Post-Myocardial Infarction and Exercise Training on Myosin Heavy Chain and Cardiac Function

Abstract

Myosin heavy chain (MyHC) acts as the chemical-mechanical transducer of motion in muscle fibers by converting energy from ATP into the sliding myofilaments. The isoform α-MyHC has about three-fold higher ATPase activity than the isoform β-MyHC. In the failing heart, however, α-MyHC expression is profoundly downregulated and β-MyHC is reciprocally upregulated. The shift of MyHC isoforms contributes to the development of myocardial systolic dysfunction and cardiomyopathy. Although this can be attributed to a multitude of factors, well-documented findings illustrate the shift as an adaptive response to chronic overload conditions resulting from the MI itself. Endurance training has been well documented as a leading technique to attenuate unfavorable post-MI cardiac dysfunction. Endurance training studies consisting of aerobic-style exercises prompts beneficial effects on cardiac function by attenuating myocardial MyHC remodeling following MI and congestive heart failure. However, endurance training promotes eccentric cardiac hypertrophy characterized by the addition of sarcomeres in series, elongation of the myocyte cell, and a consequential increase in cell size and chamber diameter, which may worsen the MI-induced cardiac dilation. In contrast, resistance training stimulates pressure-overload hemodynamic characteristics. Concentric cardiac hypertrophy is a unique resistance training adaptation characterized by cardiac wall thickening without cardiac chamber expansion. Whether resistance training also beneficially reverses MI-induced detrimental α-to β-MyHC shift and improves post-MI systolic function remains to be elucidated.