Effects of heavy resistance training on myostatin mRNA and protein expression

Purpose: Myostatin is a negative regulator of muscle mass and its effects seem to be exacerbated by glucocorticoids; however, its response to resistance training is not well known. This study examined 12 wk of resistance training on the mRNA and protein expression of myostatin, follistatin-like related gene (FLRG), activin fib receptor, cortisol, glucocorticoid receptor, myofibrillar protein, as well as the effects on muscle strength and mass and body composition. Methods: Twenty-two untrained males were randomly assigned to either a resistance-training [RTR (N = 12)] or control group [CON (N = 10)]. Muscle biopsies and blood samples were obtained before and after 6 and 12 wk of resistance training. RTR trained 3x wk(-1) using three sets of six to eight repetitions at 85-90% 1-RM on lower-body exercises, whereas CON performed no resistance training. Data were analyzed with two- and three-way ANOVA. Results: After 12 wk of training, RTR increased total body mass, fat-free mass, strength, and thigh volume and mass; however, they increased myostatin mRNA, myostatin, FLRG, cortisol, glucocorticoid receptor, and myofibrillar protein after 6 and 12 wk of training (P < 0.05). Conclusions: Resistance training and/or increased glucocorticoid receptor expression appears to up-regulate myostatin mRNA expression. Furthermore, it is possible that any plausible decreases in skeletal muscle function from the observed increase in serum myostatin were attenuated by increased serum FLRG levels and the concomitant down-regulation of the activin IIb receptor. It is therefore concluded that the increased myostatin in response to cortisol and/or resistance training appears to have no effects on training-induced increases in muscle strength and mass.