The Influence of Obstructive Sleep Apnea and Gender on Genioglossus Activity During Rapid Eye Movement Sleep

Abstract

Background The mechanisms contributing to worsening of obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep have been minimally studied. Reduced upper-airway muscle tone may be an important contributor. Because respiratory events and the associated blood gas changes can influence genioglossus (GG) activity, we compared GG activity between OSA patients and control subjects during REM sleep using continuous positive airway pressure (CPAP) to minimize the influences of upper-airway resistance (RUA) and blood gas disturbances on GG activity. Methods Twenty subjects (10 female subjects), 12 healthy individuals, and 8 OSA patients, were studied overnight. Sleep staging, epiglottic pressure, minute ventilation, and GG electromyogram (GGEMG) were recorded. GGEMG was compared between REM sleep with (phasic REM) and without (tonic REM) eye movements, non-REM (NREM) sleep, and wakefulness. Results Breathing frequency increased from stable NREM, to tonic REM to phasic REM sleep, whereas tidal volume and GGEMG decreased (ie, peak GGEMG: 3.0 ± 0.7 vs 1.7 ± 0.4 vs 1.2 ± 0.3% max, respectively; p < 0.001). Reductions in GGEMG during REM sleep were not different between OSA patients and control subjects or between genders. Conclusions When RUA and blood gas disturbances are minimized by CPAP, genioglossal activity is reduced in a stepwise manner from stable NREM, to tonic REM to phasic REM sleep to a similar extent in OSA and healthy individuals of both genders. Thus, an inherent abnormality in GG neural control in OSA patients during REM sleep is unlikely to explain the increased upper-airway collapse in this sleep stage. Rather, a generalized reduction in GG activity during REM likely renders individuals who are highly reliant on upper-airway dilator muscles vulnerable to pharyngeal collapse during REM sleep.

Trazodone Increases the Respiratory Arousal Threshold in Patients with Obstructive Sleep Apnea and a Low Arousal Threshold

“…23,24 Peak (maximum during inspiration) and tonic EMG (nadir during expiration), and respiratory parameters were quantified on a breath-by-breath basis using customdesigned semi-automated software as described previously. 25 Upper airway resistance (R UA ) was quantified as the difference in mask versus epiglottic pressure during inspiration at a flow rate of 200 mL/s. 25 Artifact-free respiratory and upper airway EMG variables were averaged for data collection periods of at least 5 min during quiet wakefulness with and without therapeutic CPAP and for the 60 sec prior to each CPAP drop while on therapeutic CPAP during NREM sleep.…”

“…25 Upper airway resistance (R UA ) was quantified as the difference in mask versus epiglottic pressure during inspiration at a flow rate of 200 mL/s. 25 Artifact-free respiratory and upper airway EMG variables were averaged for data collection periods of at least 5 min during quiet wakefulness with and without therapeutic CPAP and for the 60 sec prior to each CPAP drop while on therapeutic CPAP during NREM sleep.…”

Night-to-night Variability in Obstructive Sleep Apnea Severity: Relationship to Overnight Rostral Fluid Shift

“…During REM sleep there is maximal reduction in pharyngeal dilator muscle activity, which is probably the main mechanism of upper airway collapse. 26 Therefore, neck fluid accumulation may not have additional effects on upper airway collapsibility and the AHI during REM because the upper airway is already in its most collapsible state. However, during NREM sleep, when pharyngeal dilator muscle activity is higher and the airway is less collapsible than during REM sleep, narrowing of the upper airway due to neck fluid accumulation is likely to increase its collapsibility.…”

Sleep Apnea – Recent Updates

“…Prior to activation of the diaphragm, there is the activation of upper airway/pharyngeal dilator muscles that prevent collapse of the upper airway during inspiration. Thus, the upper airway performs an important function during respiration, and if function is compromised, obstruction could result as in OSA [26,27]. CPAP is one of the preferred treatments for moderate-to-severe OSA.…”

“…This approach would be particularly useful in patients who cannot tolerate or refuse to tolerate CPAP or other treatments. Several clinical trials have been carried out on devices implanted subcutaneously that are, once activated, triggered by the patient's own inspiratory efort [27][28][29][30][31][32][33]. The largest of these [33], a multisite clinical trial of patients with moderate-to-severe OSA, surgically implanted a hypoglossal nerve stimulator in OSA patients who were CPAP intolerant or refused CPAP treatment.…”