Chemical strength athletes who are thinking of using myostatin blockers may experience more side effects than researchers thought five years ago. The latest indications come from an animal study published by biologists at Nanyang Technological University in Singapore in AJP - Cell Physiology. According to this study, wounds incurred by mice that do not make myostatin heal less quickly than normal.
Not so long ago scientist were convinced that if you could inhibit the protein myostatin enough, then muscle fibres would grow without side effects. Myostatin was thought to inhibit the growth of muscle fibres and to only be active in muscle cells. Myostatin blockers were therefore thought to be safer than steroids and even SARMs.
Das war einmal, ladies and gentlemen. Recent studies have shown that myostatin has all sorts of functions outside the muscles in the body. If you deactivate myostatin, the muscle tendons shrink and become more brittle, reported researchers after doing an animal study at the University of Michigan in 2008. In 2010 another study appeared in which mice without myostatin have less endurance capacity than normal mice.
And the latest bad news about myostatin comes from Singapore, where researchers were curious to know whether myostatin also has a role in wound healing. A group of proteins from the TGF-beta family play a key role in the process of wound healing, and one of these proteins is myostatin. So there.
To test the theory the researchers inflicted wounds on ordinary mice [Wild Type] and mice in which the myostatin had been genetically deactivated [Mstn-Null]. The photos below show that the healing process took longer in the myostatin-less mice.
The researchers unravelled the mechanism at work and then depicted it in the diagram above. Without myostatin, new cells are produced more slowly in the dermis layer, and the cells also produce less collagen. Deactivating myostatin also inhibits the development of keratinocytes, the cells in the epidermis or outer layer of skin.
Am J Physiol Cell Physiol. 2012 Apr;302(8):C1213-25.