Hypertrophy and Load

[Adonis]

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.

[Adonis]

Part 2

The last article we discussed microtrauma and why it is essential for hypertrophy, as well as how load is linearly related to microtrauma. In this concluding part, we will look into the endocrine and metabolic factors that are often used to determine load guidelines for optimal hypertrophy.


Endocrine Factors


As the name connotes, growth hormone (GH) is anabolic in nature. The loss of strength and muscle mass characteristic of GH deficient folks, and the reversal in these performance indices upon GH supplementation, clearly reveals its anabolic role (1,2,3). This information, coupled with the presence of greater GH secretion following resistance training, leads to a barrage of GH studies which are worth discussing.

Interestingly, common to all these studies is a greater growth hormone response following moderate loads using shorter rest periods when compared with high loads using longer rest periods (4,5,6). Kraemer et al., for instance, showed that performing a 10 RM with 1 minute rest between sets showed greater GH response than performing a 5 RM with 5 minute rest periods (4). Another study reported that performance of 20 sets of 1RM produced a slight increase in GH, whereas a substantial increase in GH was observed following 10 sets of 10 repetitions with 70% of 1RM (5). Call it coincidence if you like, but the protocol that shows the greatest GH release appears to be that of a typical bodybuilding routine, while the program which showed the least GH response mirrored what we typically consider a powerlifting program.


Although researchers couldn’t find any causal evidence, this GH hypothesis was evidence enough to establish the current load and rest time guidelines for hypertrophy.


But is the evidence really enough? Let's see: one of the early processes involved in the secretions of GH is the accumulation of metabolic products like lactate (La) and proton (H) in the muscle. The acidic environment in the muscle stimulates sympathetic nerve activity through chemoreceptors, which may send signals to the hypothalamus-pituitary system, and in turn trigger the secretion of GH (6,7). Apparently, the changes in GH seen in most of the studies were in phase with changes in the lactate concentration (4,5). This suggests that metabolic accumulation during exercise is the primary stimulus influencing GH release. For example, Takarada showed a low intensity (20 RM) exercise to cause a 290-fold increase in the concentration of GH when the blood flow was blocked by occlusion (8). This magnitude of increase, even larger than that reported using heavier loads, reveals metabolic accumulation due to occlusion to be primarily responsible for GH release.

Activities that stress the metabolic pathways like hyperventilation, breath holding, hypoxia and even nicotinic acid ingestion have been shown to profoundly influence growth hormone release (9,10). The high correlation of GH and metabolic products is further supported by the decreased GH response following induced alkalosis during cycling (11). And, keep in mind that all these changes in GH are transient: the resting concentration of GH has never been altered by any sort of resistance training (12,13,14).


Researchers began to suspect that raising the resting concentration of GH through supplementation might be the key to inducing hypertrophy. After all, GH is a common ingredient in any bodybuilder's drug list. As expected, this let lose another flurry of GH supplementation studies. Surprisingly the majority of the studies, whether in young men, older men or athletes, showed little change in muscle fiber size or strength after GH supplementation (15,16,17). The inability of even supraphysiological doses to elicit a hypertrophic response clearly undermines the role these training-induced tiny spikes of GH play in hypertrophy.


The discovery of local growth factors and their central role in hypertrophy was the final blow which shifted the foundation of the growth hormone hypothesis. Studies showed muscle growth even after the depression of circulating GH and IGF-1 levels (19). Worse yet, substantial increase in muscle mass was observed even after the GH axis was surgically interrupted (20,21).


Ironically, after all these counter evidences the repetition bracket of 8-12 is still hailed as the optimum range for hypertrophy- and the same old GH hypothesis is still being quoted in its defense.


Metabolic Factors


Though mechanical factors are essential to resistance training adaptations, metabolic factors have also been shown to play a role in hypertrophy.

The feeling of "pump" or “burn” is associated with the build up of these metabolic products (H, La, P, Cr, and K) in the muscle; the higher the number of reps in a set, the greater their accumulation and effect. Traditionally, studies have used three methods to understand the influence of metabolites on hypertrophy and strength. And, all three methods have revealed conflicting roles for metabolites in hypertrophy.


