It’s been all the rage of the muscle-building press. It’s been talked as the emerging bane of the existence
of the World Anti-Doping Agency, as they try to keep athletes away from the sheer and ominous power
of the approach. While the International Olympic Committee shudders to think of all the records that will shatter, the United States Anti- Doping Agency actually went so far
as to categorically ban drugs that utilize this approach as far back as 2008 by creating a new category. Meanwhile, to this day, not a single such categorical drug exists in the marketplace or has yet to be approved for even the most extreme of medical conditions.
The approach I’m talking about is the inhibition of the blood sequence of amino acids called “myostatin.” I have written about myostatin and myostatin inhibition extensively, but it seems every time I turn around there is so much more to say about this revolutionary approach. Myostatin is the greatest single catabolic-limiting factor of extreme muscle growth, athletic performance, and aging. In short, myostatin exists in our bodies and basically works to limit muscle growth, muscle tone, strength, and body shape. Basically, too much myostatin and your muscle mass shrinks, your fat deposits grow, your strength disappears, and your body becomes formless. Similarly, a clinically significant reduction in blood myostatin levels may unchain the shackles that limit your potential to build muscles and develop.
Researchers are working on developing myostatin blockade, as muscle degradation is such a big part of major diseases like cancer, AIDS, muscle-wasting disorder
s and myopathies, endocrine dyscrasias, congenital abnormalities, and collagen vascular diseases, just to name a few. Since muscle wasting
is a hallmark of an aging physique
in the form of frailty in men and loss of tone in women, the anti-aging community has also taken notice.
In fact, myostatin levels have been conclusively shown to increase with age. Meanwhile, the athletic community remains transfixed on the latest developments of myostatin-inhibiting substances and techniques—as athletes look to gain this edge of seemingly limitless physical power—while governing organizations look to stop them. Interestingly, large pharmaceutical companies continue to fail in their efforts to produce even a single viable prescriptive myostatin inhibitor for patients. Their misguided focus continues to be on blocking myostatin completely with unnatural synthetic drugs. These experimental medications have yet
to become available and, due to the fact that they are irreversible blockers, may have potentially harmful side effects. While pharmaceutical companies have thus far struggled and failed to bring myostatin-inhibiting drugs to the market, there is a host of natural, non-pharmaceutical myostatin inhibiting techniques and substances that you can tap into right now.
But the first query that might come to mind is how much natural myostatin suppression is enough to see results? When we look at muscle-loss studies, we see a good hint as to what kinds of changes in serum myostatin represent significance. In particular, one study published in 1999 demonstrated that a plasma increase of as little as 12% in myostatin corresponded to a staggering 2.2 kilograms mean loss in lean skeletal muscle mass over 25 days. If one allows for a bit of safe extrapolation, a myostatin decrease of as little as 12% should be enough to spur a clinically significant muscle gain.
With that as our baseline of reference, we can explore the natural possibilities, the first being weight training. Yes, weight training itself is a natural myostatin inhibitor, and it makes sense. Levels are lower after weight training because myostatin naturally down-regulates in order to offset the fact that muscle is broken down and thus must rebuild.
The key is weight training in the correct way to stimulate the suppression of myostatin. Once training is challenging enough for the muscle, the recovery phase occurs, ushered in by a drop in myostatin. This transient natural drop in myostatin repairs muscles and, when the stimulus is intense enough, results in an increase in muscle size in anticipation of another similar workload. One study published in 2004 found that healthy male subjects engaged in intense resistance training had a 20% decrease in serum myostatin, which in turn resulted in a 30% gain in strength and a 12% gain in muscle mass over 10 weeks of training. So in terms of muscle gain, anything that drops serum myostatin below 20% of baseline is likely to result in clinically significant muscle gains.
Dietary manipulations will also influence myostatin. The nebulous problem is that we simply don’t know precisely how and to what extent. In past articles I have discussed animal studies that do point to the efficacy of short-term caloric restriction in helping to down-regulate myostatin as well efforts to “de-acidify” the body by “alkalinizing” the diet. The current limitations of the dietary approach are simply that we don’t have the human studies to back any particular method and lack the data to understand precisely how much one particular approach might better reduce myostatin over another. No numbers yet exist as to which dietary approaches are best for myostatin inhibition or precisely to what percentage, if any, one approach reduces serum myostatin over another.
So if you were able to get your hands on some black-market myostatin inhibitor, what can you expect? Researchers examined the effect of a single dose of myostatin gene inhibitors on muscle and strength gains. All animals treated with the myostatin inhibitors demonstrated an increase in body mass with an observable gross enhancement of muscles when analyzed two years later compared with controls. The enlarged muscle mass was accompanied by functional improvement demonstrated by an increase in hind limb grip strength. There was no effect on heart mass, indicating that myostatin inhibition was selective to skeletal muscle tissue. Effects were not restricted to the injected muscles; they were also found at sites remote from directly targeted muscles. Even a single dose of myostatin inhibitors has substantial effects on mass and strength gains. Remember the mice are not exercising, they are just sitting around eating yet they have gross muscle enhancement and increased strength.
Research on the fertile egg blastodisc brought forth the first naturally occurring, nonpharmaceutical, and now widely available myostatin inhibitor. While research I published in 2006 revealed that fertile chicken eggs actually contain biologically active follistatin, it was my work on the first human pilot trial that looked at absorption and hormonal influences that really set the stage for the subsequent studies.
