Left ventricular functional capacity in the endurance-trained rodent

• Published in: Journal of applied physiology (1985) Vol. 69; no. 1; p. 305
• Main Authors: Fitzsimons, D P, Bodell, P W, Herrick, R E, Baldwin, K M
• Format: Journal Article
• Language: English
• Published: United States 01.07.1990
• Subjects: Adaptation, Physiological; Animals; Blood Pressure - physiology; Calcium - metabolism; Female; Heart - physiology; Heart Rate - physiology; Myocardial Contraction - physiology; Myosins - metabolism; Oxygen Consumption; Phosphorylation; Physical Conditioning, Animal; Physical Endurance - physiology; Rats; Rats, Inbred Strains
• ISSN: 8750-7587
• DOI: 10.1152/jappl.1990.69.1.305

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 less than 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 less than 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 less than 0.05). For an equivalent heart rate, training evoked a significant increase in systolic pressure (26%, P less than 0.05) and caused a slight increase in P-LC(P) relative to the nontrained controls. Cardiac myosin adenosinetriphosphatase was reduced approximately 10% in the trained animals (P less than 0.05), commensurate with a 2.0-fold increase in the V3 (low adenosinetriphosphatase) isomyosin.