What would be the best way to train to take advantage of myostat blockers ie. how would you train for maximum hyperplasia/ new cell growth? I remember a few years back there was this system called the ‘matrix principle’, which basically used 21’s with very short (20 second) rest times. It was meant to maximise production of new cells, but it didn’t work in most people, mainly I guess because of the myostatin gene action. Any suggestions?
that is a GREAT question
this IS a great question!
From what I’ve read and researched the most examples of hyperplasia came from long term high intensity training. The deltoids on competitive swimmers, quads on cyclists and so on. People that undergo intense training to failure. I think that the Escalating Density programme could be a good idea, taking a body part and going to all out failure over the course of 45mins to 1h. If such is the case what about more body weight type movements, ie dips and pull ups and chins. This Myostat really could transform the way we train to put on both strength and muscle. Leg day could be a pyramid set of sprints, shoulders hitting the pool for an hour doing butterfly!!!
I’m sure it would all go down well, certainly make a nice change. As far as I know, it would most likely affect fast twitch fibers so the high intensity and speed excerises would be useful!
I’d imagine a training program that emphasized the “stretch” or eccentric portion of the lift.
THIS is a great question!
my suggestion is this… it doesn’t really matter what type of training program you use. From all the papers I’ve read on this myostatin thing, all the mice that have had the gene knocked out blew up!!! And these little suckers didn’t train at all… hahah. Joking aside, it would seem that hyperplasia, induced by myostat, would be independent of a training protocol. Now, the training comes in when you want to induce hypertrophy and become bigger than you’ve ever been!
Here’s an interesting point… the myostatin gene is conserved in almost every freakin mammal on this earth. Studies of knocking out the gene in cows have caused them a certain increase in muscle mass (i forget the number) and these same studies done on mice cause their muscle mass to increase, in proportion to the cows, by a shitload!!! The scientists have hypothesized that the super increase in the mice may be because those suckers were not bred to be big, unlike cows (agricultural reasons). So what are the implications for humans? Not sure, but then again, these guys were knocking out the gene, not trying to eliminate the protein.
I’m extremely interested in the results people get on taking myostat.
No, the examples of mice and other animals with the gene knocked out, and being huge
without training, don’t apply I think. Here is the difference. In these animals, myostatin was knocked out during early development and also during maturation, times during which satellite cell differentiation into mature muscle cells is naturally an ongoing process without training.
In the case of athletes who have reached physical maturity, my guess is that what’s needed is conditions that ordinarily would produce a little differentiation of satellite cells, or at least come close to it… and Myostat would improve this to a condition of much more cells differentiating.
With no training at all, there would probably be no effect.
And I agree with Cy: as a bet, the eccentric and particularly the stretch are probably of key importance.
This is a great QUESTION! (And deserves to be bumped…)
Years ago it was thought that high speed, high repetition sets would induce hyperplasia. The Weider superspeed principle, one could say.
BOBU - my impression of the product was that it unleashed the ability to allow hyperplasia to function, not knock out the gene completely. Could be wrong, what’s you take? I figure, like most others, that it’s going to have to be some kind of intense training that’ll give the most hyperplasia. I mean, if we took a marathon runner and an olympic gymnast, who do you think would consistently have a better environment (in their body) for hyperplasia. I’d say bets are on the gymnast. I guess my point is that it IS dependent on training. I imagine down the road some sly bugger will also figure out that there’s some diet/food combination that’ll bump things along as well…
Mark… sorry it took so long for me to reply.
I know that the Myostat binds to the protein and prohibits it from binding to the ACTRII receptor. This allows skeletal muscle cells to increase in number, resulting in more muscle.
Science generally dictates that you cannot inhibit substrate to receptor binding fully, remember sigmoidal curves?, but you can affect it. Myostat seems to have the answers. I know that this product can work. I’ve read a paper which uses follistatin as a competitive inhibitor (competes in binding the ActRII receptor). The mice that the study was done on were freakishly huge!!!
Now on the training aspect, I totally understand what you're talking about when you compare a marathon runner to a gymnast. But think about it this way. The marathon runner is so damn catabolic that he is basically causing atrophy in the muscles (shrinking them) I highly doubt, and Bill can help clarify this, that they are actually causing skeletal muscle cells to disappear. The gymnasts on the other hand, are causing hypertrophy of the muscles which explains the increased muscle size (this is not a result of hyperplasia).
Creating an environment for hyperplasia is completely different than it actually occuring. Myostat can solve this problem.
Funny thing is though, myostatin seems to be muscle specific. It’s phenotypic results (upregulation, downregulation) are seen in type II fibers. Nestor et al. (organization of the human myostatin gene and expression in healthy men and hiv-infected men with muscle wasting)–look in PNAS vol 95, pp 14938-43
They show that myostatin is specific to type II fibers as opposed to type I due to LIF (leukemia inhibitory factor), and I guess IGF-1 which counteracts myostatin effects within the type 1 fibers only.
This myostatin thing could be a tremendous breakthrough. Hopefully, one day we'll be able to genetically downregulate it in order to help those with muscular dystrophy, age and hiv related sarcopenia, and possibly cardiac development in relation to myocardial infarction.
Who knows? Maybe Biotest has created a small molecule that can do this.
Bobu, I don’t want to swear to it as it’s something I read only once (in an exercise science class about 7 or 8 years ago) but I did read something saying it was shown that running marathon distances actually can destroy muscle cells.
Check into it more before accepting it as fact though!
Judging from the appearance of the legs of these runners, though, it’s something that certainly seems believable.
Hey Bill, it definitely sounds possible.
The reasoning I took on my explanation is that of the fat cell. You can empty those sumbitches out, but the damn “shell” is still left and ready to suck in more tg’s.
I’ll try and look into it when I get a chance.
Bobu - so would you say that a marathon runner would be getting the same amount of hyperplasia as a gymnast? Interesting stuff all this… [grin] Don’t suppose you’ve got a link to some pics of these mice by any chance…?
Here’s the pdf for one paper that I found was interesting. The only other paper I have is found in Nature and you can’t get that one online even if you are a member to Nature online, you have to have the actual paper mag.
www.pnas.org/cgi/reprint/98/16/9306.pdf
This article deals with competitive binding to the receptor, but the idea is still the same.
I realize this is off topic a bit from myostatin, but your example of fat cells got me thinking. Is there any possible vector (other than liposuction) to effect destruction of fat cells? I realize that at puberty, new fat cells can be grown, but is there some way to dump them?
I’m not sure. I haven’t read any literature on the destruction of fat cells. I am, however reading up on the prevention of forming new fat cells by regulating ppar gamma. Interestingly enough, myostatin seems to have an effect on ppar gamma. Of course it’s just a correlation but an interesting one nonetheless.
Interesting link. I didn’t understand everything (a bit technical) but it seems part of the increase in muscle mass was hypertrophy. In the mice there was a 66% increase in fiber number and 28% in fiber diameter (which would be hypertrophy) from blocking myostatin. Am I getting this right?