The cardiovascular response to an arousal occurring at the termination of an obstructive apnea 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 analyzed in 13 healthy men [age 24 ± 1 (SE) yr]. 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 with a significant decrease in the R-R interval at 3 s (P <0.001); however, the magnitude of the changes was not significantly different during normoxia compared with HH (mean arterial blood pressure: normoxia, 91 ± 4 to 106 ± 4 mmHg; HH, 91 ± 4 to 109 ± 5 mmHg; P = 0.32; R-R interval: normoxia, 1.12 ± 0.04 to 1.02 ± 0.05 s; HH, 1.09 ± 0.05 to 0.92 ± 0.04 s; P = 0.78). Mean ventilation increased significantly at the second breath postarousal for both conditions (P <0.001), but the increase was not significantly different between the two conditions (normoxia, 5.35 ± 0.40 to 9.57 ± 1.69 l/min; HH, 8.57 ± 0.63 to 11.98 ± 0.70 l/min; P = 0.71). We conclude that combined central and peripheral chemoreceptor stimulation with the use of HH does not interact with the autonomic outflow associated with arousal from sleep to augment the cardiovascular response.
- Blood pressure
- Heart rate