anti-Myostatin

so there is a research chemical company that is well-known selling anti-Myostatin polyclonal anti-body. Is that myostatin inhibitor (250 mcg for $595)? Has anyone tried it yet?

They are also selling rIL-15 and rIL-2??

read my post on interleukin-15 much further down for a full description of it. il-2 would be similar but even worse.

i have no idea what a myostatin antibody would do at this point, but these tend to be extremely blunt tools. remember that antibodies in general work by marking individual cells or compounds for destruction by your immune system. given that myostatin in all likelihood has an extremely short halflife, it probably would do nothing.

i do know they've tested the genes of elite bodybuilders and found that myostatin mutations presently do not represent any part of the discrepency in size between them and the rest of the population. various (not necessarily mstn-/-) mutations in the gene just don't seem to be what's limiting muscle development in any of these individuals.

flex supposedly had one(sez balco, so take it for what it's worth). most did not. many individuals in the population have one. there are a bajillion different alleles for any individual gene, including myostatin. you can also be homozygous or heterozygous(as the german boy's parents almost certainly were for mstn+/-) for a given mutation. you should know that. a pure mstn-/- mutation is indeed rare in humans, no doubt.

http://www.musclephotos.com/myogene.html

one thing to note is the myostatin gene is *ridiculously* conserved across species. it's really kind-of surprising that it would be such a well-defended gene. apparently it's quite critical for proper function as a developing species for some reason.

yes, it will affect muscle mass dramatically. is it the limiting factor at this point? i sincerely doubt it. i haven't given any thought to what prevents the top fleet of bodybuilders from growing further but it's almost certainly not myostatin.

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=11078093
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15083369

"Myostatin genotype did not explain the hypertrophic response to ST when all 32 subjects were assessed."

"Responses to the strength-training program were not associated with the ACE I/D genotype (ANCOVA 0.057< P<0.70)."

you can argue these aren't knockouts, which is very true. but you would still expect to see some degree of variation or correlation here if it were a strong limiting or determining factor for humans involved in resistance exercise, not to mention all the other drugs we play around with.

fyi, there is a very good way you can reduce your myostatin levels dramatically right now. go to the damn gym and train your brains out. amongst the many complex transformations in muscle that occur as a result of resistance exercise, a sharp drop in myostatin production is one of them.

Ahh, but there are opposites to everything, so there would have to be mutations in the other direction. Myostatin inhibition in an individual with a mutation the other way could produce some fantastic results.

I for one, have an extremely hard time building muscle, even with the HRT I've been on. I used to have times where I'd exercise hard, get really pumped up, and then the next day have even less size than what I had before the exercise, and it took a long time for it come back--and this was when I was on HRT and eating a lot. I always thought either I overproduced cortisol in response to training, or possibly I had too much myostatin (a thought that had recently occurred to me). I would love to see what inhibiting myostatin could do for me. (I have to wonder since I have had such fantastic results from IGF.)

Perfect! Try it and tell us all how it worked!!
Ya, I think I had the same problem - If I train even a "little" too much, I have troubles sleeping and seem smaller the next day. I believe it has to do with my body over-producing cortisol.

I would love to, but I don't have that kind of money, and you have to have a special license to import the stuff because it is made via animals (don't ask me how--they didn't say).

I dont want to come off as contradicting anyone, I just want to throw this out there, b/c it happens to my thoughts on the matter, I seriously doubt that cortisol is the limiting factor in your training, given aas's effect on cortisol, i beleive it is extremely hard to overtrain. I might be wrong and everyone is diffferent, id love to see some studies on the matter, i find that my limiting factor is simplky getting enough food, I beleieve I (and others) fool ourselves into blaming things like myostatin and cortisol for our lack of growth when we are simply not taking in enough protein and or calories. However, while I do not think that myostatin is single limiting factor in todays elite BBers , it would be foolish to deny the evidence that has been seen animals (and the german monster boy) that a myostatin inhibitor would lead to a tremendous amount of muscle mass/leaness that has never been seen before. Along the same lines, I would also like to add that myostatin obviously has its place in the body and that all this gene doping business is something we, as a society, will someday regret. I consider it all a pandora's box of sorts. While there are some great things that can come all this, it also opens the door for an entirely new (and IMHO, much more terrifying) faction of problems. Anyway, all this aside, if someone wants to send me a true myostatin inhibitor, we might just all find out big and lean a human can get. Oh, i just thought of this, the main appeal of myostatin inhibitors and perhaps all these other gene doping things seems to be the fact that they require little or no effort by the user, and in our culture that potential "magic pill" is a siren song to all those lazy, want something-for-nothing peckers sitting at home muching on cheetos complaining about how they dont have the body they want.

