Acute aerobic exercise regulation of myocardial calcium homeostasis involves CASQ1, CASQ2, and TRDN

Abstract

Exercise maintains cardiac calcium homeostasis and promotes cardiovascular health. This study explored temporal changes of calcium - related myocardial transcriptome changes during the recovery phase following a single bout of moderate-intensity aerobic exercise. Healthy male Sprague-Dawley rats were sacrificed (anesthetized with sodium pentobarbital) after moderate-intensity aerobic exercise at four time points (0, 12, 24 and 72h post-exercise). The hearts were removed and RNA-seq and bioinformatics analyses were used to examine temporal transcriptional changes in the myocardium. Casq1, Casq2 and Trdn were identified as key genes in the regulation of calcium homeostasis during myocardial recovery. The highest expression of Casq1, Casq2 and Trdn genes and proteins occurred 24h after exercise. An in vitro calcium overload heart model using the Langendorff heart perfusion method was used to examine myocardial calcium buffering capacity. Calcium overload caused the least changes in left ventricular developed pressure, infarct area, LDH release, and extent of morphological damage to myocardial cells, with the highest protein expressions of Casq1, Casq2 and Trdn at 24h after acute exercise. This study indicates that maximal myocardial Ca2+ buffering capacity occurs 24h post-exercise in rats. Our study provides insights for exercise-mediated improvements in cardiovascular function and exercise preconditioning.