Obstructive sleep apnoea (OSA) is a common disorder characterised by repeated occlusions of the upper airway during sleep. Upper airway muscle dysfunction is implicated in the pathophysiology of OSA. We have shown that intermittent hypoxia – a feature of OSA due to recurrent apnoea – impairs respiratory muscle function. In this study, we tested the hypothesis that antioxidant treatment following chronic IH exposure would improve muscle function in our rat model of OSA. 15 adult male Wistar rats were placed in chambers and exposed to alternating periods (90s) of normoxia and hypoxia. Control rats (n=15) were placed in identical chambers and were exposed to an air/air cycle continuously under identical conditions in paired studies. Exposures lasted 8 hours per day for 9 days. Following the treatments, animals were killed humanely. The paired sternohyoid muscles were dissected out and prepared for in vitro examination. Isometric contractile properties of isolated strips of sternohyoid muscle were examined in tissue baths under hyperoxic (95%O₂/5%CO₂) or hypoxic (95%N₂/5%CO₂) conditions in the absence (control) or presence of the superoxide dismutase (SOD) mimetic, Tempol (10mM). Specific force was measured in response to stimulus frequencies ranging from 10-100Hz. Under in vitro hyperoxic conditions, IH caused a reduction in force at 60 to 100Hz [Peak tetanic force at 100Hz was 22.7±0.8 vs. 15.9±0.9* N/cm², control (n=8) vs. IH (n=8), *P<0.001 ANOVA]. Tempol had a positive inotropic effect at high stimulus frequencies in both normoxic and IH-treated rats [Force at 100Hz in hyperoxia was 26.4±1.0 and 22.8±1.4 N/cm², control+tempol (n=7) and IH+tempol (n=7); both significantly different from their respective controls, ANOVA. The relative increase in force was greater in the IH-treated rats compared to normoxia. Under in vitro hypoxic conditions, forces were significantly lower than hyperoxic values but there was no difference between normoxia and IH-treated rats. This study illustrates that chronic IH decreases force production of rat sternohyoid muscle but has no effect on force generation during in vitro hypoxia. Furthermore, Tempol has a positive inotropic effect on sternohyoid muscle in both groups, but the relative increase in force was greater in IH-treated animals with a recovery of force to control values. We conclude that chronic IH causes maladaptive plasticity in a pharyngeal dilator muscle and as such may be implicated in the pathophysiology of OSA. We conclude that antioxidants may be beneficial as adjunct therapies in the treatment of OSA.