Muscle sympathetic nerve activity (MSNA) and arterial pressure increase concomitantly during apnea, suggesting 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 one minute post-apnea. Apnea did not affect the sympathoinhibitory or bradycardic response to NS (P > 0.05); however, while the cardiac response to NP was maintained post-apnea, 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.