Upper airway muscle responsiveness to rising Pco(2) during NREM sleep

Although pharyngeal muscles respond robustly to increasing PCO2, during wak efulness, the effect of hypercapnia on upper airway muscle activation durin g sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO2-driven muscle activation may importantly sta bilize the upper airway during stages 3 and 4 sleep. To test this hypothesi s, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal PCO2 (PETCO2) in 18 sub jects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO2 (PETCO2 = 6 Torr above the e upneic level) were also assessed during SWS (n = 9) or stage 2 sleep (n. = 7). PETCO2 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 cha nge in GG or TP EMG. Despite a significant increase in minute ventilation w ith 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 suprap hysiological levels of PETCO2 (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-indu ced pharyngeal dilator muscle activation alone is unlikely to explain the p aucity of sleep-disordered breathing events during SWS.