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I know HGH actually makes you produce more muscle cells. But does it make you produce more receptors?
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HGH question....
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Skeletal muscle hyperplasia ( an increase in cell number ) has never been conclusively demonstrated in adult humans as a result of exercise or GH. What has been shown is that muscles grow by hypertrophy (increase in size).
Unlike other cells in the body, skeletal muscles cells have lots of nuclei because the cells (fibers) are so big. A growing muscle needs to get additional nuclei, and these come from so called satellite cells. IGF-1 is a potent inducer of satellite cell proliferation. These nuclei that are donated to the growing muscle fiber contain the genes encoding for the androgen receptor proteins (as well as everything else the muscle needs). So the now bigger muscle with more AR genes will make new androgen receptors to meet its needs.
Unlike other cells in the body, skeletal muscles cells have lots of nuclei because the cells (fibers) are so big. A growing muscle needs to get additional nuclei, and these come from so called satellite cells. IGF-1 is a potent inducer of satellite cell proliferation. These nuclei that are donated to the growing muscle fiber contain the genes encoding for the androgen receptor proteins (as well as everything else the muscle needs). So the now bigger muscle with more AR genes will make new androgen receptors to meet its needs.
monkeyballs
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So the notion that GH induces hyperplasia is a misconception?
I don't quite understand. How is the generation of new conective tissue cells any different from the generation of new muscle fibers? Unless the alleged effect of GH on conective tissues is due to some other mechanism, one which my bullshit liberal arts degee can't quite comprehend.
Enlighten us obi wan...
Good to see that your still lurking around.
I don't quite understand. How is the generation of new conective tissue cells any different from the generation of new muscle fibers? Unless the alleged effect of GH on conective tissues is due to some other mechanism, one which my bullshit liberal arts degee can't quite comprehend.
Enlighten us obi wan...
Good to see that your still lurking around.
That's a good question, Monkeyballs. As far as muscle goes, "not conclusively demonstrated" does not mean hyperplasia in adult human muscle does not happen; it very well may. The evidence is just not good enough to satisfy the community of researchers who specialize in this field. Everyone accepts hypertrophy, on the other hand.
There are quite a few studies that show stretch overload in animals produces skeletal muscle hyperplasia. In fact the results of all the studies are summarized in this meta-analysis:
http://jap.physiology.org/cgi/content/full/81/4/1584
I have never seen a study showing that GH or IGF-1 administration to an animal or human causes skeletal muscle hyperplasia.
Connective tissue seems to be different, probably because the cells responsible for connective tissue development (fibroblasts) are immature and sensitive to growth factors like IGF-1. There is a lot of research showing that IGF-1 causes fibroblasts to proliferate and end up secreting more collagen and related compounds necessary for connective tissue development.
It's debated though whether the integrity of the resulting tissue is normal, though.
There are quite a few studies that show stretch overload in animals produces skeletal muscle hyperplasia. In fact the results of all the studies are summarized in this meta-analysis:
http://jap.physiology.org/cgi/content/full/81/4/1584
I have never seen a study showing that GH or IGF-1 administration to an animal or human causes skeletal muscle hyperplasia.
Connective tissue seems to be different, probably because the cells responsible for connective tissue development (fibroblasts) are immature and sensitive to growth factors like IGF-1. There is a lot of research showing that IGF-1 causes fibroblasts to proliferate and end up secreting more collagen and related compounds necessary for connective tissue development.
It's debated though whether the integrity of the resulting tissue is normal, though.
monkeyballs
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So the new conective tissues could actually be weaker than the original ones?
You have systematically dismantled virtually every reason why I was intrested in using ex GH.
The reasons were...
1. hyperplasia
2. strengthening of connective tissues
3. Greater capacity for excercise
4. Change in body composition
I'm pretty sure that reasons 3+4 are still intact.
Also, "stretch overload"...that's no different bio-mechanically than any concentric/eccentric lift. Correct? The same stimulus has never been demonstrated to cause hyperplasia in humans.
I guess the research is of less use to us because of the need for a definitive conclusion...our intrests seem to be more anecdotally oriented.
So do you feel that hyperplasia due to exGH use is likely?
You have systematically dismantled virtually every reason why I was intrested in using ex GH.
The reasons were...
1. hyperplasia
2. strengthening of connective tissues
3. Greater capacity for excercise
4. Change in body composition
I'm pretty sure that reasons 3+4 are still intact.
Also, "stretch overload"...that's no different bio-mechanically than any concentric/eccentric lift. Correct? The same stimulus has never been demonstrated to cause hyperplasia in humans.
I guess the research is of less use to us because of the need for a definitive conclusion...our intrests seem to be more anecdotally oriented.
So do you feel that hyperplasia due to exGH use is likely?
I wish your mind weren't so fertile. You make me work too hard. As you know, IGF-1 is what is thought to be what is responsible for the muscle hypertrophy and or hyperplasia, if the latter occurs. So GH is only indirectly responsible in that it elevates IGF-1.
During development it has been shown that IGF-1 administration leads to skeletal muscle hyperplasia, i.e. new muscle cell (fiber) development. In development, new fibers arise from muscle precursor cells, called myoblasts. What IGF-1 is thought to do is induce proliferation (i.e. cell division) of these myoblasts, increasing their number. The myoblasts then fuse together into fully developed muscle fibers. Some of the myoblasts are not directly incorporated into the fiber, but remain adjacent to it. These unincorporated myoblasts are the satellite cells.
