Myostatin Blockers Break Down Bodyfat

[718si]

Bodybuilders who are thinking of using myostatin blockers in the near future are not only likely to develop mega-muscles, they're likely to become ripped too. According to researchers at the American Diabetes and Obesity Center of Excellence, blocking myostatin raises the body's sensitivity to the satiety hormone leptin.

Myostatin is a protein with which muscle cells inhibit their own growth. Myostatin no doubt has other important functions, but in adult organisms, as far as we know, blocking the effect of myostatin has no noteworthy side effects. Apart from a dramatic increase in muscle mass. And that's why bodybuilders are following the results of experiments with myostatin blockers with interest.

The experiments are not being done with athletes in mind, however. Researchers hope that myostatin blockers might help fight age-related weakness and muscle diseases. In the case of the study that the researchers at the Diabetes and Obesity Center of Excellence published in AJP – Endocrinology and Metabolism, the authors hope that myostatin may also be helpful in combatting obesity.

The researchers experimented with mice in which the gene for myostatin had been deactivated [KO] and with normal mice. According to the table below, the myostatin-less mice not only became unnaturally muscled, but also had an abnormally low fat percentage.

The researchers also gave their subjects a supplement to make up for the deficiencies, except for the vitamin B1, B2, B6 and C deficiencies.

A control group of 11 students got the same diet, plus a supplement that did make up for all the vitamins they were lacking.

As a result of their increased muscle mass, the myostatin-less mice burned more energy. You can see this in the figures for their oxygen consumption. What's strange is that deactivating the myostatin gene doesn't lead to an increase in food intake. You'd expect this to happen, but it doesn't. Mice with an inactive myostatin gene eat the same amount as mice without this gene.

When the researchers injected the mice with leptin they noticed that the myostatin-less mice lost more weight than the normal mice did. Leptin is a hormone that fat cells manufacture if they grow. This suppresses appetite and increases metabolism. The researchers conclude that deactivating myostatin increases sensitivity to leptin, and as a result reduces appetite.

The researchers suspect that myostatin blockers may therefore be interesting candidates for anti-obesity medicine, although they are careful in their formulation. "These findings suggest that myostatin signaling either directly or indirectly via increased skeletal muscle mass has far-reaching effects on energy homeostasis and raise the possibility that an unknown muscle-related factors induced by myostatin deficiency may confer metabolic benefit."

Source:
Am J Physiol Endocrinol Metab. 2011 Jun;300(6):E1031-7

 

[Solo_]

Thanks for posting this 7.

Two things....one it's one thing to turn off the myostatin gene in a mouse but entirely another to pull it off in humans (yet). The only myo blockers on the market for human research have been ineffective thus far, providing only a slight increase in intracellular water retention and some minor fat loss. These effects dissipate when you stop using the peptide.

Also...why don't any of our sponsors sell leptin? lol

 

[Jorsn]

Thanks for posting.

Very interesting

 

[JLizzle]

718si...

Which myo peps are you talking about in particular?

 

[718si]

718si...

Which myo peps are you talking about in particular?

The cited research was actually performed using mice that had a genetic modification eliminating myostatin completely. I believe this is done using viral vectors to deliver modified genes to the target cells.

There are currently several known ways to reduce myostatin:

- viral vector genetic modification,
- injecting large amounts of actual myostatin, triggering an immune response to the "foreign body", causing a net reduction of myostatin,
- follistatin, which blocks myostatin's action (like a SERM does to estrogen), or
- myostatin HMP (human myostatin propeptide) which binds to myostatin (like how shbg binds to testosterone)

Any of the above methods will either reduce the amount or effectiveness of myostatin's ability to limit muscle growth, just to varying extents.

Obviously, eliminating myostatin completely should yield the greatest potential gains in lbm in the shortest amount of time.

At this stage of research, however, there is too much uncertainty about possible negative side effects of too little myostatin (ie, weakend tendons, etc) to justify what IMHO is a radical treatment option like eliminating myostatin completely.

It seems that the best results being seen in the research community is happening when a subject's gains "hit the wall" after a month or so on a course of anabolics, as it appears that the body's 2 primary ways of attempting to reach homeostasis are increasing both shbg and myostatin.

I believe a theoretically sound protocol would be to run a standard course of anabolics, and when gains slow/stall, introduce either proviron or winstrol (control shbg) and myostatin HMP (control myostatin).