Exercise has been reported to induce autophagy. We hypothesized that exercise preconditioning (EP)-related autophagy in cardiomyocytes could be attributed to intermittent ischemia-hypoxia, allowing the heart to be protected for subsequent high-intensity exercise (HE). We applied approaches, chromotrope-2R brilliant green (C-2R BG) staining and plasma cTnI levels measuring, to characterize two periods of cardioprotection after EP: early EP (EEP) and late EP (LEP). Further addressing the relationship between ischemia-hypoxia and autophagy, key proteins, Beclin1, LC3, Cathepsin D, and p62, were determined by immunohistochemical staining, western blotting, and by their adjacent slices with C-2R BG. Results indicated that exercise-induced ischemia-hypoxia is a key factor in Beclin1-dependent autophagy. High-intensity exercise was associated with the impairment of autophagy due to high levels of LC3II and unchanged levels of p62, intermittent ischemia-hypoxia by EP itself plays a key role in autophagy, which resulted in more favorable cellular effects during EEP-cardioprotection compared to LEP.

中文翻译：

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运动预适应过程中自噬相关蛋白表达水平的改变表明自噬参与了针对运动引起的心肌损伤的心脏保护作用。

据报道，运动会引起自噬。我们假设心肌细胞中与运动预适应（EP）相关的自噬可能归因于间歇性缺血缺氧，从而可以保护心脏免受随后的高强度运动（HE）的影响。我们应用了方法，嗜铬2R艳绿（C-2R BG）染色和血浆cTnI水平测量，来表征EP后的两个心脏保护阶段：早期EP（EEP）和晚期EP（LEP）。为了进一步解决缺血缺氧与自噬之间的关系，通过免疫组织化学染色，western印迹法以及邻近的带有C-2R BG的切片来确定关键蛋白Beclin1，LC3，组织蛋白酶D和p62。结果表明，运动引起的缺血缺氧是Beclin1依赖自噬的关键因素。