Left, an example of human muscular hypertrophy.
By Benjamin J. Falk (1853-1925) - http://en.wikipedia.org/wiki/Image:Eugen_Sandow.jpg, originally uploaded 13:46, 31 August 2005 by en:User:Johnteslade, Public Domain, https://commons.wikimedia.org/w/index.php?curid=669519
People show individual variation in the ease in which they can grow muscle in response to stimulus (muscle hypertrophy). There are hard gainers (such as myself) and there are men who have bulging biceps despite never having ever touched a weight; their everyday activity suffices to stimulate growth. An example of the latter is famous American baseball player Jimmie Foxx, pictured here, who claimed to have developed his famous physique and massive strength simply as a result of doing farm work as a youth. As far as anyone knows, Foxx never did any weight training whatsoever nor did he perform any sort of exercise to maintain his muscular development apart from playing baseball. In contrast, many men spend years lifting weights and drinking protein shakes while never achieving the physique of “the natural” Foxx, and these men start losing their hard-earned gains as soon as they stop going to the gym. And when the “naturals” do work out with weights, their gains are rapid and impressive.
People also differ in their “starting” (basal) level of muscle development before they encounter muscle-growing stimuli. There are the big-boned, naturally muscular mesomorph types, the small-boned thin ectomorph types, and the big-boned and overweight endomorphs who have much more fat, and much less muscle, than the mesomorphs.
Is there are correlation between basal muscle size and the ability to put on muscle? The popular conception (see below) is that ease of muscle growth goes as follows: mesomorph>endomorph>ectomorph. Generally speaking: Is basal muscle mass a good predictor of muscle gain achieved from overload-exercise? Do people who have the most muscle before exercising tend to make the greatest gains?
Researchers performed a study using mice, and utilized eight different mouse strains to mimic the genetic variability found in humans. Male mice were used. One strain (BEH) was myostatin-mutant, another was BEH with the wild-type (normal) myostatin gene added back in (BEH+/+). Myostatin is a known inhibitor of muscle growth, and mammals born with mutant myostatin that does not function properly tend to be much more muscular than their normal counterparts. However, pharmacological interventions to inhibit myostatin have not resulted in positive results with respect to muscle growth. Therefore, myostatin status was one interesting variable to look at in this study. The other six strains were naturally wild-type for myostatin.
The muscles examined were the soleus (slow-twitch) and plantaris (fast-twitch) muscles; therefore, slow vs. fast twitch was another variable studied. Muscle growth was stimulated by ablation of the gastrocnemius muscle by removing most of the muscle from both hind legs; therefore, the soleus and plantaris muscles had to work harder to compensate for the loss of the gastrocnemius, stimulating growth.
The mice strains exhibited different levels of basal (before experiment) size of their soleus and plantaris muscles. Not surprisingly, the myostatin-mutant BEH mice were very well developed; also not surprising, there was a correlation between skeleton size and muscle weight (we can consider some mouse strains to be more “mesomorphic” than others).
The main findings from the experiment were: (a) there was significant strain-to-strain differences in the amount of muscle growth observed, (b) the well-muscled myostatin-mutant BEH mice were less (not more) responsive to muscle-growth stimulus, and (c) some mouse strains showed greater soleus growth and others showed greater plantaris growth.
Looking at those three points, we can say first that just as different people exhibit different potential for muscle growth, so do different strains of mice.
Second, and most surprising, there was no positive correlation between mouse strains with the most basal muscle (“natural” muscle before the experiment) and those mice that showed the greatest muscle growth with the experimental stimulus. Most interestingly, the myostatin-mutant mice showed the least growth, which may explain why pharmacological inhibition of myostatin hasn’t been effective. Possibly, myostatin inhibition allows for muscle growth when the myostatin function is lacking from conception or birth, but the function of myostatin may be different when considering fully-developed adult muscles. Myostatin may possibly not inhibit adult muscle growth in response to overload stimulus; or even may be necessary for such growth. More studies are needed. The “bottom-line” is that the most “naturally muscular” mice did NOT show the most muscle growth.
