Muscle Size Block and Tackle

Myostatin is a special type of protein that prevents muscular growth. You’ve probably heard of the effects of myostatin in animals: Bulls born without the gene to produce myostatin show an intense degree of muscular size and definition with no apparent bodyfat. When scientists breed rats and mice to lack the gene, the rodents look like murine versions of professional bodybuilders, with muscle mass two to three times greater than that of their normal littermates.

In the blood myostatin binds to an activin 2-B receptor. The binding can be blocked by follistatin-like related gene protein (FLRG), but if that doesn’t happen, the myostatin binds to the activin receptor and initiates a series of events that block muscle growth. The leading theory of how it does its dirty work is that myostatin inhibits the proliferation of muscle satellite cells, which are involved in muscle repair and growth after intense exercise.

Myostatin works with cortisol to produce its catabolic muscle effects. When cortisol is elevated following exercise, so is myostatin. I mentioned in this column a while ago a study showing that resistance training lowered myostatin levels nearly 40 percent. That study, however, involved only concentric muscle contractions. In a new study the subjects did the usual style of weight training, involving both concentric (raising) and eccentric (lowering) movements. That’s significant because animal studies show that the eccentric portion of weight training is the type that causes the most extensive muscle damage and, perhaps not so coincidentally, increases myostatin levels after training.

The new study featured 22 young, untrained men randomly assigned to either a weight-training group or a control group that didn’t exercise.1 The study lasted 12 weeks. Those in the weight group trained three times a week, working only the lower body with a routine consisting of leg presses, leg extensions and leg curls. Muscle biopsies and blood samples were taken from the subjects at the start and at the six- and 12-week marks.

After 12 weeks those in the weight-training group showed a 32 percent rise in myostatin mRNA, a 53 percent increase in muscle myostatin and a 56 percent increase in blood myostatin. The increases, however, were accompanied by a 127 percent rise in myostatin-blocking FLRG, along with an 18 percent decrease in activin 2-B receptor density reflecting the FLRG’s inhibiting action. That myostatin didn’t adversely affect muscle gains was seen in the 41 percent increase in muscle strength and 67 percent increase in muscle contractile protein content. Thigh volume increased 19 percent; thigh mass increased 28 percent.

What the study shows is that while weight training’especially the eccentric portion of the exercise’may increase myostatin levels, other factors effectively neutralize its ability to block gains in muscle mass and strength. Serum cortisol levels went up 40 percent, while muscle glucocorticoid receptors (which interact with cortisol) increased 104 percent. Still, neither myostatin nor cortisol had a catabolic effect on muscle because each was effectively inhibited by other substances generated during exercise. IM

1 Willoughby, D.S. (2004). Effects of heavy resistance training on myostatin mRNA and protein expression. Med Sci Sports Exer. 36:574-82.