Abstract 19023: Aerobic Exercise Training-induced Increase in Circulating Irisin Level is Associated With Reduced Arterial Stiffness in Obesity

Introduction: Aerobic exercise training reduces arterial stiffness mediated by nitric oxide (NO)-derived vasodilation in obese patients. Irisin is mainly expressed in myocytes and promotes NO release by regulating endothelial NO synthase (eNOS) expression, leading to vasodilation. Although exercise accelerates irisin secretion, the involvement of irisin in the mechanism of exercise effect on arterial stiffness in obese patients remains unclear.

Purpose: This study aimed to clarify whether aerobic exercise training-induced elevation of irisin secretion is associated with reduced arterial stiffness with elevation of NO production in obesity.

Methods: Human study; 15 obese subjects (% body fat: men≧25%, women≧35%) completed 8-week of aerobic exercise training (60-70% peak oxygen uptake [VO2peak] for 45 min, 3 days/week). Animal study; 20-week-old male obese (OLETF) rats were randomly divided into two groups; 8-week sedentary control and aerobic exercise training (treadmill running for 60min at 25m/min, 5days/week).

Results: In the obese human study, carotid-femoral pulse wave velocity (cfPWV) was significantly decreased and circulating levels of nitrite/nitrate (NOx) and irisin were significantly elevated after the exercise intervention (each P<0.05). The training-induced changes in circulating irisin level was positively correlated with circulating NOx levels (r=0.732, P<0.05) and was negatively correlated with cfPWV (r=-0.516, P<0.05). Additionally, in the obese rat study, lower cfPWV and increased aortic eNOS and Akt phosphorylation and concomitantly muscle FNDC5 protein expression, circulating irisin level were significantly increased in exercised obese rats as compared to obese control rats. Moreover, circulating irisin level was positively correlated with aortic eNOS phosphorylation (r=0.756, P<0.05).

Conclusions: These results suggest that aerobic exercise training-induced acceleration of irisin secretion may be involved in the reduced arterial stiffness in obesity. Moreover, as its underlying molecular mechanism, irisin release via increased muscle FNDC5 expression may be involved in activation of aortic eNOS signaling, leading to reduction of arterial stiffness.