Eccentric contractions recruit fewer fibers than concentric contractions when using the same load. This distinct metabolic characteristic of contractions is often exploited to examine the importance of high force stress versus metabolic stress on hypertrophy (1,2). The second method involves the manipulation of rest intervals between sets: shorter rest intervals are metabolically more taxing than longer rest intervals (3,4). The occlusion method uses a pressurized cuff to occlude or clog the blood flow to the exercising muscle and in turn also increases the metabolic fatigue (5,6).


Now let's delve deeper and look at the possible mechanisms by which the metabolic milieu can impact hypertrophy. One possibility is that the ischemic condition and/or the metabolic changes in the muscle could lead to a greater recruitment of the fast twitch muscle fibers (Type 2). This is quite evident from the greater EMG activity recorded in the occlusion studies. For instance, Moore and his team specifically investigated the neuromuscular activity accompanying occlusion and showed that there is an early activation of Type 2 fibers for the occlusive group compared to the non-occlusive group (5). Another study showed the EMG activity in the low intensity exercise (40% 1RM) with occlusion to be almost equal to that in the high intensity exercise (80% 1RM) without occlusion (6).


This, along with the greater vulnerability of Type 2 fibers to injury and subsequent hypertrophy might very well be responsible for the greater hypertrophy and strength observed in some of the occlusion and rest interval studies using lighter loads.


Muscular hypertrophy is a combination of both sarcoplasmic and sarcomeric hypertrophy. In contrast to the actual growth of muscle fibers as in sarcomeric hypertrophy, sarcoplasmic hypertrophy involves the "swelling" of the muscle mainly via increase in water and glycogen accumulation without any change in strength. As evident from the occlusion studies, this increase is prompted largely by the accumulation of metabolites. For instance, exercise in the occluded group showed greater glycogen accumulation than in the non-occluded group (7). Additionally, studies showed glucose uptake to be enhanced in response to hypoxic conditions (8,9).

The increase in sarcoplasmic volume certainly contributes to overall hypertrophy and might partly explain the increase in muscle mass observed with higher rep training. And it is likely that comparison between repetition studies is distorted, since the current methods for measuring fiber size are incapable of identifying the contribution of sarcoplasmic hypertrophy to the overall muscle size.



Another mechanism which seems to suggest a role for metabolites in hypertrophy is the production of free radicals. It has been shown that muscular xanthase activity is elevated in hypoxic conditions and produces ROS (free radicals) during subsequent reperfusions. These free radicals via ischemic/reperfusion injuries have been shown to promote growth in smooth and cardiac muscles (11). The periodic application of occlusive stimulus, without any exercise stimulus, attenuates the disuse atrophy of leg muscles. This is possibly due to the direct effect free radicals have on muscle protein synthesis (10).


All said, hypertrophy through metabolic accumulation almost always occurred in conjunction with some sort of load training. Further, the importance of load is clearly revealed by the greater need for heavier loads in the strength continuum as opposed to the endurance continuum. Hypertrophy credits only a secondary role to metabolic fatigue.

Practical Considerations


It is well established that load is the primary stimulus for strength. And if you cared to notice, I've been trying to convey how load is the primary stimulus for hypertrophy too. The greater the load, the greater your strength and muscle gains. Simply put, you can expect greater gains in strength and hypertrophy by using your 1RM for 10 reps than using your 10RM for 10 reps.


So a fair question would be: are strength increases a good measure of muscle growth? I would say that strength is a yard stick for muscle growth, as well as the BEST indicator of progress one has in a hypertrophy routine. This might seem in stark contrast to those funky neural adaptation programs claiming to selectively target hypertrophy and leave out strength or vice versa.

The expression of strength is a blend of neural and muscular adaptations. Neural adaptations are in the form of increased activation, enhanced supraspinal output, intermuscular and intramuscular coordination, antagonist co-activation and so on (1,2). Muscular adaptations can not only show up in the form of increased muscle mass but also in the form of subtle architectural changes in pennation angle, muscle fascicle length and specific tension (3,4). However, most of us have missed that all these neural and architectural adaptations can only contribute so much so far, and beyond those “optimizations” muscle size becomes the leading and indeed the only adaptation that will allow continued gains in strength.

