Decreased mitochondrial oxygen consumption and antioxidant enzyme activities in skeletal muscle of dystrophic mice after low-intensity exercise.

To evaluate low-intensity exercise training induced changes of mitochondrial metabolism in dystrophic skeletal muscle, oxygen consumption, reactive oxygen species (ROS) scavengers and antioxidant enzymes were measured in control (C57BL/10) and dystrophic (mdx) mice at 10 (young) and 22 (adult) weeks of age. Dystrophic and control mice were either kept sedentary or daily exercised on a treadmill (480 m/day, exercise training was initiated at 4 and 16 weeks of age for 6 weeks' duration). Mitochondrial oxygen consumption was significantly lower in skeletal muscle from exercised young compared to sedentary young dystrophics. Whereas oxygen consumption was unchanged in exercised adult dystrophics, exercised adult controls exhibit a significant increase vs. sedentary adult controls. Contents of TBARS and lipofuscin were increased (+48%, +24%), while alpha-tocopherol concentration tended to decrease (p > 0.05) in exercised vs. sedentary young dystrophics. Compared to sedentary groups, glutathione peroxidase activity was decreased in exercised young dystrophic muscle (-12%), but increased in exercised controls (young controls +60%, adult controls +47%). In conclusion, adaptation to exercise-induced formation of ROS was limited in young dystrophic skeletal muscle but regained in that of adults. Copyright 2001 S. Karger AG, Basel