Increases in exercise intensity resets the arterial baroreflex (ABR) control of heart rate (HR) and mean arterial pressure (MAP) in an upward and rightward direction (Fadel, PJ and Raven, PB., 2012). This resetting is measured by changes in the operating point (OP). The mechanism for ABR resetting is unknown. We hypothesized that the antioxidant N-acetylcysteine (NAC) would decrease the OP of both HR and MAP compared to control with the same exercise intensity by reducing reactive oxygen species (ROS) centrally and in the circulation. Healthy young human volunteer subjects (n = 8, 25 ± 3.8 yrs) performed upright cycling exercise at two workloads to establish HRs of 120 (e120) and 150 (e150) bpm with and without 1200mg oral NAC. HR and beat-to-beat arterial pressure were recorded. Carotid- HR and Carotid-MAP reflex responses were modeled using our established neck pressure and neck suction protocol during rest and exercise (Potts, JT. et al., 1993). In contrast to our hypothesis the OP of HR and MAP were significantly increased above rest in both intensities of exercise with and without NAC (2 factor ANOVA with repeated measures followed by a Newman Keuls post hoc analysis of significant main effects; HR e120 p = 0.02, e150 p = 0.05; MAP e120 p = 0.003, e150 p = 0.02) without significant interactions. However, the functional characteristics of the reflex, operating range (OR) and response range (RR), were not significantly different between treatment groups. We conclude that NAC increases production of glutathione resulting in a preservation of circulating catecholamines and increasing HR and the MAP operating point of the reflex. In order to identify whether NAC affected central sympathetic outflow requires ‘in vivo’ measures of muscle sympathetic nerve activity (MSNA) during rest and exercise.