Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism).

TLDR

Pharyngeal collapse in obstructive sleep apnea results from a sleep‑related drop in pharyngeal dilator muscle activity on top of abnormal airway anatomy. The authors hypothesize that awake patients with OSA increase pharyngeal dilator muscle activity to compensate for reduced airway size and preserve patency. They recorded waking genioglossus EMG in 11 OSA patients and 14 controls, using a reproducible protocol that defines maximal GG activity and expresses basal activity as a percentage of this maximum. Awake OSA patients exhibited markedly higher basal genioglossus activity (≈40.6 % vs 12.7 % of maximum), a difference that persisted in size‑matched groups, could be lowered by positive airway pressure, and may be lost during sleep, contributing to airway collapse.

Abstract

Pharyngeal collapse in obstructive sleep apnea patients is likely a product of a sleep-related decrement in pharyngeal dilator muscle activity superimposed upon abnormal airway anatomy. We postulate that during wakefulness, increased pharyngeal dilator muscle activity in apnea patients compensates for diminished airway size thus maintaining patency. We studied the waking genioglossus (GG) electromyogram (EMG) activity in 11 OSA patients and 14 age-matched controls to determine if GG activity is higher in the awake state in apnea patients than controls. To make this determination, we developed a reproducible methodology whereby true maximal GG EMG could be defined and thus basal activity quantitated as a percentage of this maximal value. Therefore, direct comparisons of basal activity between individuals was possible. We observed apnea patients to have significantly greater basal genioglossal activity compared to controls (40.6 +/- 5.6% vs. 12.7 +/- 1.7% of maximum). This difference persisted when size-matched subsets were compared. This augmented GG activity in apnea patients could be reduced with positive airway pressure. We speculate that this neuromuscular compensation present during wakefulness in apnea patients may be lost during sleep leading to airway collapse.