The stimuli controlling pharyngeal dilator muscles are poorly defined. Local mechanoreceptors are a leading possibility. To address this, we assessed the relationship between two dilator muscle electromyograms (EMGs, i.e., genioglossus [GG-an inspiratory phasic muscle], tensor palatini [TP-a tonically active muscle]) and potential stimuli (i.e., epiglottic pressure [Pepi], airflow [V], and pharyngeal resistance [Rpha]). Fifteen normal subjects were studied, during wakefulness and stable non-rapid eye movement (NREM) sleep. The GGEMG and TPEMG were assessed during basal breathing and during inspiratory resistive loading (four loads, done in triplicate), while quantifying Pepi and choanal pressures (Pcho, Millar catheters) plus V. There was a strong correlation between Pepi and GGEMG during wakefulness in most subjects (9 of 15 had absolute R > 0.7 [p < 0.05], group mean R = -0.62, p < 0.05). These correlations were less robust during NREM sleep (8 of 15 absolute R > 0.6 [p < 0.05], group mean R = -0.39, ns). The slope of the Pepi versus GGEMG relationship was greater during wakefulness than sleep (-0.67 versus -0.39% max/ cm H(2)O, p < 0.05). No significant correlations were observed between TPEMG and any of the measured potential stimuli. We conclude that intrapharyngeal pressure may modulate genioglossus activity during wakefulness, with a fall in muscle responsiveness during sleep. The activity of the TP was not clearly influenced by any measured local stimulus either awake or asleep.

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.