These satellite cells can do three things. They can just sit there, the normal state of affairs. Or they can fuse with the preexisting fully developed fiber, donating their nuclei to it (hypertrophy). The third possibility is that the satellite cells themselves can fuse together to form a new fiber (hyperplasia).
Like during development with myoblasts, in an adult, IGF-1 is thought to induce proliferation of these satellite cells, making more of them available to either form new fibers or fuse with existing fibers. Myostatin, which we've been hearing about so much, has the opposite job. It puts the brakes on satellite cell proliferation.
So IGF-1 doesn't actually cause new fiber growth. Instead it induces proliferation of the satellite cells that will eventually fuse and turn on the genes required to function as fully developed muscle.
Eccentric loading seems to be what causes hyperplasia in animal models where it has been detected.
I think it is safe to say that from reviewing the scientific literature if hyperplasia occurs as a result of GH or training in adult humans it makes only a minor contribution to muscle growth. Just speculating, maybe myostatin limits the rate of satellite cell proliferation to the point there aren't enough of them to fuse to form fibers, but there are an adequate number to fuse to preexisting muscle cells and contribute to hypertrophy.
There is no scientific evidence that GH improves athletic ability (strength or exercise capacity) in trained individuals, but there are so few randomized, double blind, placebo controlled studies (exactly 1 to my knowledge) it is impossible to draw a conclusion.
It does reduce fat and increase lean body mass in some studies, in others not. The bulk of the evidence shows no increase in LBM in trained athletes given GH. In obese people it works well in reducing fat and preserving or increasing LBM.
Overall there is little scientific justification for GH use. On the other hand there is plenty of anecdotal evidence that it works great. I don't know where the disconnect is. If you polled everyone here who has used GH they would probably to a person say it worked.
During development it has been shown that IGF-1 administration leads to skeletal muscle hyperplasia, i.e. new muscle cell (fiber) development. In development, new fibers arise from muscle precursor cells, called myoblasts. What IGF-1 is thought to do is induce proliferation (i.e. cell division) of these myoblasts, increasing their number. The myoblasts then fuse together into fully developed muscle fibers. Some of the myoblasts are not directly incorporated into the fiber, but remain adjacent to it. These unincorporated myoblasts are the satellite cells.
These satellite cells can do three things. They can just sit there, the normal state of affairs. Or they can fuse with the preexisting fully developed fiber, donating their nuclei to it (hypertrophy). The third possibility is that the satellite cells themselves can fuse together to form a new fiber (hyperplasia).
Like during development with myoblasts, in an adult, IGF-1 is thought to induce proliferation of these satellite cells, making more of them available to either form new fibers or fuse with existing fibers. Myostatin, which we've been hearing about so much, has the opposite job. It puts the brakes on satellite cell proliferation.
So IGF-1 doesn't actually cause new fiber growth. Instead it induces proliferation of the satellite cells that will eventually fuse and turn on the genes required to function as fully developed muscle.
Eccentric loading seems to be what causes hyperplasia in animal models where it has been detected.
I think it is safe to say that from reviewing the scientific literature if hyperplasia occurs as a result of GH or training in adult humans it makes only a minor contribution to muscle growth. Just speculating, maybe myostatin limits the rate of satellite cell proliferation to the point there aren't enough of them to fuse to form fibers, but there are an adequate number to fuse to preexisting muscle cells and contribute to hypertrophy.
There is no scientific evidence that GH improves athletic ability (strength or exercise capacity) in trained individuals, but there are so few randomized, double blind, placebo controlled studies (exactly 1 to my knowledge) it is impossible to draw a conclusion.
It does reduce fat and increase lean body mass in some studies, in others not. The bulk of the evidence shows no increase in LBM in trained athletes given GH. In obese people it works well in reducing fat and preserving or increasing LBM.
Overall there is little scientific justification for GH use. On the other hand there is plenty of anecdotal evidence that it works great. I don't know where the disconnect is. If you polled everyone here who has used GH they would probably to a person say it worked.
monkeyballs
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As always, thanks for the detailed response.
GH use is rampant amongst amateur athletes. The 1996 olympics in Atlanta were dubbed the "GH games" by athletes because use was so prevailant that it was almost freely discussed. Dozens of athletes were caught with paraphernalia, yet not one was actually charged with dopping. The scientific research that probably has been done by various olympic federations is not the kind that any of us will ever see. In lieu of any actual research, anecdotal evidence will have to suffice. Theoretically, all of the alleged athletic benifits of GH use make sense. Anecdotally, it's virtually assured. Ever see a german woman shot putter or a chinesse woman freestyle swimmer? They are clearly on something, but they are tested (randomly, both in and out of competition) so often that GH has to be the culprit.
I'll conduct my own little study here and keep you posted with some more anecdotal evidence.
GH use is rampant amongst amateur athletes. The 1996 olympics in Atlanta were dubbed the "GH games" by athletes because use was so prevailant that it was almost freely discussed. Dozens of athletes were caught with paraphernalia, yet not one was actually charged with dopping. The scientific research that probably has been done by various olympic federations is not the kind that any of us will ever see. In lieu of any actual research, anecdotal evidence will have to suffice. Theoretically, all of the alleged athletic benifits of GH use make sense. Anecdotally, it's virtually assured. Ever see a german woman shot putter or a chinesse woman freestyle swimmer? They are clearly on something, but they are tested (randomly, both in and out of competition) so often that GH has to be the culprit.
I'll conduct my own little study here and keep you posted with some more anecdotal evidence.
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