Non-conventional long-lasting cardioprotection induced by chronic exposure to ambient heat

Heat acclimation produces concerted favorable adaptations in the mechanical and metabolic performance of the heart. Under normoxic condition this is displayed primarily by greater pressure generation with lower oxygen consumption. Altered expression of calcium regulatory proteins, EC coupling proteins and redistribution of the myosin isoenzyme to predominancy of the V3 isoform contribute to the changes observed. An important acclimatory response is the finding that heat acclimation confers protection against ischemic/reperfusion insults. This is due to numerous factors among which greater constitutive HSP 72 kDA (Delta200 reserves and energy sparing mechanisms such as redistribution of ATPase isoforms and altered glycolytic flux leading to better intracellular pH concomitantly with continuous ATP production, are likely candidates. Collectively, our data indicate that both transcriptional and post-transcriptional processes are involved and underline the integrative response.