Exercise preconditioning (EP) is a line of scientific inquiry into the short-term biochemical mediators of cardioprotection in the heart. This study examined the involvement of autophagy induced by energy metabolism in myocardial remodelling by EP and myocardial protection. A total of 120 healthy male Sprague Dawley (SD) rats were randomly divided into six groups. Plasma cTnI, HBFP staining and electrocardiographic indicators were examined in the context of myocardial ischemic/hypoxic injury and protection. Western blotting and fluorescence double labelling were used to investigate the relationship between energy metabolism and autophagy in EP-resistant myocardial injury caused by exhaustive exercise. Compared with those in the C group, the levels of myocardial ischemic/hypoxic injury were significantly increased in the EE group. Compared with those in the EE group, the levels of myocardial ischemic/hypoxic injury were significantly decreased in the EEP + EE and LEP + EE groups. Compared with that in the EE group, the level of GLUT4 in the sarcolemma was significantly increased, and the colocalization of GLUT4 with the sarcolemma was significantly increased in the EEP + EE and LEP + EE groups (P < 0.05). LC3-II and LC3-II/LC3-I levels of the EEP + EE group were significantly elevated compared with those in the EE group (P < 0.05). The levels of p62 were significantly decreased in the EEP + EE and LEP + EE groups compared with the EE group (P < 0.05). EP promotes GLUT4 translocation and induced autophagy to alleviate exhaustive exercise-induced myocardial ischemic/hypoxic injury.

运动预适应（EP）是对心脏心脏保护的短期生化介质的一系列科学探究。本研究探讨了能量代谢诱导的自噬在 EP 心肌重塑和心肌保护中的作用。120只健康雄性SD大鼠随机分为6组。在心肌缺血/缺氧损伤和保护的背景下检查血浆cTnI、HBFP染色和心电图指标。采用Western blotting和荧光双标技术探讨力竭运动引起的EP抵抗性心肌损伤中能量代谢与自噬的关系。与C组相比，EE组心肌缺血/缺氧损伤水平明显升高。与EE组相比，EEP+EE组和LEP+EE组心肌缺血/缺氧损伤水平明显降低。与 EE 组相比，EEP + EE 组和 LEP + EE 组肌膜 GLUT4 水平显着升高，且 GLUT4 与肌膜共定位显着升高（P  < 0.05）。EEP + EE 组 LC3-II 和 LC3-II/LC3-I 水平较 EE 组显着升高（P  < 0.05）。与 EE 组相比，EEP + EE 组和 LEP + EE 组 p62 水平显着降低（P  < 0.05）。EP 促进 GLUT4 易位并诱导自噬，以减轻力竭运动引起的心肌缺血/缺氧损伤。