Apocynin Attenuates Oxidative Stress Session-Induced Strenuous Exercise

Reactive oxygen species (ROS) increase skeletal muscle response intracellular signaling during exercise. The present study investigated the role of skeletal muscle NADPH oxidase isoform 1 (NOX2) in the molecular response of skeletal muscle to physical exercise. Rats previously treated with the NOX2 inhibitor apocynin (30 mg/kg) for 3 days were subjected to exhaustive exercise. Fosfo-p47phox levels were significantly increased by exercise in the soleus muscle. Furthermore, physical exercise significantly increased the NOX2 assembly complex (p47phox – gp91phox). NOX2 and NOX4 activation induced by exercise were completely inhibited by apocynin treatment. Exercise increased mRNA levels of manganese superoxide dismutase, glutathione peroxidase, and catalase in skeletal muscle. Furthermore, an increase in thiobarbituric acid reactive substances induced by exercise decreased in rats treated with apocynin compared to the vehicle-treated group, and reduced thiol levels were increased in apocynin-treated rats. The findings demonstrate that NOX2 inhibition by apocynin changes intracellular signaling in exercise and muscle electric stimuli, suggesting that NOX2 plays a critical role in the molecular response to acute exhaustive exercise.