gandhisays
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HOW DOES MUCLE FIBER HYPERPLASIA OCCUR?
There are two primary mechanisms in
Check out these ‘split’ or branching fibers.
which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) . And perhaps the primary mechanism is via the activation and proliferation of satellite cells . Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated . Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells).
These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).
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ROLE OF MUSCLE FIBER DAMAGE
There is robust evidence which has shown the importance of eccentric contractions in producing muscle hypertrophy . It is known that eccentric contractions produces greater injury than concentric or isometric contractions. We also know that if you can induce muscle fiber injury, satellite cells are activated. Both animal and human studies point to the superiority of eccentric contractions in increasing muscle mass. However, in the real world, we don’t do pure eccentric, concentric, or isometric contractions. We do a combination of all three. So the main thing to keep in mind when performing an exercise is to allow a controlled descent of the weight
being lifted. And on occasion, one could have his/her training partner load more weight than can be lifted concentrically and spot him/her while he/she performs a pure eccentric contraction. This will really put your muscle fibers under a great deal of tension causing microtears and severe delayed-onset muscle soreness. Thus, the repeated process of injuring your fibers (via weight training) followed by a recuperation or regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect.
THE MYTH OF SARCOPLASMIC VS MYOFIBRILLAR HYPERTROPHY
This is perhaps one of the more annoying and contrived controversies in the field of skeletal muscle plasticity. Was it Joseph Goebbels who said that “if you repeat a lie often enough, it becomes the truth”? This is a perfect example of this maxim. Frankly, I don’t give a shit who started this mythical beast known as sarcoplasmic hypertrophy.
The fact of the matter is there has never been evidence to suggest that increases in skeletal muscle size can be the result of selective hypertrophy of the sarcoplasm. It’s not like you can train to increase the sarcoplasm one day; and then the next day, train for myofibrillar growth. Roughly 70-80% of the volume of a muscle fiber is the myofibrillar component.
It should be as clear as the Montana sky that gains in muscle size are largely due to increases in contractile protein. In fact there is a classic paper by Claassen et al. (Journal of Physiology, 1989, 409: 491-495) entitled “Muscle Filament Spacing and Short-term Heavy-Resistance Exercise in Humans.” They found that the “linear distance between myofilaments as well as the ratio of actin to myosin filament did not change with training.”
So the next time you hear a bodybuilder or training guru talk about achieving greater ‘muscle density,’ they’re just making shit up. And while you’re at it, if you like your doctor you can keep your doctor. And if you like your healthcare plan, you can keep it.
Moreover, don’t confuse gains in strength without gains in skeletal muscle size as evidence for sarcoplasmic hypertrophy. As my teenage daughter would say, ‘isn’t it obvy?’ Yes, it is obvy (obvious) that improvements in rate coding, muscle activation patterns and motor unit recruitment do indeed account for changes in strength without a concomitant increase in skeletal muscle size. However, if someone shows me evidence that an enlarged muscle or muscle fiber has an increase in cytoplasm with no change in the volume of actin and myosin, then I’ll alter my conclusions. Until then, show me the evidence. And if it doesn’t exist, then quit bs’ing everyone about ‘sarcoplasmic’ hypertrophy. What’s next? Pigs flying, unicorns trotting, the Jets winning? For another opinion, check out Stu Phillips PhD little ditty: https://twitpl.us/t/4Xeb
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HAS THE HYPERPLASIA DEBATE BEEN SETTLED?
To quote the genius of Yogi Berra, “I wish I had an answer to that because I’m tired of answering that question.” In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia can contribute to whole muscle hypertrophy.
There is human as well as rat, cat, and bird data which support this proposition , a veritable wild kingdom of evidence.
Does muscle fiber hyperplasia occur under all circumstances? No. There are several studies which show no change in fiber number despite significant increases in muscle mass . Is it possible that certain muscles can increase fiber number more so than others? Maybe.
Can any Joe Schmoe off the street who lifts weights to get in better shape increase the number of fibers for instance in their biceps? Maybe, maybe not. What about the elite bodybuilder who at 5’8″ tall is ripped at a body weight of 250 lbs.?
Are his large muscles purely the result of muscle fiber hypertrophy? I think it would be extremely naive to think that the massive size attained by elite bodybuilders is due solely to fiber hypertrophy.
Despite the contention that fiber number is constant once you’re born, there is an abundance of evidence which shows that muscle fiber number can increase post-natally.
Always wondered how much hyperplasia could occur in the gluteus maximus. One, two, 5999, 190000, 699699, oh my…keep counting.
Besides, there is nothing magical at birth which says that now that you’re out of the womb, you can no longer make more muscle fibers. A mechanism exists for muscle fiber hyperplasia and there is plenty of reason to believe that it occurs. Of course, the issue is not whether fiber number increases after every training program, stress, or perturbation is imposed upon an animal (or human). The issue is again, under which circumstances is it most likely to occur. For humans, I’d surmise that the average person who lifts weights and increases their muscle mass moderately probably won’t induce fiber hyperplasia in their exercised muscle(s). Yet I imagine there are exceptions. However, the elite bodybuilder who attains the massive muscular development now seen may be the more likely candidate for exercise-induced muscle fiber hyperplasia. If you are interested in a comprehensive scientific treatise on this subject, read a scientific review article that I wrote way back when Bill Clinton was President of the USA . It still holds true today.
