The cardiovascular response to an arousal occurring at the termination of an obstructive apnoea is almost double that to a spontaneous arousal. We investigated the hypothesis that central plus peripheral chemoreceptor stimulation, induced by hypercapnic hypoxia (HH), augments the cardiovascular response to arousal from sleep. Auditory induced arousals, during normoxia and HH (>10 s duration) were analysed in 13 healthy males (mean ± SEM, Age, 24 ± 1 yrs). Subjects breathed on a respiratory circuit that held arterial blood gases constant, despite the increased ventilation associated with arousal. Arousals were associated with a significant increase in mean arterial blood pressure at 5 s (p<0.001), and a significant decrease in the R-R interval at 3 s (P<0.001); however, the magnitude of the changes were not significantly different during normoxia compared to HH (MAP; normoxia, 91 ± 4 mmHg to 106 ± 4 mmHg; HH, 91 ± 4 mmHg to 109 ± 5 mmHg; p=0.32. R-R interval; normoxia, 1.12 ± 0.04 s to 1.02 ± 0.05 s; HH, 1.09 ± 0.05 s to 0.92 ± 0.04 s; p=0.78). Mean ventilation increased significantly at the second breath post arousal for both conditions (p<0.001), but the increase was not significantly different between the two conditions (normoxia, 5.35 ± 0.40 Lmin^-1 to 9.57 ± 1.69 Lmin^-1; HH, 8.57 ± 0.63 Lmin^-1 to 11.98 ± 0.70 Lmin^-1; p=0.71). We conclude that combined central and peripheral chemoreceptor stimulation using HH does not interact with the autonomic outflow associated with arousal from sleep to augment the cardiovascular response.