In vertebrates, skeletal muscle myofibers display different contractile and 
metabolic properties associated with different mitochondrial content and 
activity. We have previously identified a mitochondrial triiodothyronine 
receptor (p43) regulating mitochondrial transcription and mitochondrial 
biogenesis. When overexpressed in skeletal muscle, it increases mitochondrial 
DNA content, stimulates mitochondrial respiration, and induces a shift in the 
metabolic and contractile features of muscle fibers toward a slower and more 
oxidative phenotype. Here we show that a p43 depletion in mice decreases 
mitochondrial DNA replication and respiratory chain activity in skeletal muscle 
in association with the induction of a more glycolytic muscle phenotype and a 
decrease of capillary density. In addition, p43(-/-) mice displayed a 
significant increase in muscle mass relative to control animals and had an 
improved ability to use lipids. Our findings establish that the p43 
mitochondrial receptor strongly affects muscle mass and the metabolic and 
contractile features of myofibers and provides evidence that this receptor 
mediates, in part, the influence of thyroid hormone in skeletal muscle.