There are two primary mechanisms in
which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) . And perhaps the primary mechanism is via the activation and proliferation of satellite cells . Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated . Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells).
These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).
- - - Updated - - -
ROLE OF MUSCLE FIBER DAMAGE
There is robust evidence which has shown the importance of eccentric contractions in producing muscle hypertrophy . It is known that eccentric contractions produces greater injury than concentric or isometric contractions. We also know that if you can induce muscle fiber injury, satellite cells are activated. Both animal and human studies point to the superiority of eccentric contractions in increasing muscle mass. However, in the real world, we don’t do pure eccentric, concentric, or isometric contractions. We do a combination of all three. So the main thing to keep in mind when performing an exercise is to allow a controlled descent of the weight
THE MYTH OF SARCOPLASMIC VS MYOFIBRILLAR HYPERTROPHY
This is perhaps one of the more annoying and contrived controversies in the field of skeletal muscle plasticity. Was it Joseph Goebbels who said that “if you repeat a lie often enough, it becomes the truth”? This is a perfect example of this maxim. Frankly, I don’t give a shit who started this mythical beast known as sarcoplasmic hypertrophy.
The fact of the matter is there has never been evidence to suggest that increases in skeletal muscle size can be the result of selective hypertrophy of the sarcoplasm. It’s not like you can train to increase the sarcoplasm one day; and then the next day, train for myofibrillar growth. Roughly 70-80% of the volume of a muscle fiber is the myofibrillar component.
It should be as clear as the Montana sky that gains in muscle size are largely due to increases in contractile protein. In fact there is a classic paper by Claassen et al. (Journal of Physiology, 1989, 409: 491-495) entitled “Muscle Filament Spacing and Short-term Heavy-Resistance Exercise in Humans.” They found that the “linear distance between myofilaments as well as the ratio of actin to myosin filament did not change with training.”
Moreover, don’t confuse gains in strength without gains in skeletal muscle size as evidence for sarcoplasmic hypertrophy. As my teenage daughter would say, ‘isn’t it obvy?’ Yes, it is obvy (obvious) that improvements in rate coding, muscle activation patterns and motor unit recruitment do indeed account for changes in strength without a concomitant increase in skeletal muscle size. However, if someone shows me evidence that an enlarged muscle or muscle fiber has an increase in cytoplasm with no change in the volume of actin and myosin, then I’ll alter my conclusions. Until then, show me the evidence. And if it doesn’t exist, then quit bs’ing everyone about ‘sarcoplasmic’ hypertrophy. What’s next? Pigs flying, unicorns trotting, the Jets winning? For another opinion, check out Stu Phillips PhD little ditty: https://twitpl.us/t/4Xeb
- - - Updated - - -
HAS THE HYPERPLASIA DEBATE BEEN SETTLED?
To quote the genius of Yogi Berra, “I wish I had an answer to that because I’m tired of answering that question.” In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia can contribute to whole muscle hypertrophy.
There is human as well as rat, cat, and bird data which support this proposition , a veritable wild kingdom of evidence.
Does muscle fiber hyperplasia occur under all circumstances? No. There are several studies which show no change in fiber number despite significant increases in muscle mass . Is it possible that certain muscles can increase fiber number more so than others? Maybe.
Can any Joe Schmoe off the street who lifts weights to get in better shape increase the number of fibers for instance in their biceps? Maybe, maybe not. What about the elite bodybuilder who at 5’8″ tall is ripped at a body weight of 250 lbs.?
Are his large muscles purely the result of muscle fiber hypertrophy? I think it would be extremely naive to think that the massive size attained by elite bodybuilders is due solely to fiber hypertrophy.
Despite the contention that fiber number is constant once you’re born, there is an abundance of evidence which shows that muscle fiber number can increase post-natally.
Always wondered how much hyperplasia could occur in the gluteus maximus. One, two, 5999, 190000, 699699, oh my…keep counting.
Besides, there is nothing magical at birth which says that now that you’re out of the womb, you can no longer make more muscle fibers. A mechanism exists for muscle fiber hyperplasia and there is plenty of reason to believe that it occurs. Of course, the issue is not whether fiber number increases after every training program, stress, or perturbation is imposed upon an animal (or human). The issue is again, under which circumstances is it most likely to occur. For humans, I’d surmise that the average person who lifts weights and increases their muscle mass moderately probably won’t induce fiber hyperplasia in their exercised muscle(s). Yet I imagine there are exceptions. However, the elite bodybuilder who attains the massive muscular development now seen may be the more likely candidate for exercise-induced muscle fiber hyperplasia. If you are interested in a comprehensive scientific treatise on this subject, read a scientific review article that I wrote way back when Bill Clinton was President of the USA . It still holds true today.
