Genioglossal Activation in Patients with Obstructive Sleep Apnea versus Control Subjects

Abstract

Pharyngeal dilator muscle activation (GGEMG) during wakefulness is greater in patients with obstructive sleep apnea (OSA) than in healthy control subjects, representing a neuromuscular compensatory mechanism for a more collapsible airway. As previous work from our laboratory has demonstrated a close relationship between GGEMG and epiglottic pressure, we examined the relationship between genioglossal activity and epiglottic pressure in patients with apnea and in control subjects across a wide range of epiglottic pressures during basal breathing, negative-pressure (iron-lung) ventilation, heliox breathing, and inspiratory resistive loading. GGEMG was greater in the patients with apnea under all conditions (p < 0.05 for all comparisons), including tonic, phasic, and peak phasic GGEMG. In addition, patients with apnea generated a greater peak epiglottic pressure on a breath-by-breath basis. Although the relationship between GGEMG and epiglottic negative pressure was tight across all conditions in both groups (all R values > = 0.69), there were no significant differences in the slope of this relationship between the two groups (all p values > 0.30) under any condition. Thus, the increased GGEMG seen in the patient with apnea during wakefulness appears to be a product of an increased tonic activation of the muscle, combined with increased negative-pressure generation during inspiration.

Sleep Apnea and Cardiovascular Disease

“…Mechanoreceptors located primarily in the larynx respond reflexively to this negative pressure and increase the activity of a number of pharyngeal dilator muscles, thereby maintaining airway patency while awake. 22,23 However, during sleep, the reflex pharyngeal muscle activity that drives this neuromuscular compensation is reduced or lost, leading to reduced dilator muscle activity and ultimately to pharyngeal narrowing and intermittent complete collapse. 24 During the subsequent apnea or hypopnea, hypoxia and hypercapnia stimulate ventilatory effort and ultimately arousal from sleep to terminate the apneic event.…”

Identification of a Novel Form of Noradrenergic-Dependent Respiratory Motor Plasticity Triggered by Vagal Feedback

“…Apnea-induced LTF may therefore function to prevent or minimize airway obstructions during sleep (Mateika and Narwani, 2009;Richerson, 2010). Genioglossus motor tone is elevated in OSA patients (Mezzanotte et al, 1992;Fogel et al, 2001); however, it is unknown whether apnea-induced LTF is the underlying cause.…”

Síndrome Das Apnéias / Hipopnéias Obstrutivas Do Sono (Sahos)

“…É importante salientar que mesmo na ausência desse estí-mulo adicional durante uma apnéia, o esforço respiratório contra a via aérea ocluída, constitui o principal elemento promotor do despertar. Enfatizamos que, embora a atividade dos músculos dilatadores da faringe aumente na medida em que uma apnéia progride, o aumento é geralmente insuficiente para restabelecer a permeabilidade da faringe 14,15 . Então o paciente acor- da ou superficializa o sono, repetidamente para sair das apnéias.…”