| Abstract: | Myocardial contractility is reduced in rats following strenuous activity. Thus, the purpose of this study was to determine some of the cellular mechanisms that may contribute to the depressed contractile function. Myofibril ATPase activity was determined with varying free calcium and monomeric vanadate (Vi) concentrations. The Mg2+ stimulated myofibril ATPase activities were significantly reduced in the activity group (E). Myofibril ATPase activity from control animals increased from 0.056 +/- 0.021 to 0.216 +/- 0.030 mumol X Pi X mg-1 X min-1 with 0.1-10.0 microM Ca2+. The addition of 15.0 microM Vi resulted in a 37% decrease in ATPase activity of C animals. With regard to the experimental group, the myofibril ATPase activity at 0.1 and 1.0 microM Ca2+ were depressed (P less than 0.05) with the values at 5.0 and 10.0 microM Ca2+ being similar to the control group (P greater than 0.05). Incubations with Vi resulted in an enhanced myofibril ATPase activity for E compared to C animals. The ATPase activities were increased by 17, 10, 10 and 15% at 3.0, 5.0, 10.0 and 15.0 microM Vi. The results suggest that the exhaustive exercise raises the CA2+ requirement for half-maximal activation of cardiac myofibril ATPase activity and that the contracto-regulatory mechanism of cardiac muscle is similarly altered. |