According to the scheme proposed by D. G Sale--a pioneer in field of neural adaptations--neural mechanisms largely contribute to strength gains during the early phase of training, after which muscular adaptations dominate (1). The same can be inferred from his recent remarks: “After years of training, I suspect that there is little or no neural adaptation that can increase strength further, apart from a change in technique. Strength in the highly trained state is almost entirely a function of muscle mass. This would explain why athletes ultimately resort to anabolic steroids - increasing muscle mass is the only way to increase strength further.”

The prevailing belief that powerlifters target the nervous system more so than the muscles by using low reps is yet to be proved by science. It is clear that heavy load around the 1RM causes higher fatigue and requires longer recovery periods than a lighter load. The high fatigue experienced is not just due to nervous system fatigue alone; disruptions in the contractile system are equally responsible (5,6). Powerlifting, often seen as a "little-to-do-with-muscle-event", has been shown to indeed be a function of muscle mass, and lifting performance has been shown to be limited by the ability to accumulate muscle mass (3). And once these elite lifters hit their genetic limits with regard to muscle mass, strength increases are marginal at best (7).


Even the CNS fatigue which seems to be the buzz word these days is not just a neural phenomenon as it sounds. Overtraining as most of us might have experienced hits in the form of generalized fatigue, depression, muscle and joint pain, loss of appetite, decreased performance, decreased muscular strength and so forth. These signs/symptoms of overtraining are often blamed as a neural phenomenon. But according to the cytokine hypothesis of overtraining, repetitive trauma to the musculoskeletal system due to high intensity/volume training is the predominant cause of overtraining (8,9). That is, the many physiological and behavioral signs associated with overtraining syndrome are basically triggered by a musculoskeletal injury.


But the question remains: If strength is highly correlated with muscle size, what about those bodybuilders who are big yet not strong?


First and foremost, elite class bodybuilders are dipped in drugs. And drugs lie right to your face. Testosterone and GH administration have shown to increase retention of fluid (water/salt) within the muscle that would cause an enlargement of the muscle fibers with little strength change (15,16). Second, testosterone is shown to cause changes in strength by altering the muscle architecture in the absence of any major increase in muscle mass (4,14). And when on test you can always compromise on load unlike the natural trainees. It is now becoming increasingly clear that testosterone promotes its anabolic effects primarily through an increase in satellite cell proliferation and myonuclear number (10,4). Sadly for natural trainees the only viable option to activate satellite cell is through load mediated injury.


More important, direct comparison with highly trained athletes can be misleading because the neural patterns have probably matured in these individuals. Thus without major neural changes, the force per cross sectional area remains the same or decreased compared to less trained individuals. Further, some of the incongruity surrounding strength with enlarging muscle can be accounted by changes within the muscle cells like enlarged interstitial space, and decreased protein concentration (11). So, don’t let appearances lead your conclusions.


Whether you hit a muscle group thrice a week or once a week, whether you perform 1 set or 6 sets, high rep or low rep, if strength is climbing, stick with it. The tenets of typical bodybuilding routines like repetitions of 8-12, sets to failure, changing exercises often, and short rest intervals were all laid on the faulty premise that not load but fatigue is the primary stimulant for hypertrophy.


Opt for a periodized routine (cycling of loads to manage fatigue) built on a few basic and a few auxiliary exercises with adequate rest between sets. Additionally, stick to around 5 reps per set, and terminate each set 1 or 2 reps short of failure. A drop set of 15-20 reps right after your last work set would work well to create metabolic fatigue without sacrificing load.


Anyhow, to make a long story short, the ultimate hypertrophy routine will be the ultimate strength routine.


Good luck.

[Adonis]

Refrences 1

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Refrences 2

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17) Yarasheski, K. E., Zachweija, J. J., Angelopoulos, T. J., & Bier, D. M. (1993). Short-term growth hormone treatment does not increase muscle protein synthesis in experienced weight lifters. Journal of Applied Physiology, 74(6), 3073-6.



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Metabolic Factors

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2) Hortobagyi T, Hill JP, Houmard JA, Fraser DD, Lambert NJ, Israel RG. Adaptive responses to muscle lengthening and shortening in humans. J Appl Physiol. 1996 Mar;80(3):765-72.

