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However, how mitophagy participates in exercise preconditioning\u2010 (EP\u2010) induced cardioprotection remains unclear. EEP may involve mitochondrial protection, which presumably crosstalks with predominant H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> oxidative stress. Our EEP protocol involves four periods of 10\u2009min running with 10\u2009min recovery intervals. We added a period of exhaustive running and a pretreatment using phosphoinositide 3\u2010kinase (PI3K)\/autophagy inhibitor wortmannin to test this protective effect. By using transmission electron microscopy (TEM), laser scanning confocal microscopy, and other molecular biotechnology methods, we detected related markers and specifically analyzed the relationship between mitophagic proteins and mitochondrial translocation. We determined that exhaustive exercise associated with various elevated injuries targeted the myocardium, oxidative stress, hypoxia\u2010ischemia, and mitochondrial ultrastructure. However, exhaustion induced limited mitochondrial protection through a H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>\u2010independent manner to inhibit voltage\u2010dependent anion channel isoform 1 (VDAC1) instead of mitophagy. EEP was apparently safe to the heart. In EEP\u2010induced cardioprotection, EEP provided suppression to exhaustive exercise (EE) injuries by translocating Bnip3 to the mitochondria by recruiting the autophagosome protein LC3 to induce mitophagy, which is potentially triggered by H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and influenced by Beclin1\u2010dependent autophagy. Pretreatment with the wortmannin further attenuated these effects induced by EEP and resulted in the expression of proapoptotic phenotypes such as oxidative injury, elevated Beclin1\/Bcl\u20102 ratio, cytochrome c leakage, mitochondrial dynamin\u20101\u2010like protein (Drp\u20101) expression, and VDAC1 dephosphorylation. These observations suggest that H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> generation regulates mitochondrial protection in EEP\u2010induced cardioprotection.<\/jats:p>","DOI":"10.1155\/2018\/1916841","type":"journal-article","created":{"date-parts":[[2018,7,25]],"date-time":"2018-07-25T23:30:33Z","timestamp":1532561433000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["H<sub>2<\/sub>O<sub>2<\/sub> Signaling\u2010Triggered PI3K Mediates Mitochondrial Protection to Participate in Early Cardioprotection by Exercise 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