I’m in the middle of a cutting phase which will last for at least 5 more weeks, maybe longer. Right now i’m about -300 calories from maintainance a day; next week i will be starting a 2 week severe dieting (1300-1400) calories a day Mag 10 cycle, and then a two week recovery period at slightly under maintainance calories w/ Methoxy 7. If all goes well, and i hit my BF goals, then i will start another Mag 10 bulking cycle. My question is this: I just got a two months supply of Myostat; should i start taking it now, or wait for the bulking cycle? I’m thinking that i should start it now, as it helps with insulin sensitivity, and then hypertrophy any newly formed fibers when i start bulking. I dont need to eat big to gain more fibers right? I just need to eat big to hypertrophy those fibers…is my thinking correct?
joelm, I would use the Myostat on the bulking cycle. It just doesn’t make sense to use Myostat to gain muscle fibers, while on a calorie restricted diet. What type of training are you doing now(meltdown) I suppose? If so, then you will have, I believe if I read it right, lactic acid induced hypertrophy coupled with a GH blast. Even though you COULD use the Myoblast with Meltdown or EDT training, you should be back to a maintenence level caloric intake, especially if you are on the T-dawg diet. If I were you, I would wait, use Mag10 with Myoblast on a mass cycle; incorporating meltdown training or EDT, while on a massive eating diet. The Myoblast will do it’s part on the Myostatin protein, while the Mag10 kicks in to preserve the new precious muscle. EDT or Meltdown will ensure hypertrophy to both your existing and new fibers. The massive eating part will ensure that you are consuming enough calories and enhance the holistic anabolic effect. I hope this helps. -The Starkdog
I agree. I’d save it for when consuming
at least maintenance calories. It may be
wasted when dieting heavily.
I don’t know it for a fact, but it seems
likely that the body would not consider
a time of caloric restriction to be a time
to create (from satellite cells) new muscle cells.
Thanks for the replys, i’ll save it. I am constantly doing bulking/cutting cycles though; am i really going to get the full benefit of Myostat by going on and off it every couple of months? It seems to be a slower process; is it really a waste to stay on it year round? “30-50% reduction of body fat without a change in diet”…the insulin sensitivity/body fat reducing benefits of blocking myostatin seem to be worth it to me.
If Myostat can help reduce fat as shown in lab studies in humans especially when on a fat fast diet?
Also how much of the myostatin protein is binding with Myostat at the recommended dosage and can we double it for additional effect? How did you come to settle that the recommended dosage is the most effective one to take.
I have already bought a six months supply to try out. My goal is to use it for this time period and get back to you with what results I have had.
On a side note: Thank you for pushing the envelope when it comes to our bodies. A company like yours has been needed for a long time and I hope other companies will take note.
The problem is, I just don’t know and I don’t
think anyone does yet. It’s a guess on my part that to get the most efficient use for your dollar for muscle gains, use would be targeted for when training and diet are optimized for gains. Whether benefit in fat loss is worth the money when dieting, to me seems like something that only time will tell.
I don’t know about the insulin sensitivity part but taking myostat during a cutting cycle or a bulking cycle won’t affect hyperplasia. Interestingly enough, I read in a paper (sorry I don’t remember the paper, but I’ll try to find it again) that a restriction in calories actually caused a downregulation in myostatin.
Can murine data be properly extracted to humans? Not sure, but the sequence for the protein is highly conserved in all mammals.
Anyways, whether or not you diet, won’t affect hyperplasia. The dieting will affect hypertrophy.
I think that if you were to go on a complete starvation diet i.e. fasting for an extended period of time, then you might cause a problem.
If you happen to take myostatin during a bulking phase, you’ll see a noticeable result due to the hypertrophy of your newly made muscle. Interestingly enough, down regulation of myostatin causes hypertrophy of the muscle tissue. Stacked with mag 10 during a bulk cycle should cause tremendous growth!!!
Take myostat during a cutting cycle and hyperplasia should and most likely will occur but hypertrophy might be abrogated. Don’t worry though, when you bulk next, you’ll be able to grow bigger than you would without it. It seems to be a question of how quickly you want to see results.
The real question is whether myostatin is locally or systemically regulated. I’m working on finding that out.
Hmmmm…What I am doing for the first phase is a fat free diet. Supplements are Myostat, Mag-10 at one dose a day for the cutting cycle for two weeks and Tribex with M for the other two weeks. My goal is for fat loss and hyperplasia not hypertrophy for the first four months. My question is would this be the best way to maximize fat loss AND hyperplasia? I am not concerned in causing hypertrophy for now but to create NEW muscle cells. Thanks.
just wondering where you are getting your inforation from. Sounds like good news if calorie restrictions don’t interrupt the formation of new fibers, but just curious as to how you know this when guys like Bill don’t. Thanks.
Mike - My impression is that hyperplasia would be best induced with high intensity lifting. This type of training isn’t really in line with losing relatively large amounts of bodyfat. My guess (and yes it’s a guess), would be that you have one or the other. Not both. A proper/usual dieting training program just won’t set up the environment in your body for hyperplasia (again, I’m guessing, but noones really explained anything to the contrary to me yet…). Cheers. [Bobu - maybe you can add to this.]
Mike, why are you going on a fat free diet! That is not a good way to lose fat…at all!
