<p>Exercise has a positive effect on various cardiovascular diseases. However, it is not uncommon to experience arrhythmia events during or after exercising. To determine how to maximize the benefits of exercise while ensuring safety. We conducted a study involving 40 adult male Sprague-Dawley rats. These rats underwent exercise of different intensities for 8 weeks. We recorded electrophysiological stimulation to track the occurrence and duration of atrial fibrillation and other electrophysiological data. Additionally, we analyzed and observed the histology of cardiomyocytes. The results revealed a relationship between exercise intensity and the incidence of atrial fibrillation and myocardial lipid deposition. As exercise intensity increased, there was an increase in myocardial fibrosis, mitochondrial activity, and autophagy and a decrease in reactive oxygen species. The expression of Na/Ca Exchanger (NCX1) and Kv1.5 proteins in rat atrial cardiomyocytes exhibited varying degrees of change. The increase in myocardial lipid level after exercise is thought to significantly affect myocardial fibrosis, which may be related to the upregulation of peroxisome proliferator-activated receptor-gamma coactivator 1 alpha expression. Sustained and moderate-intensity exercise is more suitable for improving myocardial metabolic energy supply and treating atrial arrhythmias.</p>