LEFT-VENTRICULAR FUNCTIONAL-CAPACITY IN THE ENDURANCE-TRAINED RODENT

Cardiac myosin P-light chain phosphorylation [P-LC(P)] has been proposed to augment myocardial force production. This study was undertaken to examine the potential for cardiac myosin P-LC(P) for both equivalent heart rate and work load in exercising endurance-trained and nontrained rodents. A 10-wk training protocol elicited a significant reduction in submaximal running O2 uptake while enhancing peak O2 uptake (-17 and 10%, respectively, P < 0.05). Left ventricular functional index during submaximal exercise, obtained with a high-fidelity Millar ultraminiature pressure transducer, indicated that the trained animals were able to maintain peak left ventricular pressure (LVP) in comparison to their sedentary counterparts, even though both heart rate and rate of LVP development were significantly reduced (P < 0.05). When expressed on the basis of equivalent submaximal heart rate, peak LVP was augmented in the trained animals. Cardiac myosin P-LC(P) was examined under two conditions known to produce disparate responses in trained vs. sedentary animals. For an equivalent work load, we observed parallel increases in P-LC(P) (20%) and systolic pressure (17%) in both groups, even though the trained animals exhibited significantly lower heart rates (P < 0.05). For an equivalent heart rate, training evoked a significant increase in systolic pressure (26%, P < 0.05) and caused a slight increase in P-LC(P) relative to the nontrained controls. Cardiac myosin adenosinetriphosphatase was reduced ~10% in the trained animals (P < 0.05), commensurate with a 2.0-fold increase in the V3 (low adenosinetriphosphatase) isomyosin. Collectively these findings suggest that although the potential for cardiac energy turnover is reduced in the trained rodent during exercise, as reflected in cardiac adaptations at both the organ and the subcellular level, normal levels of ventricular force output are maintained at any given submaximal work load.