Late Exercise Preconditioning Promotes Autophagy against Exhaustive Exercise-Induced Myocardial Injury through the Activation of the AMPK-mTOR-ULK1 Pathway

Figure 1

LEP initiated myocardial protection alleviated exhaustive exercise-induced myocardial injury and was partially attenuated by autophagy inhibitor. (a) The changes of myocardial ischemia-hypoxia detected by HBFP staining (×400), bar = 20 μm. Nonischemic myocardial cell showed the light brown color. The ischemic tissue stained a bright crimson red color. The C, LEP, and W+LEP groups displayed a light brown color. Ischemic cardiomyocytes in the EE group stained crimson red. The LEP+EE and W+LEP+EE groups showed red patchy stain. (b) Quantitative analysis of HBFP staining. The EE group compared with the C group, the LEP+EE group compared with the EE group, and the W+LEP+EE group compared with the LEP+EE group were remarkably different. (c) The myocardial ultrastructural changes in six different conditions were observed by TEM (×3,000), bar = 1.0 μm. Exhaustive exercise led to myofibrils breaks (symbol “”), wide interfibrillar space (symbol “”), and vacuolate mitochondria (symbol “”). LEP had normal ultrastructure, but the heterochromatin was slightly marginalized (symbol “”). LEP attenuated exhaustive exercise-induced injury in the LEP + EE group. However, wortmannin alleviated the protective effect of LEP. vs. C, vs. EE, vs. LEP+EE.

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