Obstructive sleep apnoea is a common condition associated with significant morbidity and increased mortality. During sleep, the sub atmospheric pressure developed in the extra thoracic airway by the contraction of the thoracic pump muscles during inspiration causes collapse of the compliant upper airway, resulting in an episode of apnoea. Normally, upper airway collapse is prevented by contraction of upper airway muscles and if the airway does collapse, it is re-opened by a reflex augmented neural drive and greater contraction of these muscles. Therefore, the function of these muscles plays a critical role in the pathogenesis of the obstructive sleep apnoea. The multiple episodes of apnoea that occur during the course of sleep cause intermittent hypoxia. We have proposed that chronic intermittent hypoxia causes adverse changes in structure and function of upper airway muscle that result in an exacerbation of the condition. We have shown that chronic intermittent hypoxia in rats causes greater fatigability of upper airway, diaphragm and limb muscles. In general, this appears to be true also for chronic continuous hypoxia, although the diaphragm muscle is relatively tolerant of sustained hypoxia compared to limb muscle. We propose that the chronic intermittent hypoxia of obstructive sleep apnoea causes a positive feedback that exacerbates the condition by reducing upper airway muscle endurance, thus making the upper airway more vulnerable to collapse. This effect involves the generation of reactive oxygen species and treatment with antioxidants either prevents or ameliorates the adverse effects on muscle function, suggesting that antioxidants could be used as an adjunct therapy for obstructive sleep apnoea. This may be true also for respiratory disease in general since chronic continuous hypoxia is also associated with increased muscle fatigue.
Last date updated on June, 2014