We demonstrate in this study that: both PGC-1α and PGC-1β improve muscle function in dystrophic mouse models; that they do so independently of utrophin induction; that PGC-1α improves muscle function even if delivered only post-natally; and that even the more severe mdx/utrn-/- model of DMD is efficiently rescued by PGC-1α. The gene discussed is PPARGC1A; the disease is Duchenne muscular dystrophy.