Upper airway collapsibility, dilator muscle activation and resistance in sleep apnoea

¹ Institute for Breathing and Sleep, Austin Health, Heidelberg, Australia
² Brigham & Women's Hospital, Harvard Medical School, Boston
³ School of behavioural Sciences , University of Melbourne, Parkville, Australia
⁴ West Australian Institute for Medical Research, University of Western Australia, Nedlands, Australia

^* To whom correspondence should be addressed. E-mail: r.pierce{at}medicine.unimelb.edu.au.

	Abstract

The calibre of the upper airway is thought dependant upon its passive anatomy/collapsibility and the activation of pharyngeal dilator muscles. Awake, the more collapsible upper airway in obstructive sleep apnoea (OSA) increases dilator muscle activity through a negative pressure reflex (NPR).

We hypothesised a direct correlation between the closing pressure of the passive upper airway (Pcrit) as a measure of anatomy/collapsability and EMG activity of genioglossus (GGEMG) and tensor palatini (TPEMG). We also set out to determine the relationship between these indices and pharyngeal resistance (Rphar).

We studied 8 males with OSA aged 48 (46,52) years, [median (IQR)], AHI 75 (65 , 101) / hr on two nights - breathing normally and on nCPAP. Pcrit was measured during NREM sleep on nCPAP using brief, incremental reductions in Pmask. GGEMG and TPEMG were measured breath-by-breath, awake, during sleep onset and on nCPAP. Rphar was measured from airway pressures and flow.

Wakeful GGEMG, early Obstructive Sleep Apnoea sleep TPEMG and the sleep decrement in TPEMG were directly related to Pcrit. Muscle activation was negatively correlated with Rphar for TPEMG awake and GGEMG early in sleep.

These results confirm that dilator muscle activation is directly related to airway narrowing and reduces resistance across patients with OSA.

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