Third, different strains of mice showed a “preference” for which muscle grew the fastest; this is analogous to people having more responsive and less responsive body parts. For example, we hear anecdotes of one person who easily gets muscular legs from squats but who cannot build a big upper body (or vice versa), some people build chest easily but not biceps, some people develop big triceps and a big neck but small lats. Many people have trouble with the calves and forearms. This situation seems to be mimicked in the mice.
The study did not identify genes responsible for these differences, which would be an important area for future study.
If we take these findings out face value, they seem to go against popular conceptions about muscle gain. For example, casual observation would lead one to conclude that it is the “naturally muscular” mesomorph, with abundant basal muscle mass even before exercise, who shows the greatest hypertrophy with weight training, while their less muscular counterparts struggle to make gains.
Two general possible explanations for this discrepancy are as follows. First, it is possible that mice, particularly myostatin-mutant mice, are not a suitable model for human differences, and so the findings of this mouse study would not strictly apply to the human case. Second, it may be that the mouse findings do indeed apply to humans, and the confusion revolves around human perception. Perhaps, people judge physiques on their final size and not the net gain. Therefore, while the skinny ectomorph may show the greatest percentage gains, the naturally muscular mesomorph starts so far ahead in basal musculature that the mesomorph’s final physique would be much more impressive than the ectomorph’s The mouse data support this possibility. For example, looking at the findings, we can compare the myostatin-mutant BEH strain to the D2 strain. D2 mice showed significant greater growth in the soleus muscle (1.7-fold vs. 1.3-fold) and the plantaris muscle (1.5-fold vs. 1.3-fold) comparted to BEH mice. However, the BEH mice were far, far ahead of the D2 mice in basal (starting) muscle size. Basal soleus weight for the BEH mice was around 3-fold greater than that for D2 mice, and basal plantaris weight was nearly 4-fold higher. So, when all was said and done, the BEH mice ended up with bigger muscles than the D2 mice, despite showing a smaller percentage increase. Maybe there is a threshold for muscle growth, so that, for example, the BEH mice simply could not reach sizes reflecting a 1.5-1.7-fold increase?
It is of course also possible that both explanations are to some extent true.
People show individual variation in the ease in which they can grow muscle in response to stimulus (muscle hypertrophy). There are hard gainers (such as myself) and there are men who have bulging biceps despite never having ever touched a weight; their everyday activity suffices to stimulate growth. An example of the latter is famous American baseball player Jimmie Foxx, pictured here, who claimed to have developed his famous physique and massive strength simply as a result of doing farm work as a youth. As far as anyone knows, Foxx never did any weight training whatsoever nor did he perform any sort of exercise to maintain his muscular development apart from playing baseball. In contrast, many men spend years lifting weights and drinking protein shakes while never achieving the physique of “the natural” Foxx, and these men start losing their hard-earned gains as soon as they stop going to the gym. And when the “naturals” do work out with weights, their gains are rapid and impressive.
People also differ in their “starting” (basal) level of muscle development before they encounter muscle-growing stimuli. There are the big-boned, naturally muscular mesomorph types, the small-boned thin ectomorph types, and the big-boned and overweight endomorphs who have much more fat, and much less muscle, than the mesomorphs.
Is there are correlation between basal muscle size and the ability to put on muscle? The popular conception (see below) is that ease of muscle growth goes as follows: mesomorph>endomorph>ectomorph. Generally speaking: Is basal muscle mass a good predictor of muscle gain achieved from overload-exercise? Do people who have the most muscle before exercising tend to make the greatest gains?
Researchers performed a study using mice, and utilized eight different mouse strains to mimic the genetic variability found in humans. Male mice were used. One strain (BEH) was myostatin-mutant, another was BEH with the wild-type (normal) myostatin gene added back in (BEH+/+). Myostatin is a known inhibitor of muscle growth, and mammals born with mutant myostatin that does not function properly tend to be much more muscular than their normal counterparts. However, pharmacological interventions to inhibit myostatin have not resulted in positive results with respect to muscle growth. Therefore, myostatin status was one interesting variable to look at in this study. The other six strains were naturally wild-type for myostatin.
