Intermittent hypoxia is a hallmark feature of the debilitating sleep-related breathing disorder – obstructive sleep apnoea (OSA). OSA patients experience intermittent cycles of hypoxia and reoxygenation due to recurrent apnoea throughout sleep. Upper airway muscle dysfunction is implicated in the pathophysiology of OSA. Indeed, recurrent exposure to hypoxia, often employed in animal models of OSA, has been shown to drive aberrant muscle remodeling, with redox remodelling postulated as the underlying mechanism. The effects of intermittent occlusions with concomitant hypoxia on tissue oxygenation within upper airway muscles has not been explored to date. In the present study, we sought to determine sternohyoid muscle (upper airway dilator) partial pressure of oxygen (PO2) in normoxia and to characterise the dynamic tissue response to arterial oxygen desaturations associated with upper airway occlusions in anaesthetised rats. Adult male Sprague-Dawley rats (n=7) were anaesthetised (urethane 1.5g/kg; 20% w/v; i.p.) and exposed to intermittent tracheal airway occlusion trials. Respiratory airflow and arterial blood pressure were measured. Arterial oxygen saturation (SaO2, %) was measured via a pulse oximetry (sensor STARR Life™) placed on the hind paw, whilst the sternohyoidPO2was measured using an oxygen sensorprobe (Oxford Optronix™) inserted directly into the sternohyoid muscle. Sternohyoid PO2 under normoxic conditions was 41±3 mmHg (mean ± SEM, n=7). SaO2 and PO2 were significantly positively correlated; Pearson correlation r=0.4350, p<0.0001, n=7. Upper airway occlusion led to significant decreases in sternohyoid muscle PO2 at all target SaO2 desaturations: 60%, 70% and 80%, 20±3 mmHg, 25±2 mmHg and 30±2 mmHg, respectively; p=0.0001; one-way ANOVA. There were differences in the temporal relationship comparing muscle PO2 and SaO2 responses with significantly slower latency to nadir and recovery consistently observed in muscle PO2 compared with SaO2. This is the first report of sternohyoid muscle PO2 during normoxia and hypoxia. We have demonstrated and quantified sternohyoid muscle hypoxia in response to arterial oxygen desaturations that are characteristic of animal models of intermittent hypoxia modelling human OSA. We reason that tissue hypoxia characterised in our study underpins functional plasticity reported in previous studies exploring the effects of intermittent hypoxia on upper airway muscle physiology. Extending our study to a chronic model of upper airway occlusion/intermittent hypoxia to characterise and quantify respiratory muscle PO2 may help inform studies exploring the mechanisms driving intermittent hypoxia-induced muscle remodelling.