Heat acclimation improves mitochondrial function following ischemia reperfusion insult

Heat acclimation (AC) is an evolutionary conserved feature allowing organisms to adjust to prolonged/persistent changes in ambient temperature. An inseparable outcome of acclimation is the protection from novel stressors e.g. ischemia reperfusion (I/R) insult. In this study we evaluated the intrinsic apoptotic pathway and mitochondrial metabolic state of AC versus non‐acclimated rats (C) hearts. We here report that AC attenuates the death signaling pathway invoked in response to acute heat stress or I/R via increased Bcl Xl /Bad ratio, thereby abolishing cytochrome c trafficking to the cytosol. This mechanism led to an almost 3 fold reduction in apoptosis level in the AC heart. The beneficial effect of AC was also reflected in mitochondrial metabolic performance. In contrast to C hearts that demonstrated a drop in ATP production post I/R, AC hearts maintained intact mitochondrial membrane potential, respiratory chain enzyme‐complex activities and unimpaired ATP production. Concomitantly we observed upregulation of the mitochondria biogenesis gene marker PGC‐1α transcript, indicative of the beneficial AC effect on mitochondrial performance. We conclude that AC enhances mitochondrial metabolic function and cytoprotection.