Genioglossal and Diaphragmatic EMG Responses to Hypoxia during Sleep

Abstract

Activation of pharyngeal dilator muscles, such as the genioglossus, during hypoxia must be sufficient to overcome the increased subatmospheric pressure generated by the diaphragm. This is particularly important during sleep, when upper airway resistance is greater. We measured ventilatory, genioglossal (EMGgg) and diaphragmatic (EMGdi) electromyogram responses to isocapnic hypoxia during wakefulness (W), slow-wave sleep (SWS), and rapid eye movement (REM) sleep in seven chronically instrumented adult goats. We also compared the EMG responses to hypoxia to response to CO2 during W. delta EMGdi/delta SaO2 decreased progressively from W to SWS (p less than 0.05) to REM sleep (p less than 0.05 versus SWS), paralleling the corresponding ventilatory responses. EMGgg was activated only below an SaO2 threshold, similar during W (69.8 +/- 6.3%) and SWS (67.2 +/- 4.3%), beyond which there was a brisk linear increase. During REM sleep, arousal preceded activation of EMGgg in each animal, although SaO2 at arousal (61.3 +/- 4.4%) was less than the SaO2 threshold for EMGgg activation during W or SWS (p less than 0.05). Despite state-related differences in the individual muscle responses, simultaneous EMGgg and EMGdi during hypoxia or hypercapnia in W, and during hypoxia in SWS and REM sleep, were linked in a constant manner. This suggests common integration of central and peripheral chemoreceptor inputs. Furthermore, these relationships are unaffected by either SWS or REM sleep.

Application of histamine or serotonin to the hypoglossal nucleus increases genioglossus muscle activity across the wake–sleep cycle

“…Interestingly, the present study showed that phasic GG reductions were accompanied by PGO wave bursts and REMs (PS+ period). Consistent with this finding, a reduction in GG muscle activity was found specifically during REMs in goats, even in the presence of strong excitatory drives induced by hypercapnia (Parisi et al, 1987). These GG phasic decreases may result from a similar glycinergic postsynaptic inhibitory process in the HMN to that which occurs in lumbar motoneurons during PS+ periods (Lopez-Rodriguez et al, 1990).…”

Pathophysiology of obstructive sleep apnoea

“…Phasic inspiratory GG activity decreases with sleep in normal subjects [60,105,119], and almost ceases during REM sleep [117,120]; whilst it increases significantly from wakefulness to NREM sleep, between apnoeas in OSA patients, and in older obese control subjects [121]. Thus, normal subjects have less activity than patients with OSA, yet do not have occlusive apnoeas, and such augmented activation of GG in OSA subjects may be viewed as a protective mechanism that occurs when patency of the pharyngeal airway is compromised.…”

“…An arterial carbon dioxide tension (Pa,CO 2 ) threshold well above the eupnoeic level is observed for GG muscle stimulation during all stages of sleep and wakefulness, whilst the DIA shows increased activity at even minor degrees of hypercapnia [120]. This imbalance of activity, which favours upper airway collapse, seems to be greatest during phasic REM sleep.…”

Nasal continuous positive airway pressure with supplemental oxygen in coexistent sleep apnoea-hypopnoea syndrome and severe chronic obstructive pulmonary disease

“…This transition may have been caused by the decrease in upper airway muscle activity normally present at the start of obstructive episodes [29]. Studies in animals [12,13,30,31], normal humans [14], and SAHS patients [32] have shown that hypoxia and marked hypercapnia determine a preferential increase in upper airway muscle activity compared with that of the diaphragm, and an inverse effect of hyperoxia, hypocapnia and mild hypercapnia. Furthermore, in the range of Sa,O 2 values considered in our study, a strong linear relationship has been observed between Sa,O 2 and upper airway muscle activity [33] and upper airway resistance [34] (inverse and positive relationships, respectively).…”