Here’s the scoop… do a search on pubmed. You’ll get a lot of abstracts and some free articles related to the myostatin gene. Also, www.pnas.org has free articles on myostatin. Most of the articles found there are by the founders of the gene when it was originally called GDF-8 (growth differentiation
factor 8). Those scientists are at John’s Hopkins, freaky good med school, and really know their shit. Their original discovery of the gene in 1997 was published in Nature!!!
Mike, maximizing fat loss would be better served through t-dawg diet, ketogenic diet, don’t diet diet, or any other low carb diet.
Seems though that you would be wasting your money using mag 10 that way, but maybe you have the money to burn? If your concern is to create new muscle cells, then the myostat is all you need.
Mark Aus…I haven’t read the papers on whether or not hyperplasia is induced by high intensity lifting. But it seems to me that high intensity lifting is more of a neural based training. You definitely activate more fibers and possibly cause hypertrophy (which can be misinterpreted for hyperplasia).
Shit, who knows? Neural training could cause a spike in IGF-1 and LIF which are myostatin antagonists possibly lead to hyperplasia. Not sure on this, I haven’t done the research. But get this, it seems that diet has nothing to do or at least very little to do with myostatin expression. If anything, a restriction diet can actually cause a decrease in myostatin expression. Fuck me if I can remember the paper I read it in (I got roughly 13 of em) but I’m gonna have to read them again anyways, and when I find that data, I’ll post it. So, setting up an environment for hyperplasia is not necessary. What you are setting an environment for is hypertrophy or atrophy.
Bill Roberts is the man. No doubt about it. His knowledge in the field of drugs and their effects on the human system is phenomenal. I’m guessing, sorry Bill, that he wants you to eat big during the myostat loading so you can see OPTIMAL effects and not bitch later about how myostat didn’t work. If you were to cut up and take myostat, hyperplasia should be induced but not hypertrophy. This could lead
you to believe that myostat didn’t work. Then when you started to bulk up, you’d think that your mass gains were due to bulking. However, if myostat does it’s job, you’ll be able to get bigger than you’ve ever been!!!
Now if I can just find out if that son of a bitch (myostatin) is locally or systemically regulated.
I’ll keep you guys posted.
Bill, Bobu is saying that caloric intake has nothing to do with hyperplasia; this seems to be contrary to your post earlier on this thread. Is there a reason why the formation of new muscle cells would not occur; does bobu have some valid points? And does it have to do with how much myostatin is being blocked? From my understanding, only 10% of myostatin is blocked with myostat, is that true? And, is that the reason why it wont work on a cutting cycle? thanks
At this point, for me it’s guessing as to when hyperplasia occurs. If Bobu has specific
information that hyperplasia is independent
of caloric intake, then my guess is wrong.
I could not tell from his post whether he
had such specific information, or was himself guessing based on the suggestive evidence
of myostatin levels decreasing with reduced caloric intake. (Which does not prove that
hyperplasia occurs then.)
Bill is right… the data that I’ve been reading doesn’t mean that decreased myostatin through a caloric restriction can induce hyperplasia. I’m going with the assumption that decreased myostatin will induce hyperplasia. I think it would be best to follow Bill’s suggestions since he has much more experience and knowledge than I do. Lookout Bill, someday I’ll catch up to you, hopefully.
I hope you are doing more than just reading abstracts on pubmed. Trust me, you won’t get to far that way. I used to think this was a good idea and did it all of the time. But after taking biostats in grad school, I’ve learned that so much of the research done on supplements and the like are horribly flawed and unless you do your OWN statistical analysis, the abstract and the researchers conclusions mean almost nil. I’m not flaming you here, I’m just trying to give some useful advice. Have you heard the saying, “Statistics don’t lie but people do”. A study can easily be biased or calculations performed incorrectly.
Oh hell yeah!!! Reading abstracts isn’t anywhere near enough. I’ve managed to get all the papers for every abstract. The company I work for, Sangamo Biosciences, has memberships for many scientific journals. I also took stat and agree with you wholeheartedly on scientists biasing their data. Even so, most of the papers out there show good promise for myostatin inhibitors.
Kudos to you BOBU. Keep up the good work then.
Just a tidbit on provoking hyperplasia. I recall reading in a book somewhere that a study of competitive swimmers’ deltoids revealed that they had approximately twice the number of muscle fibers per cross sectional area as ordinary folks. The implication was that the type of exercise involved in swimming provoked hyperplasia. (On the other hand, perhaps those gifted in swimming are so gifted by virtue of having more muscle fibers per cross sectional area…)The book also noted that hyperplasia has been confirmed in cats, but no similar “smoking gun” evidence had been found (at least at the writing of this book)in humans, but the swimmers’ results strongly suggested that training could induce it. The book also noted that this increase in muscle fibers per cross sectional area was also seen in anabolic steroid users and offered a possible avenue for monitoring for steroid use in athletic settings where this is forbidden. Just thought this might be an interesting aside given the speculation about what induces hyperplasia.
I also noticed the thing on cats, and in the same book by Wilmore & Costill (check) about an increased fibre number in bodybuilders and the extrapolation of hyperplasia. No before & after studies disproving were sited so the mystery remains. Did hyperplasia occur?, Were a larger amount fo fibres present originally?, or are they naturally gifted with low myostatin like a certain famous group of genetically modified rats who had the gene switched off?. Does anyone know off hand where to find that article/study.