Short-Term Exercise Does Not Increase ER Stress Protein Expression in Cardiac Muscle

Abstract

Both short-term (three to five consecutive days) and long-term (weeks to months) endurance exercise training provides cardioprotection against ischemia-reperfusion (IR)-induced injury. However, the mechanisms responsible for exercise-induced cardioprotection are not well understood. Emerging evidence indicates that endoplasmic reticulum (ER) damage contributes to IR-induced myocardial injury. It follows that exercise-induced expression of ER stress proteins could serve as the mediators of exercise-induced cardioprotection against IR injury. Hence, these experiments tested the hypothesis that exercise training is associated with an increase in ER stress proteins in the heart. Adult male Sprague-Dawley rats (N=13) were habituated to treadmill running for 5 d, followed by five 60-min exercise bouts (approximately 70% of VO2max) on consecutive days. Infarct area resulting from IR was determined by a standard histological (triphenyltetrazolium chloride (TTC)) method. Cardiac levels of ER stress proteins Grp78, Grp94, and calreticulin were analyzed via Western blot. Moreover, we determined myocardial levels of heat shock protein 72 (HSP72) along with ER proteins associated with cellular injury, including CHOP, caspase 12, Puma, Noxa, and ATF3. Our exercise protocol resulted in cardioprotection as evidenced by reduced infarct size (P<0.05) and increased myocardial HSP72 levels (+227%; P<0.01) in the exercise-trained animals. Nonetheless, exercise training did not increase (P>0.05) cardiac levels of the ER stress proteins, Grp78, Grp94, and calreticulin. Moreover, exercise did not alter myocardial levels of CHOP, caspase 12, Puma, Noxa, or ATF3. These data reveal that short-term exercise training does not elevate ER stress proteins in the heart. Hence, the cardioprotective effect of short-term exercise training does not seem to be linked to ER stress adaptation.