Exercise Training Normalizes Sympathetic Outflow by Central Antioxidant Mechanisms in Rabbits With Pacing-Induced Chronic Heart Failure

Abstract

Background— In a recent study, we demonstrated that an increase in oxidative stress in the rostral ventrolateral medulla plays a critical role in the sympathoexcitation observed in chronic heart failure (CHF). Growing evidence indicates that exercise training evokes an antioxidative effect in CHF. In the present study, we therefore hypothesized that long-term exercise exerts its beneficial effect on autonomic activity in CHF via central antioxidative mechanisms. Methods and Results— Experiments were performed on New Zealand White rabbits. All rabbits were instrumented to measure mean arterial pressure, heart rate, and renal sympathetic nerve activity and to test baroreflex sensitivity. Exercise training significantly decreased baseline renal sympathetic nerve activity (65.8±5.2% to 41.3±3.9% of Max [where “Max” is the maximum renal sympathetic nerve activity induced by a 50-mL puff of smoke directed to the external nares of the rabbit], P P P P phox protein expression (1.9±0.2 to 1.2±0.1 [ratio of gp91 ^phox to tubulin], P 10 particles of adenovirus, 53.2±4.4% of Max; and 10 ¹¹ particles of adenovirus, 33.7±3.5% of Max; P Conclusions— These results suggest that an upregulation in central antioxidative mechanisms and suppressed central prooxidant mechanisms may contribute to the exercise training–induced beneficial effects on autonomic activity in CHF.