We have recently demonstrated that the severity of sleep-disordered breathing in obstructive sleep apnoea hypopnoea syndrome (OSAHS) can be reduced by lowering the surface tension (γ) of the upper airway lining liquid (UAL). Morning xerostomia (related to oral breathing during sleep) is reported by most OSAHS patients. In the present study we examine relationships between breathing route, oral mucosal 'wetness' and the γ of UAL. We studied eight healthy subjects ( with oral breathing (P < 0.001). For the group and all conditions studied, γ of UAL values strongly correlated with upper airway mucosal 'wetness' (correlation coefficient, r 2 = −0.34, P < 0.001; linear regression). We conclude that oral breathing increases and nasal breathing decreases the γ of UAL in healthy subjects during wakefulness. We speculate that nasal breathing in OSAHS patients during sleep may promote a low γ of UAL that may contribute to reducing the severity of sleep-disordered breathing.

Hysteresis of the nasal airway pressure-flow relationship (PFR) is seen during hyperpnea, with lower nasal resistance during increasing inspiratory flow than during decreasing flow. We hypothesized that the nasal PFR hysteresis arose in the nasal vestibule airway because of progressive collapse during the inspiration. We measured the inspiratory transnasal and transvestibular PFR for one nasal passage in five normal subjects breathing via a nasal mask during voluntary hyperventilation, both with voluntary nostril flaring and without flaring. The inspiratory hysteresis (IH) was quantified as the ratio of the areas under the descending and ascending pressure-flow curves. Flaring reduced the vestibular IH from 1.96 +/- 0.06 to 1.15 +/- 0.06 and the nasal IH from 2.05 +/- 0.13 to 1.28 +/- 0.06 (both P < 0.01). Our results demonstrate that hysteresis arises in the compliant vestibule segment of the nasal airway, likely because of progressive collapse of the nasal vestibule during inspiration. The findings suggest that hysteresis is prevented by voluntary nostril flaring maintained throughout inspiration.

Exercise (Ex) and hypercapnia (HC) both lead to increases in ventilation and upper airway muscle (UAM) activity. To determine whether different breathing routes (nasal vs. oral) or stimuli produced differential UAM activation, electromyographic (EMG) activity of the alae nasi (AN) and genioglossus (GG) were measured in seven normal subjects seated on a bicycle ergometer. Subjects performed paired runs during both progressive Ex and HC while breathing through the nose alone (N) or the mouth alone (O). During hyperpnea, AN EMG was greater when the subjects were breathing via N [81 +/- 6% maximum (HC) and 69 +/- 7% maximum (Ex)] than when they were breathing via O [30 +/- 5% maximum (HC) and 27 +/- 5% maximum (Ex); both P < 0.01], whereas the GG EMG did not differ between N and O. Both AN and GG EMG were similar for Ex and HC when the subjects were breathing via the same route. We conclude that UAM activation was independent of the nature of the stimulus. However, the AN muscle but not the GG muscle demonstrated breathing-route dependence of activity.

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