Myostatin Blockers

(By David Steen)

Anyone familiar with the world of bodybuilding will agree that return to the era when power sports were completely free of steroids and various other substances supporting muscle growth (like Human Growth Hormone or Insulin) is not realistic.

Steroids, even if proven very harmful, are not like cigarettes or even narcotics: steroids rather resemble the philosopher´s stone of ancient alchemists a substance that can profoundly alter your body and soul. The quest for such transformation is eternal, deep seated in human character and present in every cultural tradition.

Thus, in my opinion, the only solution to anabolic-steroid abuse is to find a harmless substance (or treatment) with similar effects. So far, the only such promising treatment is blocking of myostatin, a protein that limits the muscle growth.

First of all, I have to warn you that there is no treatment or drug that could block myostatin and thus lead to uncontrolled muscle growth in humans at present. Although the early results in animals (especially mice) were very promising, anyone claiming to actually own such substance and possibly trying to sell it is a scammer, so do not get fooled and don´t buy any products claiming to have myostatin-inhibiting properties. However, according to scientists, the day when a working myostatin inhibitor will be produced is very close (probably couple of years).

Myostatin and its associated gene were first discovered by a group of scientists at John Hopkins University in 1997. Alexandra McFarren, Se-Jin Lee and Ravi Kambadur tried to block the gene associated with myostatin production in mice and the result was a mouse with doubled muscle mass. Since then it became clear that defects of myostatin hormone cause significant growth in muscle mass in both animals and humans. The very muscular Piedmontese and Belgian Blue bulls, for instance, were found to have defective myostatin genes.

At present, there are two approaches to myostatin inhibition/blocking: the first, more conservative, is to produce a substance that would block the myostatin production or it´s binding on myostatin receptors, thus causing muscle growth.

The second, more radical approach is to target the myostatin gene directly, disabling it and thus make the results of the treatment permanent. This is what H. Lee Sweeney, physiologist at University of Pennsylvania, is trying to do. As I said earlier, both approaches have yet to yield some results. Wyeth Pharmaceuticals, drug maker based in Madison, New Jersey, caused much excitement by its myostatin blocking compound called MYO-029. However, after several years of development and clinical testing, the company announced in March 2008 that the drug, although harmless, simply doesn´t work. The gene therapy is also currently not working in humans, because of immune response.

Another problem with blocking myostatin is the fact that it apparently causes the tendons to be „small, brittle and hypocellular“ according to a 2007 study (on mice) by scientists at University of Michigan.

Anyway, as I said earlier, there is little doubt among the scientists that myostatin inhibition will soon be achieved. In fact, the anti-doping agencies are already busy to develop tests for blocked myostatin. If the test will be successfully implemented (and this is a big IF) and if they will indeed eliminate myostatin blockers from sports (even more doubtful) the professional athletes may find themselves in a strange situation when every senior treated for muscle dystrophy will be more muscular than them.

Resources: Scientific American, August 2005 and August 2008 McPherron A., Lee S. Double muscling in cattle due to mutations in the myostatin gene Proc Natl Acad Sci USA, 1997 Mosher D.S., Quignon P., Bustamante C.D., Sutter N.B., Mellersh C.S., et al. A Mutation in the Myostatin Gene Increases Muscle Mass and Enhances Racing Performance in Heterozygote Dogs. PLOS Genetics, 2007 Mendias C.L., Bakhurin K.I. ,Faulkner J.A.; Tendons of myostatin-deficient mice are small, brittle, and hypocellular; PNAS, 2008 vol 105 no. 1 388-393