The effect of sleep onset on upper airway muscle activity in patients with sleep apnoea versus controls

Abstract

Pharyngeal dilator muscles are important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that during wakefulness, the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) is greater in patients with OSA compared with controls. Further, EMG activity decreases at sleep onset, and the decrement is greater in apnoea patients than in healthy controls. In addition, it is known that the prevalence of OSA is greater in middle-aged compared with younger men. Thus, we had two goals in this study. First we compared upper airway muscle activity between young and middle-aged healthy men compared with men with OSA. We also explored the mechanisms responsible for the decrement in muscle activity at sleep onset in these groups. We investigated muscle activity, ventilation (V e ), and upper airway resistance (UAR) during wakefulness and sleep onset (transition from α to θ EEG activity) in all three groups. Measurements were obtained during basal breathing (BB) and nasal continuous positive airway pressure (CPAP) was applied to reduce negative pressure-mediated muscle activation). We found that during wakefulness there was a gradation of GGEMG and UAR (younger < older < OSA) and that muscle activity was reduced by the application of nasal CPAP (to a greater degree in the OSA patients). Although CPAP eliminated differences in UAR during wakefulness and sleep, GGEMG remained greater in the OSA patients. During sleep onset, a greater initial fall in GGEMG was seen in the OSA patients followed by subsequent muscle recruitment in the third to fifth breaths following the α to θ transition. On the CPAP night,V e and GGEMG still fell further in the OSA patients compared with control subjects. CPAP prevented the rise in UAR at sleep onset along with the associated recruitment in GGEMG. Differences in TPEMG among the groups were not significant. These data suggest that the middle-aged men had upper airway function midway between that of young normal men and the abnormal airway of those with OSA. Furthermore it suggests that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefulness' stimulus, rather than to loss of responsiveness to negative pressure, and that this wakefulness stimulus may be greater in the OSA patient than in healthy controls.

Dissociation of electromyogram and mechanical response in sleep apnoea during propofol anaesthesia

“…This assumption is supported by the decline in pharyngeal dilator muscle electromyogram (EMG) activity observed during the onset of sleep [8,9]. However, there is abundant evidence suggesting that this decline does not persist throughout sleep.…”

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

“…This defect in neuromuscular control was independent of age, obesity, and sex (86), and may be caused by sleep-related reductions in dilator activity during sleep compared with wakefulness (87,88) or by a loss of compensatory responses during sleep (87)(88)(89)(90)(91)(92)(93)(94)(95)(96)(97)(98)(99). Thus, current evidence indicates that sleep apnea is associated with fundamental disturbances in upper airway mechanical (68,100,101) and neuromuscular control (80,(102)(103)(104)(105)(106)) (see Figure 1, left), and suggests that a combined defect is required to produce sleep apnea (86). Nevertheless, the impact of obesity on upper airway mechanical and neural properties has not been elucidated.…”

Adult Obstructive Sleep Apnea

“…23,[32][33][34][35][36] These studies imply that upper airway structural differences distinguish OSA patients from normal subjects, and may predispose to upper airway obstruction when protective neuromuscular mechanisms wane at sleep onset. 37 Obesity, the major risk factor for OSA, has been linked with elevations in neck circumference and increased amounts of peripharyngeal fat, 38,39 which could narrow and compress the upper airway. Furthermore, increased parapharyngeal fat has been correlated with increased sleep apnea severity.…”

“…Thus, reductions in upper airway muscle activity with sleep onset through serotonergic, cholinergic, noradrenergic, and histaminergic pathways may lead to upper airway obstruction and have been hypothesized to be due to the loss of a "wakefulness stimulus" that may be greater in OSA patients than healthy control subjects. 37,49,50 Pressure-sensing mechanisms play a prominent role in modulating upper airway neuromuscular activity during wakefulness and sleep. A negative pressure reflex within the upper airway serves to stabilize the upper airway during inspiration.…”