AHEART Mar. 45/3

Taylor, Ryan P., M. Brennan Harris, and Joseph W. Starnes. Acute exercise can improve cardioprotection without increasing heat shock protein content. Am. J. Physiol. 276 (Heart Circ. Physiol. 45): H1098–H1102, 1999.—The aim of this study was to determine the effects of acute bouts of exercise on myocardial recovery after ischemia and heat shock protein expression. Adult female Sprague-Dawley rats were divided into five groups: 1) 1-day run (1DR; n 5 6) and 2) 3-day run (3DR; n 5 7), in which rats ran for 100 min at a speed of 20 m/min up a 6° 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°C, which prevented an elevation of core temperature (n 5 8); 4) heat shock sedentary (HS), in which rats had their core temperatures raised to 42°C one time for 15 min (n 5 5); and 5) sedentary control (n515). Cardiac function was analyzed 24 h after the last treatment using an isolated, working heart model. Nonpaced hearts were initially perfused under normoxic conditions, then underwent 17 min of global, normothermic (37°C) ischemia, and, finally, were allowed to recover for 30 min under normoxic conditions. The concentration of the 72-kDa heat shock protein (HSP 72) was measured in each left ventricle. Compared with that in the sedentary group, recovery of cardiac output 3 systolic pressure (CO 3 SP) was enhanced (P , 0.05) in all treatment groups when the postischemic value was covaried with the preischemic value. No differences in CO 3 SP were found (P . 0.05) between the following groups: 1DR vs. 3DR, 1DR vs. HS, and 1DR vs. 1CR. 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 1CR. The concentration of HSP 72 was not significantly correlated with postischemic CO 3 SP (R2 5 0.197, P . 0.05). We conclude that acute bouts of exercise can produce cardioprotective effects without an elevation of HSP 72.