Wei Zhan, Ahmad Mujahid, Chen Rongzhi, Fatima Sana, Shah Shahab
International College of Football, Tongji University, China.
Department of Kinesiology, Henan University, Kaifeng, China.
Int J Cardiol Heart Vasc. 2025 Jul 25;60:101756. doi: 10.1016/j.ijcha.2025.101756. eCollection 2025 Oct.
Ischemic heart disease remains a leading cause of global mortality and morbidity, underscoring the urgent need for effective therapies particularly for patients recovering from ischemic cardiac events. High-intensity interval training (HIIT) has emerged as a promising non-pharmacological intervention with substantial cardioprotective potential. Both clinical studies and animal models demonstrate that HIIT attenuates cardiac damage induced by ischemia-reperfusion injury. However, the precise cellular and molecular mechanisms underlying these benefits remain incompletely elucidated. Mitochondria play a pivotal yet dual role in ischemia-reperfusion injury, serving as central regulators of both cell survival and death pathways. Although HIIT is recognized to modulate mitochondrial function, its specific impact on cardiac susceptibility to ischemic injury requires further clarification. This review synthesizes current evidence on the beneficial effects of HIIT on cardiac mitochondrial function, with a focus on the mechanisms through which it confers cardioprotection. We examine how HIIT may enhance mitochondrial resilience by activating critical signaling pathways that mitigate ischemia-reperfusion injury. Despite significant advances, key knowledge gaps persist. This review emphasizes the necessity of further research to fully unravel HIIT's cardioprotective potential and its role in promoting mitochondrial adaptation under ischemic stress.
缺血性心脏病仍然是全球死亡率和发病率的主要原因，这凸显了对有效治疗方法的迫切需求，特别是对于从缺血性心脏事件中恢复的患者。高强度间歇训练（HIIT）已成为一种有前景的非药物干预措施，具有巨大的心脏保护潜力。临床研究和动物模型均表明，HIIT可减轻缺血再灌注损伤所致的心脏损伤。然而，这些益处背后确切的细胞和分子机制仍未完全阐明。线粒体在缺血再灌注损伤中起关键的双重作用，是细胞存活和死亡途径的核心调节因子。尽管HIIT被认为可调节线粒体功能，但其对心脏缺血损伤易感性的具体影响仍需进一步阐明。本综述综合了关于HIIT对心脏线粒体功能有益作用的现有证据，重点关注其赋予心脏保护作用的机制。我们研究了HIIT如何通过激活减轻缺血再灌注损伤的关键信号通路来增强线粒体弹性。尽管取得了重大进展，但关键的知识空白仍然存在。本综述强调了进一步研究的必要性，以全面揭示HIIT的心脏保护潜力及其在缺血应激下促进线粒体适应中的作用。
