Protective mechanisms of skeletal muscle against oxidative stress by physical exercise: the role of uncoupling protein via NO

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Exercise is considered to serve as one of useful tools for the prevention and remedy against lifestyle-related diseases. On the other hand, physical exercise markedly enhances a flow of blood in skeletal muscle, thereby leading to an increase in the production of reactive oxygen species (ROS). In 2003 we demonstrated that the increased production of ROS by acute eccentric exercise in mouse skeletal muscle might be due to factors other than leukocytes, and that extracellular superoxide dismutase (EC-SOD) had a part in antiarteriosclerotic effects of exercise. Unexpectedly, there were no significant changes in uncoupling proteins (UCP2 and UCP3) or nitric oxide synthases (NOS-I, II, III) in skeletal muscle from mice after the exercise.In 2004 we made a human study. The physical training executed consisted of 30-min interval training (swimming or running) in addition to 30-min long-distance training (swimming or running) per day, 5 times per week, during 3 months. Muscle biopsies were taken before and after the training. All the subjects notably increased their VO_2max levels, indicating an improvement in aerobic capacity. After training, there were significant decreases in the expression of mRNAs for HSP70, CuZn-SOD, and Mn-SOD but a significant increase in UCP2 mRNA expression, whereas no definite changes were observed in the levels of mRNAs for VEGF, bFGF, HIF1α, myoglobin, or UCP3. Moreover, the changes in HIF1α mRNA expression correlated well with those in VEGF mRNA expression after training. The increased expression of UCP2 mRNA might attenuate the generation of ROS during the training period. Taken together, it is envisioned that cumulative effects of transient changes in transcription during recovery from successive bouts of exercise may represent the underlying kinetic basis for the cellular adaptations associated with endurance training.