Exercise Preconditioning Induces Cellular Autophagy by Intermittent Ischemia-Hypoxia to Participate in Early Myocardial Protection

Objective: By analyzing the relationships between myocardial ischemia-hypoxia and cellular autophagy in exercise, and by detecting changes of autophagy-associated proteins Beclin1/Bcl-2 in early exercise preconditioning (EEP) and in early protective phase, the effects of cellular autophagy on EEP-cardioprotection were discussed. Methods: SD rats were randomly divided into the groups of control (C group) , early exercise preconditioning (EEP group) , exhaustive exercise (EE group) , and early exercise preconditioning+exhaustive exercise (EEP+EE group) . 1) The plasma cTnI contents were detected by chemiluminescence immunoassay (CLIA) method, which were combined with the adjacent slices between HE-staining and HBFP-staining, to comprehensively assess the extents of myocardial ischemia-hypoxia, and to verify the EEP-cardioprotection. 2) The expressional changes and the dissociated degrees in Beclin1/Bcl-2 were detected by immune-blotting, and were observed by double-labeling immunofluorescence, respectively. 3) The relationships between exercise-induced hypoxia-ischemia and cellular autophagy were assessed by the correlational analysis. Results: 1) Compared with the C group, the plasma cTnI levels and the MOD values in the EEP group to both have increasing tendencies (P>0.05) , and these in the EE group and in the EEP+EE group to were both significant increase (P<0.05) . Compared with the EE group, the plasma cTnI levels and the MOD values in the EEP group to were both significant decrease (P<0.05) . Compared with the C group, all other groups to represent ischemia-hypoxia changes in different degree, which were as the acidophilyenhanced positions in HE-staining approaching to the positive areas of crimson in HBFP-staining. 2) Compared with the C group, all other groups to have significantly increased Beclin1 levels (P<0.05) , and to have increased extents of Beclin1/Bcl-2 dissociations (P<0.05) , but which were without any changes in Bcl-2 levels. Compared with the EE group, the extents of Beclin1/Bcl-2 co-localization were significant increase (P<0.05) . All groups represented with significantly negative correlations between the Beclin1/Bcl-2 co-localization and the ischemia-hypoxia areas, and the IOD values respectively. Conclusion: EP can induces autophagy in cardiomyocytes by intermittent ischemiahypoxia, in which the cellular autophagy participates in the early myocardial protection against the exercise-induced myocardial injury.