Endurance exercise causes mitochondrial and oxidative stress in rat liver: Effects of a combination of mitochondrial targeting nutrients

Abstract

Aims Endurance exercise causes fatigue due to mitochondrial dysfunction and oxidative stress. In order to find an effective strategy to prevent fatigue or enhance recovery, the effects of a combination of mitochondrial targeting nutrients on physical activity, mitochondrial function and oxidative stress in exercised rats were studied. Main methods Rats were subjected to a four-week endurance exercise regimen following four weeks of training. The effects of exercise and nutrient treatment in rat liver were investigated by assaying oxidative stress biomarkers and activities of mitochondrial complexes. Key findings Endurance exercise induced an increase in activities of complexes I, IV, and V and an increase in glutathione (GSH) levels in liver mitochondria; however, levels of ROS and malondialdehyde (MDA) and activities of complexes II and III remained unchanged. Exercise also induced a significant increase in MDA and activities of glutathione S-transferase and NADPH-quinone-oxidoreductase 1 (NQO-1) in the liver homogenate. Nutrient treatment caused amelioration of complex V and NQO-1 activities and enhancement of activities of complex I and IV, but had no effect on other parameters. Significance These results show that endurance exercise can cause oxidative and mitochondrial stress in liver and that nutrient treatment can either ameliorate or enhance this effect, suggesting that endurance exercise-induced oxidative and mitochondrial stress may be either damaging by causing injury or beneficial by activating defense systems.