstrated similar hypertrophic responses (10, 29). Influenced by the above said discrepancies, this article will look into the factors implicated in skeletal muscle hypertrophy and examine how they are impacted by the manipulation of load.

Before we continue, I will give an introduction to the well orchestrated events leading to skeletal muscle hypertrophy. Studies, both in vivo and in vitro have repeatedly demonstrated the involvement of two fundamental events in the hypertrophy of muscle fibers. The first and foremost is an increase in protein synthesis, mainly attributed to increased mRNA activity (translational capacity). The unstable relationship between protein synthesis and protein degradation represents the basis for hypertrophy. Muscle growth follows when a positive protein balance is established and maintained by an increase in protein synthesis that exceeds the rate of protein breakdown (24).

The second facet of hypertrophy involves an increase in mRNA abundance (transcriptional capacity) via differentiation and proliferation of satellite cells, which is critical for donating additional myonuclei to the enlarging myofibers. Unlike most other cells, mammalian skeletal muscle is multinucleated. Each and every nucleus is responsible for a particular volume of the cell, known as a nuclear domain (16). This domain is tightly regulated and any increase in the fiber cross-sectional area requires a concomitant increase in the number of myonuclei (6). Conversely, if the cell experiences serious atrophy as seen in immobilization, space flight, malnutrition, or tenotomy, the number of myonuclei decreases by a process of programmed cell death (20, 26). This indicates that the tight regulation of the domain is preserved in either direction.

The concept of a finite relationship between fiber size and myonuclei number predicts that the hypertrophying fibers must increase their myonuclear number proportionally. However, shortly after birth, mammalian myofibers are permanently differentiated, and thus cannot undergo mitotic division or directly increase their myonuclear number by means of the usual myonuclear division process (11). Therefore, hypertrophying fibers require an external source of new nuclei to maintain a relatively constant nucleus-to-fiber size ratio. A significant body of evidence blames satellite (stem) cells as the probable source of the new myonuclei (8, 28).The role of satellite cells in hypertrophy has been further corroborated by studies using radiation to prevent satellite cell activity, thereby negating any potential hypertrophic response (5, 25).

In short, with utter disregard for the set tone, satellite cell activity is required for you to get big while protein synthesis is necessary for you to stay big. Frankly, at first, I thought of painting a scientific tone to the article, but soon realized that the complexity of the topic at hand would undermine the message. Perhaps, ignoring my mom’s words, there was never a scientist in me to begin with. Without further delay and resuming a laid back tone, let us cruise towards our next topic: how satellite cells are triggered and how load can have any bearing on this.

Mechanical Factors
Staying true to the principle of specificity, the cellular level changes discussed above are specific to the muscle that is experiencing functional changes. That is, the factors that confine for example almost exclusively the growth of the biceps when the biceps are exercised alone are largely mediated by things that are intrinsic or local to the exercised muscle (19). As it turns out, mounting evidence has revealed growth factors to be responsible for these localized changes.

Among these growth factors, insulin like growth factor (IGF-1) is known to stimulate satellite cell activity as well as protein synthesis, and has received increasing attention in the studies of hypertrophy. This increasing attention to IGF-1 is understandable, given its ability to stimulate both proliferation and differentiation, making it unique within the ranks of growth factors. Lest you get confused, this locally expressed IGF-1 acts independently of any change in the serum growth hormone or the serum IGF-1.

More importantly, IGF-1 is sensitive to mechanical load, as observed in a number of in vivo activity models, such as increased loading, stretch, and eccentric contraction (recently discovered, a specific isoform of IGF-1 called mechano growth factor is exclusively regulated by mechanical loading and/stretch) (1, 2, 3). To further seal IGF-1’s fate, infusion of local IGF-1 directly to skeletal muscles has shown increased muscle mass (4). Looking at all the studies (and the studies which I have omitted for the fear of turning this article into an IGF-1 review paper), I cannot help but conclude that locally expressed IGF-1 is the CHIEF player in mediating muscle growth.

