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Duchenne muscular dystrophy (DMD) is characterized by devastating muscle degeneration associated with oxidative stress, loss of contractile tissue, muscle atrophy, muscle weakness and increased fibrosis in respiratory and locomotor muscles. We tested the hypothesis that protection against oxidative stress via the catalase/superoxide dismutase mimetic EUK‐134 will prevent reduction of diaphragm and skeletal muscle mass/body mass during the early inflammatory phase (20‐28 days) in mdx mice. C57BL(wild type) and mdx mice were given EUK‐134 (30mg/kg body weight/day, i.p., injection) for 8 days, beginning at 20 days of age. Body mass was significantly lower in mdx mice (‐37.7%) than wild type but, EUK‐134 increased body mass by 15.5% in mdx mice. Absolute muscle mass was lower in diaphragm (‐44.3%), gastrocnemius (‐53.6%), tibialis anterior (‐58.1%) in mdx mice. Muscle mass/body mass was lower in diaphragm (‐11.4%), gastrocnemius (‐26.3%), tibialis anterior (‐34.4%), but not heart, plantaris, soleus, extensor digitorum longus in mdx mice. EUK‐134 had a significant positive effect in protecting against reduced muscle mass/body mass in diaphragm (+38.7%) and gastrocnemius (+27.1%) in mdx mice. These data indicate that EUK‐134 provide protection against reduced muscle mass/body mass in diaphragm and gastrocnemius in mdx mice during this early phase of muscular dystrophy. Supported by NIH Grant (AR054084).

Exercise may reduce oxidative stress, mitochondrial dysfunction, and mitochondrial caspase‐dependent apoptosis with age. However, it is unclear whether the caspase‐independent apoptosis via EndonucleaseG (EndoG) and Apoptosis Inducing Factor (AIF) is affected by exercise in aging skeletal muscle. We hypothesize that exercise will attenuate apoptosis brought on by the translocation of EndoG and AIF from the mitochondria to the nucleosome in aging white gastrocnemius. Twenty‐four Fischer Brown Norway rats were randomly assigned to four groups, young sedentary, old sedentary, young exercisers and old exercisers. In the soluble fraction there was an 86.4 % increase in the old sedentary group in EndoG, but there was no change in the young groups. EndoG protein level in the nucleosome fraction of young exercisers decreased 49 % and old sedentary increased by 86.5% when compared to young sedentary controls. The data indicated that exercise was protective against apoptosis by decreasing the translocation of EndoG to the nucleosome in aged skeletal muscle.