Contribution of oxidative stress to skeletal muscle fatigue following acute exercise

Abstract

Skeletal muscle fatigue is defined as muscle force depression following exercise or repeated contractions that mimic exercise. Oxidative stress, caused by excessive production of reactive oxygen species (ROS), has long been thought to contribute to muscle fatigue after acute exercise. However, recent studies on antioxidant treatments have suggested little impacts of oxidative stress on muscle fatigue. This review examines the chemical properties of various ROS, their source, their effects on the contractile mechanism, and their production during muscle fatigue. Based on these, this review discusses cellular mechanisms behind the limited ROS influence on muscle fatigue, with a focus on the primary ROS produced during exercise such as superoxide, hydrogen peroxide and hydroxyl radical. These ROS have been shown to exert both positive and negative effects on muscle force. Therefore, the limited effectiveness of antioxidants is thought to be due to their capacity to suppress not only the negative effects but also the positive effects of ROS. This antioxidant effect provides an important insight into the relationship between oxidative stress and muscle force. Previous studies suggest that the low levels of ROS can enhance muscle force, whereas higher levels impair it, which is referred to here as the “invert U” relationship. Developing this concept further, I proposed a hypothesis that the relationship between oxidative stress and muscle force can be divided into two phases: in phase 1, the positive and negative effects of ROS balance out, resulting in minimal impact on muscle force, while oxidative stress dramatically decreases force in phase 2 which occurs under more sever condition.