Just when you thought it was over, I’d like to share what Bamman and his crew discovered when investigating IGF-1’s role in resistance training (9). Not surprisingly, they found that eccentric exercise showed the greatest muscle damage and muscle soreness. As suspected, they found significant increases in IGF-1 mRNA concentration for eccentric than concentric exercises (p<0.05). Based on the soreness and the creatine kinase (CK) data, the researchers concluded myofibrillar disruption and/or sarcolemma damage most likely to play a role in activating the IGF-1 system, and in turn activating the satellite cells

The conclusion is in accord with the results observed in vitro, suggesting that the release of other growth factors like hepatocyte growth factor and fibroblast growth factor are also injury-mediated, and their expression is proportional to the degree of injury (13, 27). Another study of note also revealed that the magnitude of protein synthesis was shown to depend on the extent of muscle damage (14). And, as you know very well, muscle damage has been consistently observed in resistance training studies (21).

As an example of the infamous Repeated Bout Effect (RBE), it was shown using electron microscope that untrained subjects suffered 35% more myofibrillar disruption than strength trained individuals after a typical weight training session, and 40% of fibers of the untrained group displayed severe disruption compared to 3% of the strength trained participants (I guess that’s one more study for Bryan to stack in his HST archives) (17, 18). Now you tell me why you think you stopped growing? Connecting the dots, we get the picture of IGF-1 expression being injury-mediated, with its expression being dependent on the severity of the injury.

It can be clearly inferred from the previous passages that as the load goes up, the magnitude of the injury should go up too. And this is precisely what Nosake, Newton and Saka concluded after their study (23). They found that the group performing 12 maximal eccentric elbow flexion exercises compared to the group who performed 3600 elbow flexion showed significantly greater muscle damage as tested from B-mode ultrasound and creatine kinase (p<0.05).

In their second study, Nosake, Newton and Saka concluded that though the magnitude of damage was similar for maximal and submaximal eccentric loading (50% RM), the secondary damage was less after the submaximal loading (22). Though low load activities like endurance training and downhill protocols are said to cause marked muscle damage, the damage appears to be relatively low compared to maximal eccentric exercise of the elbow flexors (12). As an attempt to link hypertrophy and load, an extensive review of weight training studies illustrated greater hypertrophic responses associated with greater load in both Type 1 and Type 2 fibers (16) (29).

Taken together, all these studies has given me enough confidence to state that the extent of muscle damage is dependent primarily on load, and the degree of damage traces a linear relationship with load.

So the moral of the story is that microtrauma is mandatory for continued hypertrophy, and the extent of hypertrophy is dictated largely by the load on the bar. The endocrine and metabolic factors implicated in hypertrophy and how load affects those factors will be explored in the next article. Until then, happy loading.

References
1) Adams, G. (1998). Role of insulin-like growth factor-I in the regulation of skeletal muscle adaptation to increased loading. Exercise and Sports Sciences Reviews, 26, 31-60.

2) Adams, G. R., & Haddad, F. (1996). The relationships between IGF-1, DNA content, and protein accumulation during skeletal muscle hypertrophy. Journal of Applied Physiology, 81, 2509-2516.

3) Adams, G. R., Haddad, F., & Baldwin, K. M. (1999). Time course of changes in markers of myogenesis in overloaded rat skeletal muscles. Journal of Applied Physiology, 87, 1705-1712

4) Adams, G. R., & McCue, S. A.(1998). Localized infusion of IGF-I results in skeletal muscle hypertrophy in rats. Journal of Applied Physiology, 84(5),1716-1722.

5)Adams, G. R, Vincent, J. C., Fadia, H., & Kenneth, M. B.(2002). Cellular and molecular responses to increased skeletal muscle loading after irradiation. American Journal of Physiology, 283(4), 1182-1195.

6) Allen, D. L., Yasui, T., Tanaka, Y., Ohira, S., Nagaoka, C., Sekiguchi, W. E., Hinds, R. R., Roy, & Edgerton. (1996). Myonuclear number and myosin heavy chain expression in rat soleus single muscle fibers after spaceflight. Journal of Applied Physiology, 81, 145-151.

7) Baechle, T. R., & Earle, R. W. (2000). Essentials of strength and conditioning (2nd ed.). Champaign, IL: Human Kinetics.

8) Barton-Davis, E. R., Shoturma, D. I., & Sweeney, H. L. (1999). Contribution of satellite cells to IGF-I induced hypertrophy of skeletal muscle. Acta Physiologica Scandinavica 167, 301-305.

9) Bamman, M. M., Shipp, J. R., Jiang, J., Gower, B. A., Hunter, G. R., Goodman, A., McLafferty, C. L., & Urban, R. J. (2001). Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans. American Journal Physiology and Endocrinology Metabolism, 280(3), E383-90.
10) Campos, G. E., Leucke, T. J., Wendeln, H. K., Toma, K., Hagerman, F. C., Murray, T. F., Ratamess, N. A., Kramer, W. J., & Staron, R. S. (2002). Muscular adaptations in response to three different resistance-training regimens: specificity of repetition maximum training zones. European Journal of Applied Physiology, 88(1-2), 50-60.

