Acute exercise can improve cardioprotection without increasing heat shock protein content

The aim of this study was to determine the effects of acute bouts of exerci se on myocardial recovery after ischemia and heat shock protein expression. Adult female Sprague-Dawley rats were divided into five groups: 1) 1-day r un (1DR; n = 6) and 2) 3-day run (3DR; n = 7), in which rats ran for 100 mi n at a speed of 20 m/min up a 6 degrees grade for 1 or 3 consecutive days; 3) 1-day cold run (1CR), in which rats ran the same as 1DR but with wet fur at 8 degrees C, which prevented an elevation of core temperature(n = 8); 4 ) heat shock sedentary (HS), in which rats had their core temperatures rais ed to 42 degrees C one time for 15 min (n = 5); and 5) sedentary control (n =15). Cardiac function was analyzed 24 h after the last treatment using an isolated, working heart model. Nonpaced hearts were initially perfused unde r normoxic conditions, then underwent; 17 min of global, normothermic (37 d egrees C) ischemia, and, finally, were allowed to recover for 30 min under normoxic conditions. The concentration of the 72-kDa heat shock protein (HS P 72) was measured in each left ventricle. Compared with that in the sedent ary group, recovery of cardiac output x systolic pressure (CO x SP) was enh anced (P < 0.05) in all treatment groups when the postischemic value was co varied with the preischemic value. No differences in CO x SP were found (P > 0.05) between the following groups: 1DR vs. 3DR, 1DR vs. HS, and 1DR vs. ICR. Heat shock protein concentration was significantly greater (P < 0.05) than that in the sedentary controls in HS, 1DR, and 3DR groups, but not for ICR. The concentration of HSP 72 was not significantly correlated with pos tischemic CO x SP (R-2 = 0.197, P > 0.05). We conclude that acute bouts of exercise can produce cardioprotective effects without an elevation of HSP 7 2.