kiwiol says that Mysotatin Inhibition is a myth. It can only work in the embryonic stage.
It`s not a myth, myostatin is a negative regulator of skeletal muscle growth. Gene knockouts in embryonic mice result in hypermuscular adult mice. Recent work in which gene expression 'knockouts' were effected in adult mice showed that "Tamoxifen administration to 4-mo-old Mstn[f/f]/Cre+ mice reduced myostatin mRNA expression to less than 1% of normal, which increased muscle mass ~25% over the following 3 mo in both male and female mice". It was concluded that "even after developmental muscle growth has ceased, knockout of the myostatin gene induces a significant increase in muscle mass".
As far as bodybuilding goes, it'll be sometime before it`s possible to start messing with a person`s genes directly in a clandestine lab, at least without significant and irreversible effects. The easiest way will be to use antibodies or better anti-sense RNA; this will become a reality over the next decade or so. Basically the DNA (usually double-stranded, of course) that defines this particular gene produces an mRNA (messenger RNA which is single-stranded). This mRNA is then used as a template for protein synthesis. Antisense RNA is, essentially, the introduction of anti-sense (or complimentary sequence) RNA that binds to the mRNA. When it is double-stranded, the mRNA cant be used in protein synthesis and so protein expression (in this case myostatin expression) is inhibited.
The problem is, there are numerous genes involved in muscular hypertrophy, and also muscular dystrophy. The function of myostatin itself is not fully understood either, so those at the forefront will have to weigh up the significant risks with the rewards.
