Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

Abstract

The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean ± SE: age, 25 ± 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s ( P < 0.001) and a significant decrease in R-R interval at 3 s ( P < 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 ± 3 to 104 ± 3 mmHg; O, 86 ± 3 to 105 ± 3 mmHg; P = 0.99. R-R interval: C, 1.12 ± 0.03 to 0.89 ± 0.04 s; O, 1.11 ± 0.02 to 0.87 ± 0.02 s, P = 0.99). Ventilation significantly increased during arousals under both conditions at the second breath ( P < 0.001); this increase was not different between the two conditions (C: 4.40 ± 0.29 to 6.76 ± 0.61 l/min, O: 4.35 ± 0.34 to 7.65 ± 0.73 l/min; P = 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men.