SUMMARY1. To determine the afferent pathways mediating pharyngeal dilator muscle activation in response to negative airway pressure in man, we recorded genioglossus electromyogram (EMG) activity (via intra-oral bipolar surface electrodes) in response to 500 ms duration pressure stimuli of -15 and -25 cmH20 in normal, conscious, supine subjects relaxed at end-expiration; responses were compared before and after upper airway anaesthesia.2. Six rectified and integrated EMG responses were bin averaged for pressure stimuli applied with the glottis open (GO) and closed (GC) and to the outside of the face only (controls). Response magnitude was quantified as the ratio of the EMG activity for an 80 ms post-stimulus period (before the subject's reaction time for tongue protrusion) to an 80 ms pre-stimulus period.3. In eight subjects, upper airway anaesthesia reduced the EMG responses with GC to a level indistinguishable from controls. After anaesthesia, responses with GO remained higher than those with GC.4. With GC, the mean EMG responses decreased by 43 % after selective anaesthesia of the nasal mucosa (trigeminal nerves) in two subjects, 32 % after selective anaesthesia of the laryngeal mucosa (superior laryngeal nerves) in six subjects and by 21 % after selective anaesthesia of the oropharyngeal mucosa (glossopharyngeal and lingual nerves) in four subjects.5. We conclude that upper airway afferents mediate pharyngeal dilator muscle activation in response to negative pressure with GC and that subglottal receptors cause the increased activation with GO. With GC, the trigeminal and superior laryngeal nerves mediate an important component of the responses with the glossopharyngeal nerves playing a less important role.

1. The present study was designed to determine the effect of sleep on reflex pharyngeal dilator muscle activation by stimuli of negative airway pressure in human subjects. 2. Intra-oral bipolar surface electrodes were used to record genioglossus electromyogram (EMG) responses to 500 ms duration pressure stimuli of 0 and -25 cmH2O applied, via a face-mask, in four normal subjects. Stimuli were applied during early inspiration in wakefulness and in periods of non-rapid-eye-movement (non-REM) sleep, defined by electroencephalographic (EEG) criteria. 3. The rectified and integrated EMG responses to repeated interventions were bin averaged for the 0 and -25 cmH2O stimuli applied in wakefulness and sleep. Response latency was defined as the time when the EMG activity significantly increased above prestimulus levels. Response magnitude was quantified as the In ratio of the EMG activity for an 80 ms post-stimulus period to an 80 ms prestimulus period; data from after the subject's voluntary reaction time for tongue protrusion (range, 150-230 ms) were not analysed. 4. Application of the -25 cmH2O stimuli caused genioglossus muscle activation in wakefulness and sleep, but in all subjects response magnitude was reduced in sleep (mean decrease, 61 %; range, 52-82 %; P = 0-011, Student's paired t test).

It has been suggested that deposition of fat in the soft tissues surrounding the upper airway may be an important factor in the pathogenesis of obstructive sleep apnoea (OSA) in obese subjects. We have used magnetic resonance imaging to determine the site(s) and size(s) of fat deposits around the upper airway in six obese patients with OSA (116-153% of ideal body weight) and five weight-matched controls without OSA (107-152% of ideal body weight). In all subjects, large deposits of fat were present postero-lateral to the oropharyngeal airspace at the level of the soft palate. Significantly more fat was present in these regions in the patients with OSA (p = 0.03). Fat deposits in the soft palate were observed in 4 of the 6 patients with OSA but none of the controls. Fatty streaks were observed in the tongue in 2 of the 5 controls and 3 of the 6 patients with OSA. Fat deposits were observed anterior to the laryngopharyngeal airspace, in submental regions, in all obese subjects. This study shows that more fat is present in those areas surrounding the collapsable segment of the pharynx in patients with OSA, compared to equally obese control subjects without OSA.

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