Ultimately it was all about debulking and naturally processing to create a powder by way of a high-grade handling technique that really ended up producing the very first naturally occurring, clinically tested myostatin inhibitor of its kind, MYO-T12 (currently available from MHP as MYO-X, a breakthrough in body-transformation science). In 2009 I published results confirming that the active ingredients in this fertile egg isolate were not only absorbed and active in the human but also resulted in average serum myostatin temporarily dropping by an average of 46% in all study subjects over 12 hours.
In summary, the excitement around myostatin inhibition will only continue to grow as the popularity of this approach takes off. Not only will we see the ceiling of human performance raised to a new height, but we are already seeing staggering improvements in quality of life. We may even one day soon see this approach curing disease and dramatically lengthening our existence here on earth. Certainly if/when myostatin blocking drugs ever arrive, the abuses will invariably happen. But nothing can stop the juggernaut of the natural myostatin-inhibiting evolution that is just now in its infancy.
The approach I’m talking about is the inhibition of the blood sequence of amino acids called “myostatin.” I have written about myostatin and myostatin inhibition extensively, but it seems every time I turn around there is so much more to say about this revolutionary approach. Myostatin is the greatest single catabolic-limiting factor of extreme muscle growth, athletic performance, and aging. In short, myostatin exists in our bodies and basically works to limit muscle growth, muscle tone, strength, and body shape. Basically, too much myostatin and your muscle mass shrinks, your fat deposits grow, your strength disappears, and your body becomes formless. Similarly, a clinically significant reduction in blood myostatin levels may unchain the shackles that limit your potential to build muscles and develop.
Researchers are working on developing myostatin blockade, as muscle degradation is such a big part of major diseases like cancer, AIDS, muscle-wasting disorder
But the first query that might come to mind is how much natural myostatin suppression is enough to see results? When we look at muscle-loss studies, we see a good hint as to what kinds of changes in serum myostatin represent significance. In particular, one study published in 1999 demonstrated that a plasma increase of as little as 12% in myostatin corresponded to a staggering 2.2 kilograms mean loss in lean skeletal muscle mass over 25 days. If one allows for a bit of safe extrapolation, a myostatin decrease of as little as 12% should be enough to spur a clinically significant muscle gain.
With that as our baseline of reference, we can explore the natural possibilities, the first being weight training. Yes, weight training itself is a natural myostatin inhibitor, and it makes sense. Levels are lower after weight training because myostatin naturally down-regulates in order to offset the fact that muscle is broken down and thus must rebuild.
The key is weight training in the correct way to stimulate the suppression of myostatin. Once training is challenging enough for the muscle, the recovery phase occurs, ushered in by a drop in myostatin. This transient natural drop in myostatin repairs muscles and, when the stimulus is intense enough, results in an increase in muscle size in anticipation of another similar workload. One study published in 2004 found that healthy male subjects engaged in intense resistance training had a 20% decrease in serum myostatin, which in turn resulted in a 30% gain in strength and a 12% gain in muscle mass over 10 weeks of training. So in terms of muscle gain, anything that drops serum myostatin below 20% of baseline is likely to result in clinically significant muscle gains.
Dietary manipulations will also influence myostatin. The nebulous problem is that we simply don’t know precisely how and to what extent. In past articles I have discussed animal studies that do point to the efficacy of short-term caloric restriction in helping to down-regulate myostatin as well efforts to “de-acidify” the body by “alkalinizing” the diet. The current limitations of the dietary approach are simply that we don’t have the human studies to back any particular method and lack the data to understand precisely how much one particular approach might better reduce myostatin over another. No numbers yet exist as to which dietary approaches are best for myostatin inhibition or precisely to what percentage, if any, one approach reduces serum myostatin over another.
So if you were able to get your hands on some black-market myostatin inhibitor, what can you expect? Researchers examined the effect of a single dose of myostatin gene inhibitors on muscle and strength gains. All animals treated with the myostatin inhibitors demonstrated an increase in body mass with an observable gross enhancement of muscles when analyzed two years later compared with controls. The enlarged muscle mass was accompanied by functional improvement demonstrated by an increase in hind limb grip strength. There was no effect on heart mass, indicating that myostatin inhibition was selective to skeletal muscle tissue. Effects were not restricted to the injected muscles; they were also found at sites remote from directly targeted muscles. Even a single dose of myostatin inhibitors has substantial effects on mass and strength gains. Remember the mice are not exercising, they are just sitting around eating yet they have gross muscle enhancement and increased strength.
Research on the fertile egg blastodisc brought forth the first naturally occurring, nonpharmaceutical, and now widely available myostatin inhibitor. While research I published in 2006 revealed that fertile chicken eggs actually contain biologically active follistatin, it was my work on the first human pilot trial that looked at absorption and hormonal influences that really set the stage for the subsequent studies.
Ultimately it was all about debulking and naturally processing to create a powder by way of a high-grade handling technique that really ended up producing the very first naturally occurring, clinically tested myostatin inhibitor of its kind, MYO-T12 (currently available from MHP as MYO-X, a breakthrough in body-transformation science). In 2009 I published results confirming that the active ingredients in this fertile egg isolate were not only absorbed and active in the human but also resulted in average serum myostatin temporarily dropping by an average of 46% in all study subjects over 12 hours.
In summary, the excitement around myostatin inhibition will only continue to grow as the popularity of this approach takes off. Not only will we see the ceiling of human performance raised to a new height, but we are already seeing staggering improvements in quality of life. We may even one day soon see this approach curing disease and dramatically lengthening our existence here on earth. Certainly if/when myostatin blocking drugs ever arrive, the abuses will invariably happen. But nothing can stop the juggernaut of the natural myostatin-inhibiting evolution that is just now in its infancy.
