Nocturnal swallowing augments arousal intensity and arousal tachycardia in healthy individuals and in obstructive sleep apnea

Cortical arousals from sleep vary considerably in their frequency, duration and in their effects on the autonomic nervous system. Yet mechanisms that modify the arousal intensity and autonomic activity remain unclear. Here we examined the effects of nocturnal episodic swallowing on spontaneous and respiratory evoked arousal from sleep and on the arousal tachycardia. Methods. 24 healthy and 18 obstructive sleep apnoea (OSA) subjects participated. One group (N=14; 8 female; none with OSA) were examined for supine blood pressure and heart rate responses to swallows during wakefulness. The second group (N=28; 8 female) undertook an overnight in-laboratory physiology sleep study to examine the relationships between breathing and airway obstruction, arousal from sleep, arousal tachycardia and spontaneous swallows.Results. In all participants we observed swallows trigger robust and patterned tachycardia conserved across wake, sleep, spontaneous arousal, or arousal preceded by hypopnoea or apnoea. Tachycardia onset was temporally matched to glottic closure - the first phase of the swallow motor program. Multiple swallows increased the magnitude of tachycardia via temporal summation, and blood pressure increased as a function of the degree of tachycardia. During sleep, 98% of nocturnal swallows were associated with arousal in healthy individuals and people with sleep apnoea. Swallows were causally linked to the intense, prolonged cortical arousals and marked tachycardia for all spontaneous and respiratory-evoked arousal in all participants. The tachycardia at arousal increased as a function of swallow incidence (spontaneous arousal and no swallow: 6 ± 3 bpm; one swallow: 18 ± 4 bpm; two swallows: 26 ± 5 bpm; P< 0.001). Arousal intensity also increased as a function of swallow incidence (arousal duration and no swallow: 9±2 sec; one swallow: 19 ± 6 sec; two swallows: 25±8 sec; P< 0.001) Conclusions. Our findings identify a fundamental mechanism driving both autonomic activity and heightened arousal via cortical feedback from swallow Central Pattern Generator networks of the brainstem. In healthy individuals, the swallowing-tachycardia makes up a large component of the cardiovascular activation during arousal from sleep, and may also explain the variation in arousal duration and intensity. In OSA, spontaneous swallowing intensifies respiratory-evoked arousal and tachycardia.