While a propensity towards upper airway collapse, as seen in obesity, has classically been considered the principle determinate of OSA pathogenesis, more recent work has shown that non-anatomical variables including the ventilatory arousal threshold (ArTH) are also important. During wakefulness pharyngeal dilator muscles remain active to maintain airway patency however during sleep these muscles lose activity in all individuals but in those with OSA airway collapse occurs and results hypoxia and hypercapnia. Both accumulation of carbon dioxide and increased negative pressure can cause recruitment of the upper airway dilator muscles resulting in pharyngeal patency if sleep is maintained. Cortical arousal during apnea for most individuals represents a protective mechanism as the airway is restored with resolution of hypoxia and hypercarbia. However individuals with low ArTH (individuals who wake easily) do not have sufficient time for accumulation of respiratory stimuli, recruitment of pharyngeal muscles is then unable to occur which results in disruption of sleep. ArTH is variable amongst individuals and is dependent on the magnitude of negative intrathoracic pressure tolerated before awakening occurs and is independent from other factors.