Abstract
Recurrent apneas associated with sleep-disordered breathing increase sympathetic nerve activity and arterial blood pressure, and enhance sympathetic and ventilatory responses to acute hypoxia [14, 19]. Chronic intermittent hypoxia (CIH) and activation of arterial carotid body chemoreceptors are primarily responsible for driving the increase in sympathetic activity [4, 17]. The excessive sympathetic activity and hypertension are sustained and contribute to high morbidity and mortality in afflicted patients [15, 19]. Certain recreational and vocational activities involve episodes of volitional apnea. One example is underwater breath-hold diving. In this issue of Clinical Autonomic Research, Breskovic and colleagues [1] address the question: Do elite breath-hold divers exhibit exaggerated increases in muscle sympathetic nerve activity (MSNA) and ventilation during exposure to acute hypoxia? Such a finding would raise concern that the CIH imposed by these types of activities may increase cardiovascular risk in otherwise healthy individuals. The investigators measured arterial oxygen saturation, ventilation, MSNA, blood pressure, heart rate and stroke volume in elite divers and healthy control subjects at baseline (while breathing room air) and during progressive isocapnic hypoxia [1]. Resting blood pressure and MSNA were not significantly different in divers versus control subjects. Furthermore, hypoxia-induced increases in ventilation and MSNA were also not different between the groups. While good news for the divers, these negative results raise several important questions.
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