Myostatin inhibitors are a perfect example of the latter phenomenon. There are only a couple of fringe products still around on the market. Nobody I know of uses them, and it’s been aaaages since anyone’s even asked about them.
So why bother reviewing Myostatin inhibitors at all? Two reasons:
- The myostatin “story” is a cautionary tale about how supplement companies—and their customers—can jump to conclusions based on incomplete data.
- Myostatin inhibition is the subject of intensive mainstream research. This makes it a tempting target, so it’ll help to know something about the subject…just in case more supplements are introduced.
Ok, enough moralizing: let’s get to the heart of the matter…what is myostatin?
Myostatin is an regulatory protein expressed in skeletal muscle. It’s a “negative regulator”—that is, myostatin, in its unbound, active form, suppresses muscle growth. Conversely, myostatin inactivation amplifies muscle growth. This can be seen in certain animal models with inactive, myostatin mutations, such as “double-muscled” Belgian Blue cattle. Various animal models have also been created, such as myostatin-deficient “knockout” mice, in order to study its effects on muscle growth.
Myostatin mutations have also been found in humans with unusually muscular phenotypes. The best-known example in bodybuilding is Flex Wheeler. A young German boy with the mutation has also been identified.
Mutations, however, are not the only way to take myostatin out of the picture. Myostatin has naturally occurring inhibitors that can bind to it and render it inactive. Animals injected with inhibitors also pack on extra muscle. Thus, it should come as no surprise that myostatin inhibition is now being viewed as a viable therapeutic strategy for muscle-wasting diseases such as Duchenne Muscular Dystrophy (DMD).
To sum up: animals and people with inactive myostatin are able to add a lot of muscle mass naturally. Thus, you can understand the “buzz” surrounding the discovery of a natural, non-physiological myostatin inhibitor. This was a sulfated polysaccharide fraction (SP) from the brown seaweed, Cystoseira canariensis, which could bind serum myostatin in-vitro. The fact that no animal or human studies had been performed was irrelevant: Cystoseira canariensis was hailed as the next big thing.
Reality, however, soon set in. Despite the appearance of a report in a Russian journal that showed a small increase in lean mass for trainees taking creatine/whey protein/SP extract vs. trainees consuming whey protein/creatine alone, the fate of Cystoseira canariensis was sealed by two studies at Baylor University. The first, by Darryn Willoughby, showed SP supplementation had no effect on serum myostatin, lean mass gains or strength. The second, performed in Richard Kreider’s lab, confirmed this finding.
So much for Cystoseira canariensis…the only products I know of that are still on the market are Champion MyoStim and Pinnacle’s AnabolX Plus, Fuse and Esterified Creatine.
Beyond that, there’s one other supplemental approach to myostatin inhibition that I know of. This is Folstaxan, which is alleged to be a source of follistatin.
Follistatin is yet another regulatory protein, which—among other functions—plays an indirect role in regulating follicle stimulating hormone (FSH). But the importance of follistatin in this scenario lies in its ability to bind to—and inhibit myostatin.
Follistatin is expressed during embryonic development. The manufacturers of Folstaxan claim that fertilized egg yolks are a rich source of it. They claim Folstaxan provides sufficient egg yolk follistatin to reduce serum myostatin in human subjects. Their patent application indicates Folstaxan is simply freeze dried fertilized egg yolk powder, and their web site offers no credible proof that Folstaxan results in any muscle mass gains.
Nonetheless, if you find the concept compelling, there’s a homespun alternative: just find a health food store that sells fertilized eggs, and have a few yolks “Rocky” style—I expect your results (if any) will be just as good.
As I noted above, myostatin inhibition is a legitimate therapeutic target for muscle-wasting diseases. Currently, there are a number of approaches being investigated: gene therapy, modified RNA oligonucleotides, DNA vaccines, and injected inhibitors, such as myostatin propeptide (an inactive form that can bind to—and inhibit—active myostatin) and anti-myostatin antibodies. This last strategy is currently being used in human clinical trials on patients with muscular dystrophy.
Naturally, there are those who hope this research will eventually lead to physique/performance enhancing therapies that will be just as effective—and safer—than anabolic steroids. This hope may be misplaced, however. While myostatin inhibition may be a promising therapeutic strategy, there are also some potentially undesirable effects. For example, force production in mice carrying myostatin mutations is not improved, and is even reduced, when expressed as a function of muscle size. In addition, the tendons of myostatin deficient mice are smaller and more brittle than those of wild type contols. Double-muscled cattle are known to be more susceptible to stress than normal cattle. The performance of myostatin-deficient, “bully” racing whippets is also impaired.
These concerns are based on full, homozygous mutants, however. An interesting finding of the whippet study is that heterozygous dogs (that is, dogs with only one copy of the mutation), are actually superior racers. As such, there may be an athletic performance benefit to partial myostatin inhibition.
This makes it clear, however, that myostatin inhibition is nothing to fool around with: there are potential benefits, but also potential liabilities associated with it, if taken too far. Thus, even a supplement that actually “worked”—however improbable that may seem—would not be something to take lightly. At this point, myostatin inhibition is best left to the pharmaceutical companies, rather than the supplement companies.