Objective To investigate the mechanism of resveratrol protecting exercise-induced liver injury in rats. Methods Thirty-two 7-week-old male SPF SD rats were randomly divided into a control group (Group C), resveratrol RM) with eight rats in each group. Group C and Group R did not undergo any exercise. Group M and Group RM underwent 4 weeks of high-intensity treadmill training (10° slope; velocity started from 10 m/ min, which was increased by 5 m/ min every 5 min and would not increase until 35 m/ min, and then the rats were trained to exhaustion). One hour before training, Group R and Group RM were intragastrically injected with 150 mg/ (kg·bw) resveratrol in 5 mL/ (kg·bw). Group C and Group M were injected with an equal volume of solvent at the same time point. Rats were sacrificed at 24 hours after the end of the last training session, and blood and liver were collected. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity were detected by an automatic biochemical analyzer. Hepatic histomorphology was observed by hematoxylin-eosin (HE) staining. Hepatic nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), apoptosis-related protein B-cell lymphoma-2 (Bcl-2), and bcl-2-associated X protein (Bax) protein expression was detected by immunohistochemistry. Hepatic apoptosis was detected by TdT-mediated dUTP nick-end labeling. Hepatic superoxide dismutase (SOD) and malondialdehyde (MDA) activity was detected by colorimetry. Results Compared with Group M, serum ALT, AST activity, the hepatic MDA level, and hepatic apoptosis were significantly decreased in Group RM (P< 0. 05 or P< 0. 01), hepatic Nrf2 and HO-1 protein expression, SOD activity, the and Bcl-2/ Bax ratio were increased significantly (P< 0. 05 or P< 0. 01), and liver histopathological changes had effectively improved. Conclusions Four weeks of resveratrol treatment alleviates exercise-induced liver injury in rats, and the mechanism of its protective effect might be related to activation of the Nrf2 signaling pathway, which relieved oxidative stress in the liver, thereby antagonizing excessive occurrence of apoptosis induced by oxidative stress.