11) Chambers, R. L., & McDermott, J. C. (1996). Molecular basis of skeletal muscle regeneration. Canadian Journal of applied physiology, 21, 155-184.

12) Clarkson, P. M. & Hubal, M. J.. (2002). Exercise-induced muscle damage in humans. American Journal of Physical Medicine and Rehabilitation, 81(11), S52-S69.

13) Clarke, M. S., Khakee, R., & McNeil, P.L. (1993). Loss of cytoplasmic basic fibroblast growth factor from physiologically wounded myofibers of normal and dystrophic muscle. Journal of Cell Science, 106, 121-133.

14) Dolezal, B. A., Potteiger, J. A., Jacobsen, D. J., & Benedict, S. H. (2000). Muscle damage and resting metabolic rate after acute resistance exercise with an eccentric overload. Medicine and science in sports and exercise, 32 (7), 1202–1207.

15) Edgerton, V. R., & Roy, R. R. (1991). Regulation of skeletal muscle fiber size, shape and function. Journal of Biomechanics, 1, 123-133.

16) Fry, A. C. (2004). The role of resistance exercise intensity on muscle fiber adaptations. Sports Medicine, 34(10), 663-679.

17) Gibala, M. J., Interisano, S. A., Tarnopolsky, M. A., Roy, B. D., MacDonald, J. R., Yarasheski, K. E., & MacDougall, J, D. (2000). Myofibrillar disruption following acute concentric and eccentric resistance exercise in strength-trained men. Canadian Journal of Physiology and Pharmacology, 78(8), 656-661.
18) Gibala, M. J., MacDougall, J. D., Tarnopolsky, M. A., Stauber, W. T., & Elorriaga, A. (1995). Changes in human skeletal muscle ultrastructure and force production after acute resistance exercise. Journal of Applied Physiology, 78(2),702-708.

19) Goldberg, A. L. (1967). Work induced growth of skeletal muscle in normal and hypophsectomized rats. American journal of applied physiology, 213, 1193-1198.

20) Grounds, M. D. (1998). Muscle regeneration: Molecular aspects and therapeutic implications. Current Opinion in Neurology, 12, 535-543.

21) Kraemer, W. J., Ratamess, N. A., & Duncan, N. F. (2002). Resistance training for health and performance. Current Sports Medicine Reports, 1, 165-171.

22) Nosaka, K., & Newton, M. (2002). Difference in the magnitude of muscle damage between maximal and submaximal eccentric loading. Journal of Strength and Conditioning Research, 16(2), 202-208.

23) Nosaka, K., Newton, M., & Sacco, P. (2002). Muscle damage and soreness after endurance exercise of the elbow flexors. Medicine and science in sports and exercise, 34(6), 920-927.

24) Pitkanen, H.T., Mykanen, T., Knuutinen, J., Lahti, K., Keinanen, O., Alen, M., Komi, P.V., & Mero, A. A. (2003). Free amino acid pool and muscle protein balance after resistance exercise. Medicine and science in sports and exercise, 35(5), 784-792.

25)Phelan, J. N., & Gonyea, W. J. (1997). Effect of radiation on satellite cell activity and protein. Anatomical Records, 247(2), 179-188.

26) Schultz, E. (1989). Satellite cell behavior during skeletal muscle growth and regeneration. Medicine and science in sports and exercise, 21, 181-186.

27) Sheehan, S. M., Tatsumi, R., Temm-Grove, C.J., & Allen, R. E. (2000). HGF is an autocrine growth factor for skeletal muscle satellite cells in vitro. Muscle Nerve, 23, 239-245.

28) Sinha-Hikim, S. M., Roth, M. I., Lee, H., & Bhasin, S. (2003). Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men. American Journal Physiology and Endocrinology Metabolism, 285(1), E197 – 205.

29) Florini, J. R., Ewton, D. Z., & Coolican, S. A. (2002). I knew that you were gonna fall for it. Don’t worry, I wont tell anybody.

30) Weiss. W., Coney, H. D., & Clark, F. C. (2000). Gross measures of exercised induced muscular hypertrophy. Journal of orthopedic and sports physical Therapy, 30, 143-148.

 





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