Exercise and calcium in the heart

Abstract

Cardiomyocyte Ca²⁺ dictates cardiac contraction via excitation–contraction coupling (ECC) and excitation–transcription coupling. Adaptation to these processes also majorly contributes to enhanced contractile function and capacity following exercise training. Cytoplasmic Ca²⁺ release controls sarcomeric contraction, with important modulation by the voltage-sensitive plasma membrane L-type Ca²⁺ channel and the Ryanodine receptor, as well as the sarcoplasmic reticulum Ca²⁺ ATPase. Exercise training increases and enhances these ECC subprocesses, in a manner that increases and enhances cardiac contraction. Also, adaptation to exercise training further includes myofilament Ca²⁺ sensitization. Then, there are several aspects linked to postexercise training cardiomyocyte Ca²⁺ handling that remains speculative and inconclusive, but could if proven true to be of special importance. This includes Ca²⁺-linked muscle-specific gene transcription to alter cell architecture and size, and it includes the scenario whereby Ca²⁺ cycling and adaptations may alter arrhythmogenicity. These aspects of cardiac Ca²⁺ adaptations to exercise training are discussed in this review article.