The muscles examined were the soleus (slow-twitch) and plantaris (fast-twitch) muscles; therefore, slow vs. fast twitch was another variable studied. Muscle growth was stimulated by ablation of the gastrocnemius muscle by removing most of the muscle from both hind legs; therefore, the soleus and plantaris muscles had to work harder to compensate for the loss of the gastrocnemius, stimulating growth.
The mice strains exhibited different levels of basal (before experiment) size of their soleus and plantaris muscles. Not surprisingly, the myostatin-mutant BEH mice were very well developed; also not surprising, there was a correlation between skeleton size and muscle weight (we can consider some mouse strains to be more “mesomorphic” than others).
The main findings from the experiment were: (a) there was significant strain-to-strain differences in the amount of muscle growth observed, (b) the well-muscled myostatin-mutant BEH mice were less (not more) responsive to muscle-growth stimulus, and (c) some mouse strains showed greater soleus growth and others showed greater plantaris growth.
Looking at those three points, we can say first that just as different people exhibit different potential for muscle growth, so do different strains of mice.
Second, and most surprising, there was no positive correlation between mouse strains with the most basal muscle (“natural” muscle before the experiment) and those mice that showed the greatest muscle growth with the experimental stimulus. Most interestingly, the myostatin-mutant mice showed the least growth, which may explain why pharmacological inhibition of myostatin hasn’t been effective. Possibly, myostatin inhibition allows for muscle growth when the myostatin function is lacking from conception or birth, but the function of myostatin may be different when considering fully-developed adult muscles. Myostatin may possibly not inhibit adult muscle growth in response to overload stimulus; or even may be necessary for such growth. More studies are needed. The “bottom-line” is that the most “naturally muscular” mice did NOT show the most muscle growth.
Third, different strains of mice showed a “preference” for which muscle grew the fastest; this is analogous to people having more responsive and less responsive body parts. For example, we hear anecdotes of one person who easily gets muscular legs from squats but who cannot build a big upper body (or vice versa), some people build chest easily but not biceps, some people develop big triceps and a big neck but small lats. Many people have trouble with the calves and forearms. This situation seems to be mimicked in the mice.
The study did not identify genes responsible for these differences, which would be an important area for future study.
If we take these findings out face value, they seem to go against popular conceptions about muscle gain. For example, casual observation would lead one to conclude that it is the “naturally muscular” mesomorph, with abundant basal muscle mass even before exercise, who shows the greatest hypertrophy with weight training, while their less muscular counterparts struggle to make gains.
Two general possible explanations for this discrepancy are as follows. First, it is possible that mice, particularly myostatin-mutant mice, are not a suitable model for human differences, and so the findings of this mouse study would not strictly apply to the human case. Second, it may be that the mouse findings do indeed apply to humans, and the confusion revolves around human perception. Perhaps, people judge physiques on their final size and not the net gain. Therefore, while the skinny ectomorph may show the greatest percentage gains, the naturally muscular mesomorph starts so far ahead in basal musculature that the mesomorph’s final physique would be much more impressive than the ectomorph’s The mouse data support this possibility. For example, looking at the findings, we can compare the myostatin-mutant BEH strain to the D2 strain. D2 mice showed significant greater growth in the soleus muscle (1.7-fold vs. 1.3-fold) and the plantaris muscle (1.5-fold vs. 1.3-fold) comparted to BEH mice. However, the BEH mice were far, far ahead of the D2 mice in basal (starting) muscle size. Basal soleus weight for the BEH mice was around 3-fold greater than that for D2 mice, and basal plantaris weight was nearly 4-fold higher. So, when all was said and done, the BEH mice ended up with bigger muscles than the D2 mice, despite showing a smaller percentage increase. Maybe there is a threshold for muscle growth, so that, for example, the BEH mice simply could not reach sizes reflecting a 1.5-1.7-fold increase?
It is of course also possible that both explanations are to some extent true.
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