Effect of thyroid state on cardiac myosin P-light chain phosphorylation during exercise

Abstract

This study ascertained the effects of thyroid deficiency (TD) and hyperthyroidism (H) on in vivo cardiovascular functional capacity in the context of cardiac myosin light chain 2 phosphorylation [P-LC(P)], a proposed modulator of myocardial function, at rest and during exercise. Compared with normal controls (NC), Ca2(+)-regulated myofibril adenosinetriphosphatase was reduced by 39% in TD and increased by 9% in H rats. This response was associated with a 20-fold increase in the V3 isoform and an 11% increase in the V1 isoform in TD and H rats, respectively. Submaximal treadmill exercise elicited significant elevations in all myocardial functional indexes examined in H rats compared with the NC group, whereas the opposite occurred for the TD group. Despite the marked contrast in cardiac function among the three groups, intrinsic levels of P-LC(P) were similar at rest among the groups and were significantly reduced in both TD and H groups relative to controls during exercise. These data suggest that although thyroid state exerts a profound impact on intrinsic myocardial functional state, it exerts little control over cellular processes regulating P-LC(P) during rest and exercise.