Altered expression levels of autophagy-associated proteins during exercise preconditioning indicate the involvement of autophagy in cardioprotection against exercise-induced myocardial injury

Jian-Qi Yuan,Ke Cai,Yang Yuan,Shan-Shan Pan

doi:10.1186/s12576-020-00738-1

Jian-Qi Yuan, Ke Cai + Show 2 more

Open Access

https://doi.org/10.1186/s12576-020-00738-1

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Abstract

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.

Highlights

Strategies that encourage endogenous cardiac adaptations have increasingly been used as non-pharmacological therapies to mitigate the risks of cardiovascular events
Exercise preconditioning reduced myocardial ischemia– hypoxia injury from high‐intensity exercise Changes in plasma cardiac troponin I (cTnI) levels reflect the degree of myocardial injury (Fig. 1a)
The normal cardiomyocytes were green in C-2R Chromotrope-2R brilliant green staining (BG) staining, while the ischemia–hypoxia cardiomyocytes were stained red. c Image analysis of chromotrope-2R brilliant green (C-2R BG) ischemia–hypoxia staining. *P < 0.05 vs. group C; #P < 0.05 vs. group high-intensity exercise (HE)

Summary

Introduction

Strategies that encourage endogenous cardiac adaptations have increasingly been used as non-pharmacological therapies to mitigate the risks of cardiovascular events. Known as cardiac preconditioning, involves vigorous exercise prior to ischemic events to prevent lethal myocardial injury [1,2,3,4]. Ischemic preconditioning (IP), known as intermittent ischemia/reperfusion (I/R), can result in cardioprotection in the myocardium, alleviating subsequent myocardial ischemia–hypoxia-like injury or. EP has been shown to induce an adaptive promotion that generates dualprotective windows similar to those generated during IP [8,9,10]. This EP-induced protection is associated with early exercise preconditioning (EEP), which occurs immediately after EP, and late exercise preconditioning (LEP), which occurs 12–24 h after EP [11]. There is not yet clear evidence of the relationship between exercise-induced ischemia–hypoxia and autophagy

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