Background: Exercise induces a multitude of physiological and biochemical changes in blood that can affect its redox status. Exercise causes an increase in oxygen consumption by the whole body and particularly by the exercising muscle. As a result of this process there is a rise in the production of reactive oxygen species (ROS), which are capable to trigger a chain of damaging biochemical and physiological changes known as lipid peroxidation and oxidative stress. Since the early work of Dillard et al. in 1978, and findings of increased lipid peroxidation following acute aerobic exercise, the topic of exercise-induced oxidative stress has received considerable attention.
Objectives: The aim of this study was to examine how swimming to the point of exhaustion affects oxidative stress generation and nonenzymatic antioxidant activity in an animal model.
Material and methods: The experiments were conducted on 10 male Dunkin-Hartley guinea pigs, and the swimming program used in the study, described as swimming to exhaustion, was defined by Dawson and Horvath. Peripheral blood samples were taken at rest and immediately after the exercise test, and the following parameters were evaluated: total plasma peroxide concentration (TPPC), total plasma thiols (TPT), plasma xanthine oxidase activity (XOD), plasma antioxidant capacity and total plasma proteins.
Results: No significant difference was found between TPPC measured at rest and immediately after exercise swimming test (p = 0.138). Two other parameters--TPT and XOD activity--showed significant differences before and after the swimming exercise test: After the test the TPT value decreased significantly (p = 0.022), while XOD activity increased significantly (p = 0.039). Comparing antioxidant activity in plasma before and after the exercise test, although the value decreased, the difference was not statistically significant (p = 0.755).
Conclusions: The results of this study show that exercise to exhaustion induces the generation of oxidative stress primarily by oxidative modification of protein molecules. The results also indicated that the prooxidative enzyme xanthine oxidase is an important source of ROS during exercise-induced oxidative injury.