Oxidative stress in training, overtraining and detraining: From experimental to applied research

Abstract

According to the hormesis theory, the responses of biological systems to stressors in exercise training may be explained by a U-shaped curve with inactivity and overtraining as the two endpoints. Both of these endpoints decrease physiological functions. Markers of oxidative stress may be important parameters for biological monitoring of athletes. Numerous studies have shown that acute exercise has the potential to induce oxidative stress, but regular exposure to an increased level of prooxidants leads to upregulation of the endogenous antioxidative defence system (ADS) of an athlete. Studies that explored the redox state in athletes during the competitive season showed that the antioxidative status changes depending on the training load and training phase. During the training season, a state of fatigue known as overtraining may occur, which results from an excessive training load. Oxidative stress has been suggested as one of the causes of overtraining syndrome. Based on the existing studies, it can be said that a connection exists, but whether oxidative stress is a cause or a consequence of overtraining is yet to be clarified. Furthermore, detraining (training reduction or cessation) leads to a partial or complete loss of training-induced anatomical, physiological and performance adaptations; therefore, it seems reasonable to assume that changes in ADS are also reversible.