I'm all for gene doping that would be SIC.

Im all for it for me, (and maybe you too chaps if your lucky, LMAO) i just worry about all the greg valentinos out there in the world

I'm still sketchy on it....especially the viral anti-myostatin. There could be a immune response that could cause your body to attack other structurally similar peptides circulating in your body, of which control things like cell division. (I.E....causing leukemia or other cancers.)

diseases in which myostatin production is messed up are commonly referred to as muscular dystrophies. from here you don't appear severely ill and/or dead, so no, i don't think you have major defects in your myostatin production.

i think ton's first post was excellent. i'd like to re-emphasize that myostatin is not remotely the only thing regulating the extent to which muscle can grow. that's a very narrow view of an extremely complex process. i hate to quote at such length, but from a study looking at precisely how myostatin limits muscle hypertrophy(emphasis mine):

http://ajpendo.physiology.org/cgi/content/full/280/2/E221

"Muscle mass in humans and animals reflects a balance between anabolic factors such as IGF-I/growth factor 1/growth hormone, testosterone, nutrition, and exercise, and catabolic factors such as glucocorticoids, thyroid hormones, mediators of systemic inflammatory response, and cytokines. Sarcopenia that occurs in association with aging and chronic illness is a complex process that involves changes in systemic metabolism and intramuscular gene expression (2). Myostatin should be added to the list of catabolic factors that inhibit muscle growth and contribute to the multifactorial pathophysiology of muscle loss that occurs in association with aging and chronic illnesses such as HIV infection."

you can produce more dramatic hypertrophy in animal models by making them overexpress igf-i.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9335610
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=14766764

in fact, immobilization results in much greater muscle loss with no myostatin production:

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=12618358

go figure. this is extremely dodgy stuff and not to be trifled with. the good news is that the antibody is likely to do jack shit.

In response to ton's comments above, I believe it is possible to overtrain even with AAS. Most of my problems did stem from not eating enough or even working out too much for my body to recover by the next workout time--that in of itself causes overtraining doesn't it? That doesn't happen so much to me now. I've been able since those times to make slow but steady progress because I've learned (well, I'm still learning) how to eat and I'm letting myself recover better.

And though the process of building muscle is very complex, involving many factors, inhibiting myostatin may work very well though it be a single component. Adding more testosterone to your system is also a single component, and it causes more muscle growth. These single components act on or affect many different processes in the body, which is why I believe that inhibiting myostatin could produce substantial muscle gains, perhaps depending on how it is used. As far as the antibody is concerned, I agree that it may be dangerous to use. Something that has been shown to inhibit myostatin temporarily, such as follistatin and other chemicals, would be better IMO.

Tonykemp you may be right, i suppose its a very induvidual thing about overtraining. However i do love the skinny peckerhead at the gym who only does one set of 15 and dosent even workout and then claim she dosent want to overtrain.

If your running AAS very androgenic compounds will really help to prevent over training.

nah, the antibody just won't really work well at all. it's certainly not going to be permanent. if it's keyed to myostatin -- as the name obviously implies -- it won't do anything to curtail myostatin production, but instead attempts to destroy it quickly once it's produced.

pharmacological approaches targetting myostatin itself will be difficult to make work simply because myostatin is locally produced and rapidly used. disrupting production is a much more likely strategy and adenoviral vectors encoding mstn -/- or a similar mutation is the most straightforward approach, scary though that is.

Can't a brother dream? lol

hell yeah, but you can probably find a cheaper way to do that with similar results.

Seems to me that they shouldn't be wasting research on an antibody then. We should try to get the inhibitors out there instead. There was an article on the net a while back about the results of follistatin, and I contacted the author to see if he could provide any more information on it. He right away told me that he first will never tell anyone where to get follistatin (the source used in the article), citing something about journalism, ethics, and how you don't reveal your sources or something like that. IMO, he was just being a jerk.

hmm...I think it would be a very bad idea to try follistatin. I wrote some info about it awhile back. Basically follistatin binds myostatin and several other key tgfb family members that controls different functions...such as cell division. Gasp-1 seemed to be the only one with the highest binding affinity for myostatin and with low binding affinity for the others.

BTW Tony....if it's who I think it is then he supposedly works for some bio-research center or something so he has access to different peptides and chemicals...I would be sketchy of trying it to be completely honest. If you do a search on the internet you can probably see what companies make each peptide, but more often than not you'll need to verify that you're a research facility.

Anyone have any info on interleukin 6? Dave Palumbo mentioned it in an interview recently, i've only heard of interleukin 15.