The transcriptional coactivator PGC-1? is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling.

ABSTRACT: Skeletal muscle mass loss and dysfunction have been linked to many diseases. Conversely, resistance exercise, mainly by activating mammalian target of rapamycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effects. Moreover, mTORC1, along with peroxisome proliferator-activated receptor ? coactivator 1? (PGC-1?), regulates skeletal muscle metabolism. However, it is unclear whether PGC-1? is required for skeletal muscle adaptations after overload. Here we show that although chronic overload of skeletal muscle via synergist ablation (SA) strongly induces hypertrophy and a switch toward a slow-contractile phenotype, these effects were independent of PGC-1?. In fact, SA down-regulated PGC-1? expression and led to a repression of energy metabolism. Interestingly, however, PGC-1? deletion preserved peak force after SA. Taken together, our data suggest that PGC-1? is not involved in skeletal muscle remodeling induced by SA.

SUBMITTER: Perez-Schindler J 

PROVIDER: S-EPMC3864298 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature