Sympathetic responses to exercise in myocardial infarction: a role played by central command

Abstract

Central command is a feed-forward neural mechanism originating in higher brain, stimulating medulla, and evoking both motor and cardiorespiratory activation in exercise. Whether this contributes to the exaggerated cardiovascular responses to exercise in heart failure (HF) is unknown. We hypothesized that HF augments sympathetic responses to central command. Thus, renal and lumbar sympathetic nerve activities (RSNA and LSNA) responses to fictive locomotion were examined in healthy control rats (n=8) and rats with myocardial infarction (MI) (≥8 weeks after coronary artery ligation, n=8). Fictive locomotion was evoked by electrical stimulation of mesencephalic locomotor region (MLR) of the decerebrate and paralyzed rats. Mild stimulation (20 μA) of the MLR did not result in significant differences in RSNA and LSNA responses between control and MI groups. Intense stimulation (50 μA) induced greater RSNA and LSNA responses in MI (120 % and 55 %, P<0.05 vs control) as compared with controls (65 % and 15 %). These data suggest that the sympathetic responses to activation of central command are sensitized in HF animals after MI. This study was supported by NIH R01 HL075533 & HL078866 (Li) and HL060800 (Sinoway).