The depression of EMG activity in upper airway muscles during sleep is known to be a predisposing factor causing upper airway obstruction in patients with obstructive sleep apnea syndrome (OSAS). To clarify whether or not the selective depression of upper airway muscles could be associated with the hypoxic ventilatory depression, we performed sustained hypercapnic hypoxia tests during wakefulness in 11 control subjects and 10 patients with OSAS. Isocapnic sustained hypoxia around SaO2 80% with mild hypercapnia [PETO2: 45.8 ± 1.6 (SD) and 46.7 ± 2.8 mm Hg and PETCO2: 44.2 ± 4.7 and ± 5.0 mm Hg in control and OSAS groups, respectively] was applied for 20 min. Electromyogram activities were recorded from the genioglossal muscle (EMGGG) and diaphragm (EMGDIA) with ventilatory variables. The magnitudes of hypoxic depression in terms of minute ventilation (VI) and minute EMGDIA (EMGDIA/min) were compared in percentage between peak value and the value at the late period. These values were not significantly different between two groups (VI: 79.2 ± 10.7 and 66.9 ± 12.8% and EMGDIA/min: ± 17.1 and 60.4 ± 24.0% in control and OSAS, respectively). On the contrary, the depression in EMGgg was not consistently observed in control (86.1 ± 38.6% of the peak value) whereas EMGgg was markedly depressed in OSAS (38.6 ± 15.7% of the peak value; p < O.Ol). It is concluded that sustained hypoxia attenuates the activity in genioglossal muscle in patients with OSAS, but not in control subjects. We speculate that the lack of a compensatory response of genioglossal muscle to sustained hypoxia could be responsible for the pathogenesis of OS A.

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