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4) Folland, J. P, Irish, C. S., Roberts, J. C., Tarr, J. E., and Jones, D. A. (2002). Fatigue is not a necessary stimulus for strength gains during resistance training. Br J Sports Med 2002;36:370-373.

5) Moore, D. R, Burgomaster, K. A, Schofield, L. M, Gibala, J. M, Sale, D. G, and Phillips, S. M. (2004). Neuromuscular adapataions in human muscle following low intensity resistance training with vascular occlusion. European Journal of Applied Physiology, 92, 399-406.



6) Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N.Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans.J Appl Physiol. 2000 Jun;88(6):2097-106.

7) Burgomaster, K. A, Moore, D. R., Schofield LM, Phillips SM, Sale DG, Gibala MJ.(2003).Resistance training with vascular occlusion: metabolic adaptations in human muscle. 35(7),1203-8.

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6) Fry AC, Kraemer WJ, van Borselen F, Lynch JM, Marsit JL, Roy EP, Triplett NT, Knuttgen HG. Performance decrements with high-intensity resistance exercise overtraining. Med Sci Sports Exerc. 1994 Sep;26(9):1165-73.

7) Hakkinen K, Pakarinen A, Alen M, Kauhanen H, Komi PV.Neuromuscular and hormonal adaptations in athletes to strength training in two years.J Appl Physiol. 1988 Dec;65(6):2406-12.

8) Smith, L. L.Tissue trauma: the underlying cause of overtraining syndrome? J Strength Cond Res. 2004 Feb;18(1):185-93. Review.
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12) Forbes G. B. Exercise and lean weight: the influence of body weight.
Nutr Rev. 1992 Jun;50(6):157-61. Review.

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14) Storer TW, Magliano L, Woodhouse L, Lee ML, Dzekov C, Dzekov J, Casaburi R, Bhasin S.estosterone Dose-Dependently Increases Maximal Voluntary Strength and Leg Power, but Does Not Affect Fatigability or Specific Tension. Clin Endocrinol Metab. 2003 Apr;88(4):1478-85.

15) Creutzberg, Eva C.; Schols, Annemie M.W.J. Anabolic Steroids. Current Opinion in Clinical Nutrition & Metabolic Care. 2(3):243-253, May 1999.

16) Yarasheski, K. E., Zachwieja, J. J., Campbell, J. A., & Bier, D. M. (1995). Effect of growth hormone and resistance exercise on muscle growth and strength in older men. American Journal of Applied Physiology, 268(2), E268-E276.

[Old_Fart2]

Opt for a periodized routine (cycling of loads to manage fatigue) built on a few basic and a few auxiliary exercises with adequate rest between sets. Additionally, stick to around 5 reps per set, and terminate each set 1 or 2 reps short of failure. A drop set of 15-20 reps right after your last work set would work well to create metabolic fatigue without sacrificing load.

How do you "cycle loads to manage fatigue" yet stick to 5 reps per set? Does that mean you train at less than maximum effort some days and at maximum effort on other days? 5 reps would be about 90% of your 1RM.

[Adonis]

By that, 5 reps per set for the majoirty of your wokouts, but a rep range of 1-7 reps would be optimal for hypertrophy.

[mkruzel88]

I was just reading an article that said 3-6 sets of 8-15 reps for hypertrophy
1-3 sets of 15-20 reps for endurance
2-4 sets of 6-8 reps for strength
2-4 sets of 3-5 reps for power

Something like that

It got me worried that uping my sets and lowering my reps was the wrong thing to do. It would be nice to be strong but honestly I care more about looking strong. I lift to build muscle.

So I searched around here and it's nice to read an article with some real info from actual studies. It makes sence to me that muscle mass and strength go hand in hand. It seems that you would need one in order to have the other.

So I'll stick withmy 4-6 reps and if I get strong too it's a bonus.

Adonis, this is a fantastic article. I'm suprised there are not more comments here. Maybe that's because it was a little tough to read. Lots of big words. Don't tell me true what they say that muscleheads lift to make up for lack of uuuummmmm, reading ability. ; )

I just wanted to comment and bump this up so people look it over again.

And it looks like it's your own. Hope you got a good grade. I'd give it at worst a B+. Probobly better.

Thanks

Mike