Myostatin!!

[bigorse]

I am tempted to try yk myself. Im just trying to figure out how to best incorporate it.
I am running mk677 & cjc w/dac right now and have no intention of stopping.
What I have been thinking about doing is running a tried and true cycle, one I know what i can expect from and add in the yk11. This will allow me to see what kind of difference, if any, the YK11 brings to the table. I am thinking that would be the fairest way for me personally to judge its effectiveness. If I were to run my standby test/deca/winstrol cycle I could add in the yk and get a darn good idea how effective it is. I can almost tell you right now what I would get out of the cycle alone having run it so many times in my present condition. The only thing is then to really be fair I would have to drop the mk/cjc stack and to be honest I just do not want to do that. Quite frankly I am loving that combo. I only pin E3D with it and am getting some really nice gh/igf benefits.
Decisions, decisions.....

well from what i have read myostatin inhibition should allow proliferation easier. (il try sight a study) so using something like your current gh stack plus some MGF should make YK even more effective. anabolic wise there are animal studies showing hyperplasia from tren so if you were going an all out blast based on the hope for muscle proliferation i would reccomend something like this

1-indefinitely your gh peps stack
1-4 and 8-12 pegMGF 200mcg eod
1-12 tren a where your comfortable
1-12 test prop where your comfortable
yk11 through out.

that would be how i see it most effective.

the other would be incorporated into long cycle like deca/eq cycle. gains ussually slow around week 10, myostatin inhibition is what seems to be the causr so inhibiting it should allow for continued gains in longer cycles.

1-16 test e 500mg
1-16 deca 500mg
8-16 yk11

this is where i see it beneficial.

 

[bigorse]

pub med abstract on myostatin deficient animals

Abstract

Myostatin, which is a member of the TGF-beta superfamily, is a negative regulator of skeletal muscle formation. Double-muscled Piedmontese cattle have a C313Y mutation in myostatin and show increased skeletal muscle mass which resulted from an increase of myofiber number (hyperplasia) without that of myofiber size (hypertrophy). To examine whether this mutation in myostatin gene affects muscle development in a dominant negative manner, we generated transgenic mice overexpressing the mutated gene. The transgenic mice exhibited dramatic increases in the skeletal muscle mass resulting from hyperplasia without hypertrophy. In contrast, it has been reported that a myostatin mutated at its cleavage site produces hypertrophy without hyperplasia in the muscle. Thus, these results suggest that (1) the myostatin containing the missense mutation exhibits a dominant negative activity and that (2) there are two types in the dominant negative form of myostatin, causing either hypertrophy or hyperplasia.

 

[j_p]

Yes please post up logs guys! I would love that myself!