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Animal studies have demonstrated an increase in BP with repeated upper airway closure and intermittent hypoxia. 25–28 Studies of human subjects have demonstrated increased sympathetic activity and mean arterial BP in acute and chronic intermittent hypoxic conditions. 29–34 It is thought that hypoxia is the main stimulus for the increased sympathetic response seen in sleep apneics, but hypercapnia and the apnea itself are also implicated. 19, 35–37 Additionally, in subjects with OSA, repeated arousals from sleep at the end of disordered breathing events may contribute to persistent sympathetic overactivity and to the development of systemic hypertension over time. 38, 39

Higher sympathetic activity that is seen during sleep in subjects with OSA may eventually be noted during wakefulness as well. Cortical autonomic network gray matter changes relating directly to the intensity of sympathetic discharges during …