Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.
Cardiol Res Pract. 2011 Mar 6;2011:972807. doi: 10.4061/2011/972807.
Physical inactivity is increasingly recognized as modifiable behavioral risk factor for cardiovascular diseases. A partial list of proposed mechanisms for exercise-induced cardioprotection include induction of heat shock proteins, increase in cardiac antioxidant capacity, expression of endoplasmic reticulum stress proteins, anatomical and physiological changes in the coronary arteries, changes in nitric oxide production, adaptational changes in cardiac mitochondria, increased autophagy, and improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels. It is currently unclear which of these protective mechanisms are essential for exercise-induced cardioprotection. However, most investigations focus on sarcolemmal KATP channels, NO production, and mitochondrial changes although it is very likely that other mechanisms may also exist. This paper discusses current information about these aforementioned topics and does not consider potentially important adaptations within blood or the autonomic nervous system. A better understanding of the molecular basis of exercise-induced cardioprotection will help to develop better therapeutic strategies.
身体活动不足日益被认为是心血管疾病可改变的行为风险因素。运动诱导的心脏保护作用的部分提出的机制包括热休克蛋白的诱导、心脏抗氧化能力的增加、内质网应激蛋白的表达、冠状动脉的解剖和生理变化、一氧化氮生成的变化、心脏线粒体的适应性变化、自噬增加以及肌浆网和/或线粒体三磷酸腺苷敏感性钾通道功能的改善。目前尚不清楚这些保护机制中哪些对于运动诱导的心脏保护是必需的。然而，尽管很可能还存在其他机制，但大多数研究都集中在肌浆网 KATP 通道、NO 生成和线粒体变化上。本文讨论了关于这些上述主题的当前信息，并不考虑血液或自主神经系统内可能重要的适应性变化。更好地了解运动诱导的心脏保护的分子基础将有助于开发更好的治疗策略。
