Exercise training suppresses central command‐evoked sympathoexcitation in rats with heart failure

Abstract

Sympathoexcitation evoked by central command, a parallel activation of the locomotor and autonomic neural circuits in the brain, has been shown to become exaggerated in heart failure (HF). In the present study, we tested whether exercise training (ET) in HF normalizes central command‐evoked sympathoexcitation. HF was induced in rats > 6 wks after coronary artery ligation. A subset of the HF rats was treadmill trained (20 m/min, 5% grade, 60 min/day, 5 days/wk, 8–14 wks) (HF+ET). Central command was activated by fictive locomotion in decerebrate rats. Fictive locomotion induced by 30‐s electrical stimulation at 35 μA of the mesencephalic locomotor region evoked a larger (P<0.05) increase in renal sympathetic nerve activity in HF rats [269 ± 45 arbitrary unit (AU), fractional shortening (FS) = 20 ± 3%, N12] than that in HF+ET (121 ± 33 AU, FS = 20 ± 2%, N10) and sham (111 ± 37 AU, FS=46 ± 3%, N6) rats. The sympathoexcitation in the HF rats was significantly reduced by bilateral injection into the rostral ventrolateral medulla of Tempol (10 mM, 100 nl), a superoxide dismutase mimetic. In the HF+ET and sham rats, Tempol had no effect on the response. These results suggest that ET has a therapeutic effect to suppress sympathoexcitation evoked by central command in HF. Further, the role played by central superoxide in amplifying central command‐evoked sympathoexcitation in HF may be altered by ET. Supported by JSPS Kaken 22790226 (SK).