Intermittent hypoxia elicits plasticity in sensory and motor pathways involved in the control of breathing with potentially adaptive and maladaptive consequences for respiratory homeostasis. We and others have shown that chronic intermittent hypoxia (CIH) – a major feature of sleep-disordered breathing – has deleterious effects on rat upper airway dilator muscle contractile function and motor control (1-3). In the present study, we sought to test the hypothesis that CIH impairs reflex recruitment of sternohyoid (pharyngeal dilator) EMG during obstructive airway events. Adult male Wistar rats were exposed to 20 cycles of normoxia and hypoxia (5% O2 at nadir) per hour, 8 hours a day for 7 days (CIH, N=7). The sham group (N=7) were exposed to normoxia in parallel. Following gas treatments, rats were anaesthetised with an i.p. injection of urethane (1.5g/kg; 20% w/v). Fine concentric needle electrodes were inserted into the sternohyoid (pharyngeal dilator) and the costal diaphragm. Discriminated sternohyoid motor unit potentials and whole EMG, together with arterial blood pressure, tracheal pressure and O2 saturation were recorded during quiet basal breathing and during nasal or tracheal airway occlusion. Arterial blood samples were taken intermittently to determine arterial PO2, PCO2, pH and haematocrit. During basal breathing, the commonest discharge frequency of individual sternohyoid motor units determined from autocorrelograms was decreased in CIH rats but this did not achieve statistical significance (53±6Hz vs. 36±7Hz; sham vs. CIH; mean±SEM, Student’s t test, p=0.09). Area under the curve analysis of the integrated EMG recordings revealed that basal sternohyoid EMG activity was increased in CIH-treated rats but this did not achieve statistical significance (18±5a.u. vs. 37±13a.u.; p=0.2). Airway obstruction increased sternohyoid EMG activity in all animals; there was no difference in the reflex response to airway occlusion between sham and CIH-treated animals (+47±3% vs. +49±6%, % increase from baseline, p=0.75). We conclude that neither basal nor reflexly evoked motor discharge to the sternohyoid is affected by CIH. This is surprising since we have previously established that CIH causes sternohyoid muscle weakness – an effect blocked by antioxidant supplementation (3). Of interest, upper airway muscle activity is enhanced in sleep apnoea patients compared to controls, but this adaptation is not seen in this rat model. Though we have recently demonstrated that 7 days of CIH is sufficient to alter the control of breathing in sleeping rats (4), longer durations of CIH may be necessary to elicit plasticity in the neural pathways regulating upper airway calibre (1, 2).