Effect of aerobic exercise on the susceptibility of atrial fibrillation among aged mice.

BACKGROUND

Regular aerobic exercise has been shown to improve mitochondrial function and delay mitochondrial aging. Mitochondria play a crucial role in maintaining cardiac function and metabolism in myocardial cells. However, the effect of aerobic exercise on the incidence of atrial fibrillation (AF) is unclear. The aim of this study was to investigate the effects of aerobic exercise of different intensities on the susceptibility of aged mice to AF, and the relationship between altered mitochondrial structure and function and susceptibility to AF.

METHODS

Thirty-two 18-month-old C57BL/6N aged mice were selected and divided into low-, medium-, and high-speed aerobic exercise groups, and a no-exercise control group. Electrophysiological characteristics, susceptibility to AF, mitochondrial morphology and structure, mitochondrial membrane potential, adenosine triphosphate (ATP)ase activity, cytosolic calcium ion concentration, and mitochondrial function were assessed in each group of aged mice using the intracardiac catheterization technique, transmission electron microscopy, cellular flow technique, and Seahorse mitochondrial stress test.

RESULTS

A negative correlation was found between the success rate of AF induction/AF duration and the speed of exercise, such that the success rate of AF induction/AF duration was significantly lower in the high-speed group than the no-exercise group (P=0.01/P=0.02). Transmission electron microscopy revealed that the number and density of mitochondria in mouse atrial myocytes were positively correlated with exercise velocity. The basal oxygen consumption, mitochondrial energy supply, and maximum mitochondrial energy supply potential of atrial myocytes increased as exercise speed increased (P<0.001).

CONCLUSIONS

Both moderate- and vigorous-intensity aerobic exercise significantly reduced the susceptibility of the aged mice to develop AF while concurrently enhancing mitochondrial morphology and structural integrity, ultimately leading to improved mitochondrial bioenergetic function.