ABSTRACT
<p><b>OBJECTIVES</b>In addition to having health-promoting effects, exercise is considered to induce oxidative stress. To clarify whether increased oxygen consumption during exercise induces oxidative stress, we investigated the effects of aerobic exercise and anaerobic exercise on a series of oxidative damage markers.</p><p><b>METHODS</b>One group of subjects performed aerobic exercise and another group performed anaerobic exercise with similar workloads, but with different levels of oxygen consumption. Blood and urine samples were collected before, immediately after, and 3, 9, and 24 h after exercise. Serum uric acid (UA) and creatine phosphokinase were evaluated. As markers of oxidative damage to lipids, proteins and DNA, we evaluated serum 4-hydroxy-2-nonenal, urinary F(2)-isoprostanes, serum protein carbonyls, and leukocyte 8-hydroxydeoxyguanosine.</p><p><b>RESULTS</b>Oxygen consumption was significantly greater during aerobic exercise. Although UA level increased immediately after aerobic exercise and decreased thereafter, UA level did not change after anaerobic exercise. The two types of exercise had significantly different effects on the change in UA level. After anaerobic exercise, the levels of 8-hydroxydeoxyguanosine and 4-hydroxy-2-nonenal significantly increased at 24 h and 3 h, respectively. The levels of creatine phosphokinase and F(2)-isoprostanes decreased after exercise. The two types of exercise caused no apparent significant differences in the levels of these biomarkers.</p><p><b>CONCLUSION</b>The findings suggest that similar workloads of anaerobic exercise and aerobic exercise induce reactive oxygen species (ROS) differently: aerobic exercise seems to initially generate more ROS, whereas anaerobic exercise may induce prolonged ROS generation. Although more oxygen was consumed during aerobic exercise, the generated ROS did not induce significant oxidative damage. Oxygen consumption per se may not be the major cause of exercise-induced oxidative damage.</p>
ABSTRACT
Objectives: In addition to having health-promoting effects, exercise is considered to induce oxidative stress. To clarify whether increased oxygen consumption during exercise induces oxidative stress, we investigated the effects of aerobic exercise and anaerobic exercise on a series of oxidative damage markers. Methods: One group of subjects performed aerobic exercise and another group performed anaerobic exercise with similar workloads, but with different levels of oxygen consumption. Blood and urine samples were collected before, immediately after, and 3, 9, and 24 h after exercise. Serum uric acid (UA) and creatine phosphokinase were evaluated. As markers of oxidative damage to lipids, proteins and DNA, we evaluated serum 4-hydroxy-2-nonenal, urinary F2-isoprostanes, serum protein carbonyls, and leukocyte 8-hydroxydeoxyguanosine. Results: Oxygen consumption was significantly greater during aerobic exercise. Although UA level increased immediately after aerobic exercise and decreased thereafter, UA level did not change after anaerobic exercise. The two types of exercise had significantly different effects on the change in UA level. After anaerobic exercise, the levels of 8-hydroxydeoxyguanosine and 4-hydroxy-2-nonenal significantly increased at 24 h and 3 h, respectively. The levels of creatine phosphokinase and F2-isoprostanes decreased after exercise. The two types of exercise caused no apparent significant differences in the levels of these biomarkers. Conclusion: The findings suggest that similar workloads of anaerobic exercise and aerobic exercise induce reactive oxygen species (ROS) differently: aerobic exercise seems to initially generate more ROS, whereas anaerobic exercise may induce prolonged ROS generation. Although more oxygen was consumed during aerobic exercise, the generated ROS did not induce significant oxidative damage. Oxygen consumption per se may not be the major cause of exercise-induced oxidative damage.