
Obstructive sleep apnea (OSA) affects between 2% and 4% of the middle aged workforce ¹ and is characterized by repetitive collapse and partial closure of the upper airway during sleep. These respiratory disturbances occur as ‘awake’ muscle tone is withdrawn from pharyngeal dilator muscles, usually as sleep develops from awake towards stage two. Each event is associated with a period of hypoxia and hypercapnia which the patient opposes with increasing inspiratory efforts until the episode is terminated by an arousal from sleep, the return of wakefulness related muscle tone, and finally re-establishment of upper airway patency. This results in sleep fragmentation and daytime sleepiness, although evidence also suggests an increased risk for cardiovascular disease ² and metabolic dysregulation ³, although the mechanisms for these latter associations remain unclear.