Exercise preconditioning-induced early and late phase of cardioprotection is associated with protein kinase C epsilon translocation.

BACKGROUND Exercise preconditioning (EP) can provide powerful protection to the heart. Evidence supports the contention that EP directly enhances myocardial tolerance to ischaemia through a protein kinase C (PKC)-mediated mechanism. However, studies investigating the role of isoform-specific PKC after EP are lacking. METHODS AND RESULTS In this study, a male Sprague-Dawley rat model of EP was established (4 periods of 30 m/min for 10 min exercise then a 10 min rest at 0% grade treadmill exercise). Rats were subjected to exhaustive exercise to induce myocardial injury. Chelerythrine (5 mg/kg) was injected before EP to investigate the role of PKC in EP. EP was found to attenuate exhaustive exercise-induced myocardial injury in both of EP's 2 protective phases, especially the latter phase. After EP, PKCε was markedly upregulated, and PKCε was translocated to myocardial intercalated disks, and p-PKCε(Ser729) was translocated to the myocardial cytomembrane. Even though PKCε was markedly upregulated and translocated to intercalated disks during exhaustive exercise, p-PKCε(Ser729) was mainly distributed in the cytoplasm. A chelerythrine injection before EP did not suppress the activation of PKC and the protection of EP. CONCLUSIONS These results indicate that PKCε plays an important role in EP-mediated protection of the myocardium during exhaustive exercise-induced myocardial injury, and that a chelerythrine injection during exercise is not suitable for demonstrating the role of PKCε.