ENHANCING CARDIAC RECOVERY: THE ROLE OF HIF-1 IN MITOCHONDRIAL AUTOPHAGY AND THE THERAPEUTIC EFFECTS OF THYROXINE ON MYOCARDIAL ISCHEMIA-REPERFUSION INJURY IN ATHLETES

Abstract

Objective: This study investigates the role of Hypoxia-Inducible Factor 1 (HIF-1) in regulating mitochondrial autophagy and assesses the therapeutic effects of thyroxine on mitigating myocardial ischemia-reperfusion injury, focusing on its application in athletes who may experience such cardiac events due to intense physical exertion. Methods: We examined the activation of HIF-1 and its regulatory effects on mitochondrial autophagy in a controlled experimental model of myocardial ischemia-reperfusion injury. Athletes subjected to simulated high-intensity training were treated with thyroxine post-injury to evaluate its protective effects on cardiac function. Results: Preliminary data indicate that activation of HIF-1 enhances mitochondrial autophagy, thereby reducing cellular damage in ischemic cardiac tissue. Thyroxine treatment was found to significantly improve recovery outcomes, enhancing myocardial function and reducing infarct size. These benefits suggest a critical role for HIF-1 in the cellular response to ischemic stress and highlight the potential of thyroxine as a therapeutic agent in the sports setting. Conclusion: The study underscores the importance of HIF-1 in mitochondrial health during ischemic events and supports the use of thyroxine to enhance cardiac recovery in athletes. By improving understanding of these molecular mechanisms, we can better design targeted interventions to protect athlete heart health under extreme physical stress, contributing to safer training practices and enhanced performance sustainability.