Influence of breathing route on upper airway lining liquid surface tension in humans

Abstract

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 (gamma) 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 gamma of UAL. We studied eight healthy subjects (age, 25 +/- 5 years [mean +/- S.D.]; body-mass index, 23 +/- 2 kg m(-2)) during a 120 min challenge of both nasal-only breathing (mouth taped) and oral-only breathing (nose clip), each on a separate day (randomized). Both oral mucosal 'wetness' (5 s contact gravimetric absorbent paper strip method) and the gamma ('pull-off' force technique) of 0.2 microl samples of UAL obtained from the posterior pharyngeal wall were measured at 15 min intervals (mouth tape removed and replaced as required). Upper airway mucosal 'wetness' increased during 120 min of nasal breathing from 4.0 +/- 0.4 (mean +/- S.E.M.) to 5.3 +/- 0.3 microl (5 s)(-1) but decreased from 4.5 +/- 0.4 to 0.1 +/- 0.2 microl (5 s)(-1) with oral breathing (both P < 0.001, repeated-measures ANOVA, Tukey's multiple comparison test, post hoc test). Concurrently, the gamma of UAL decreased from 59.3 +/- 2.2 to 51.8 +/- 0.98 mN m(-1) with nasal breathing but increased from 64.4 +/- 2.7 to 77.4 +/- 1.1 mN m(-1) with oral breathing (P < 0.001). For the group and all conditions studied, gamma of UAL values strongly correlated with upper airway mucosal 'wetness' (correlation coefficient, r2 = -0.34, P < 0.001; linear regression). We conclude that oral breathing increases and nasal breathing decreases the gamma of UAL in healthy subjects during wakefulness. We speculate that nasal breathing in OSAHS patients during sleep may promote a low gamma of UAL that may contribute to reducing the severity of sleep-disordered breathing.

Figure 1. A 1 min raw data period obtained from one subject during both the nasal and oral breathing challenges

The traces show signals from respiratory inductance plethysmography (thorax, abdomen, thorax + abdomen = sum), breathing route thermocouples (nasal and oral) and submental electromyography (EMG). Note that there is no oral breathing during the nasal breathing challenge and similarly no nasal breathing during the oral breathing challenge. A single swallow is evident on the EMG trace during nasal and oral breathing.

Figure 2. Group mean ± s.e.m. upper airway mucosal ‘wetness’ values during nasal and oral breathing challenge periods

*P < 0.001 compared to time 0 min nasal breathing challenge; †P < 0.001 compared to time 0 min oral breathing challenge; and ‡P < 0.001 nasal compared to oral breathing challenge at respective 15 min intervals.

Figure 3. Group mean ± s.e.m. γ of UAL values during nasal and oral breathing challenge periods

*P < 0.001 compared to time 0 min nasal breathing challenge; †P < 0.001 compared to time 0 min oral breathing challenge; and ‡P < 0.001 nasal compared to oral breathing challenge at respective 15 min intervals.

Figure 4. There was a highly significant, inverse (negative) relationship between UA mucosal ‘wetness’ and γ of UAL

r² = −0.34, P < 0.001. The line represents the regression line.