Short‐term exercise does not affect ER stress protein expression in cardiac muscle

Abstract

Cardiac muscle damage resulting from ischemia-reperfusion (IR) injury remains a major health problem around the world. We and others have shown that short-term exercise training provides protection against IR-induced cardiac injury. However, the mechanisms responsible for this protection are not well understood. Emerging evidence indicates that the endoplasmic reticulum (ER) stress is involved in IR-induced myocardial injury. Indeed IR-induced ER dysfunction can initiate cell death in the event of prolonged ER stress. Therefore, this study investigated the effect of short-term exercise training on ER stress protein levels in the heart. Adult male Sprague-Dawley rats (n=10) were habituated to treadmill running for 5 days, followed by three 60-minute exercise bouts (@~70% of VO2 max) on consecutive days. The trained animals, along with sedentary controls, were sacrificed 24 hours after the last exercise bout and the hearts were excised following a sham surgery. Cardiac levels of ER stress proteins Grp78, Grp94 along with the 72kDa Heat Shock Protein (HSP72) and PKR were analyzed via Western blot. Although our exercise protocol elevated myocardial HSP72 levels by 227% compared to controls (p<0.01), cardiac levels of Grp78, Grp94 and PKR were unaltered (p>0.05) by exercise. These data reveal that short-term exercise training does not elevate ER stress proteins in the heart. Hence the cardioprotective effect of exercise training does not appear to be linked to ER stress adaptation. Supported by NIH HL072789 (SKP)