Objective To explore the effect of aerobic exercise on endothelial dysfunction in obese rats and determine its mechanism of action. Methods An obese rat model was established by feeding with a high-fat diet for 8 weeks, then the rats were divided into three groups: the normal group, model group, and aerobic exercise group. The exercise protocol consisted of 8 weeks of medium-intensity aerobic exercise, six times per week. Body weight, body length, visceral weight, and visceral fat weight were measured, and Lee’ s index and the liposome ratio were calculated. Blood lipids were detected using a biochemical analyzer. The levels of serum thrombomodulin (TM) and visfatin were detected using an ELISA kit. Visfatin mRNA expression in epicardial adipose tissue was detected by an RT-PCR assay. Pathological changes in aorta morphology and structure were compared using the hematoxylin-eosin staining method. Results Compared with the normal group, the body weight, body length, Lee’ s index, visceral weight, visceral fat weight, liposome ratio, and the levels of TG, TC, LDL, TM, and visfatin in the model group were significantly increased (P< 0.05), the level of HDL was significantly decreased ( P< 0.01), and the expression of visfatin mRNA in epicardial adipose tissue was significantly upregulated (P< 0.01). Compared with the model group, body weight, Lee’s index, liver weight, perrenal fat weight, and the levels of TG, TC, LDL, TM, and visfatin in the aerobic exercise group were significantly decreased (P< 0.05), the level of HDL was significantly increased (P< 0.01), and the expression of visfatin mRNA in the epicardial adipose tissue was significantly downregulated (P< 0.05). Conclusions Aerobic exercise can reduce fat accumulation in obese rats, improve fat metabolism, downregulate the expression of visfatin in epicardial adipose tissue, inhibit visfatin secretion, and reduce pathological damage of the aorta to delay the process of endothelial dysfunction.