Abstract: Objective:To investigate the change of endurance training on mitophagy and its mechanism in alcohol-induced acute hepatic injury rats.Methods:It analyzed the expressions of BNIP3, NIX and HIF-1α mRNA and content of HIF-1α protein, mitochondrial reactive oxygen species production, content of mitochondrial MDA, activity of aconitase, and mitochondrial potential in liver tissue and ALT and AST in serum in alcohol-induced acute hepatic injury rats after 12 week unload swimming training.Results:The acute alcohol treatment induces mitochondrial ROS production, increases mitochondrial MDA content, decreases aconitase activity and mitochondrial potential, up-regulates expressions of BNIP3, NIX and HIF-1α mRNA and content of HIF-1α protein in liver and increases ALT and AST in serum in alcohol-induced acute hepatic injury rats.The parameters of all above indicate the same change in alcohol-induced acute hepatic injury rats after endurance training but the extent is lower.When rats are injected YC-1 (inhibitor of HIF-1) , the expressions of BNIP3 and NIX mRNA are lower than that of no injection of YC-1 in trained and untrained rats, however, there is no change of the expression of HIF-1α mRNA but HIF-1α protein increases significantly.Conclusion:Acute alcohol treatment enhances mitophagy, which related to HIF-1 up-regulated expression, but endurance training can increase liver oxygen supply, and that decreases HIF-1expression, which results in the decrease of mitophagy in liver.