Carotid baroreflex function during and following voluntary apnea in humans

Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas 76107 Submitted 19 February 2003 ; accepted in final form 29 July 2003 Muscle sympathetic nerve activity (MSNA) and arterial pressure increase concomitantly during apnea, suggesting a possible overriding of arterial baroreflex inhibitory input to sympathoregulatory centers by apnea-induced excitatory mechanisms. Apnea termination is accompanied by strong sympathoinhibition while arterial pressure remains elevated. Therefore, we hypothesized that the sensitivity of carotid baroreflex control of MSNA would decrease during apnea and return upon apnea termination. MSNA and heart rate responses to –60-Torr neck suction (NS) were evaluated during baseline and throughout apnea. Responses to +30-Torr neck pressure (NP) were evaluated during baseline and throughout 1 min postapnea. Apnea did not affect the sympathoinhibitory or bradycardic response to NS ( P > 0.05); however, whereas the cardiac response to NP was maintained postapnea, the sympathoexcitatory response was reduced for 50 s ( P < 0.05). These data demonstrate that the sensitivity of carotid baroreflex control of MSNA is not attenuated during apnea. We propose a transient rightward and upward resetting of the carotid baroreflex-MSNA function curve during apnea and that return of the function curve to, or more likely beyond, baseline (i.e., a downward and leftward shift) upon apnea termination may importantly contribute to the reduced sympathoexcitatory response to NP. sympathetic nerve activity; heart rate; arterial blood pressure; neck suction; neck pressure Address for reprint requests and present address of N. Muenter Swift, Dept. of Neurology/Autonomic Disorders Center, Mayo Clinic, 200 First St. SW, Charlton 7-158, Rochester, MN 55905 (E-mail: muenterswift.nicolette{at}mayo.edu ).