Upper airway muscle responsiveness to rising Pco₂during NREM sleep

Abstract

Although pharyngeal muscles respond robustly to increasing PCO(2) during wakefulness, the effect of hypercapnia on upper airway muscle activation during sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO(2)-driven muscle activation may importantly stabilize the upper airway during stages 3 and 4 sleep. To test this hypothesis, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal PCO(2) (PET(CO(2))) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO(2) (PET(CO(2)) = 6 Torr above the eupneic level) were also assessed during SWS (n = 9) or stage 2 sleep (n = 7). PET(CO(2)) increased spontaneously by 0.8 +/- 0.1 Torr from stage 2 to SWS (from 43.3 +/- 0.6 to 44.1 +/- 0.5 Torr, P < 0.05), with no significant change in GG or TP EMG. Despite a significant increase in minute ventilation with induced hypercapnia (from 8.3 +/- 0.1 to 11.9 +/- 0.3 l/min in stage 2 and 8.6 +/- 0.4 to 12.7 +/- 0.4 l/min in SWS, P < 0.05 for both), there was no significant change in the GG or TP EMG. These data indicate that supraphysiological levels of PET(CO(2)) (50.4 +/- 1.6 Torr in stage 2, and 50.4 +/- 0.9 Torr in SWS) are not a major independent stimulus to pharyngeal dilator muscle activation during either SWS or stage 2 sleep. Thus hypercapnia-induced pharyngeal dilator muscle activation alone is unlikely to explain the paucity of sleep-disordered breathing events during SWS.

Recruitment and rate-coding strategies of the human genioglossus muscle

“…5, 9, 46) and human studies (e.g., Refs. 31,32,47). The excitation of hypoglossal motoneurons achieved with increased ventilation is consistent with the effect produced at the motoneuron pools of the parasternal intercostals and scalenes that show more prominent recruitment than frequency modulation (16).…”

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

“…In general, upper airway obstruction elicits compensatory neuromuscular responses that maintain upper airway patency and prevent sleep apnea from developing. These responses can restore airway patency by recruiting muscles that dilate and elongate the airway (63,65,66,67,(78)(79)(80)(81)(82)(83)(84). In patients with sleep apnea, impaired neural responses to airway obstruction account for the marked elevation in Pcrit during sleep compared with normal individuals (54)(55)(56).…”

Dissociation of electromyogram and mechanical response in sleep apnoea during propofol anaesthesia

“…Since the pioneering studies of REMMERS et al [18], it is believed that the forces preventing pharyngeal obstruction are produced primarily by the upper airway dilator muscles. The reduction in GG-EMG activity with the onset of sleep [8,9] and the diminution of the reflex response of the GG to negative pressure [19] and chemical drive [20] during sleep suggested that the increase in pharyngeal collapsibility during sleep is due primarily to sleep-associated decrease in dilator muscle activity.…”