Reactive oxygen species may contribute to the pathogenesis of muscular dystrophy. High intensity exercise clearly induces muscle damage in mdx mice; however, the effects of low intensity exercise training (LIT) on mdx muscle are less clear. We examined the effect of LIT on markers of oxidative stress (malondialdehyde and protein carbonyls), antioxidant (superoxide dismutase, catalase, and glutathione peroxidase), and mitochondrial (2-oxoglutarate dehydrogenase and cytochrome oxidase) enzymes in skeletal muscle of mdx and wild-type mice. Mdx and wild-type mice were allocated to LIT and sedentary groups. Malondialdehyde levels were higher in white muscle from sedentary mdx as compared to both sedentary and LIT wild-type mice (P<0.001). Protein carbonyl content was higher in white and red muscle of mdx versus wild-type mice (P<0.05). LIT was associated with lower levels of malondialdehyde and protein carbonyls in white muscle of mdx mice (decreased 38 and 44%, P<0.001 and P<0.01, respectively). Antioxidant and mitochondrial enzyme activities were higher in white muscle of mdx than in wild-type mice (P<0.05). LIT in mdx mice induced physiological adaptation resulting in lower levels of markers of oxidative stress that were not different than those from wild type. These results are of relevance for therapeutic exercise in patients with dystrophinopathy where exercise prescription remains controversial.