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1 Physiology, University of Otago, New Zealand
2 Peninsula Private Sleep Laboratory Sydney, Australia
3 Medicine, Institute of Medicine, Nepal
4 Medicine, University of Sydney, Australia
* To whom correspondence should be addressed. E-mail: philip.ainslie{at}stonebow.otago.ac.nz.
We tested the hypothesis that following exposure to high altitude (HA), cerebrovascular reactivity to CO2 and cerebral autoregulation (CA) would be attenuated. Such alterations may predispose to central sleep apnea (CSA) at HA by promoting changes in brain PCO2 and thus breathing stability. We measured middle cerebral artery blood flow velocity (MCAv) and arterial blood pressure (BP) during wakefulness in conditions of eucapnia (room air), hypocapnia (hyperventilation) and hypercapnia (isooxic rebeathing), and also during non-rapid eye movement (stage 2) sleep at low altitude (LA, 1400m) and at HA (3840m) in five individuals. At each altitude, sleep was studied using full polysomography, and resting arterial blood gases were obtained. During wakefulness, and polysomnographic-monitored sleep, dynamic CA and steady-state changes in MCAv in relation to changes in BP were evaluated using transfer function analysis. HA was associated with an increase in CSA apnea index (0.2±0.4 to 20.7±23.2 /h), and an increase in mean BP and cerebrovascular resistance during wakefulness and sleep. MCAv was unchanged during wakefulness whereas there was greater decrease during sleep at HA when compared with LA (-9.1±1.7 verses -4.8±0.7 cm/s, respectively; P<0.05). At HA, compared with LA, the cerebrovascular reactivity to CO2 in the hypercapnic range was unchanged, whilst it was lowered in the hypocapnic range (3.1±0.7 vs. 2.2±0.6 %/mm Hg: P<0.05). Further, dynamic CA was further reduced during sleep (P<0.05 vs. LA). A lowered cerebrovascular reactivity to CO2 and reduction in both dynamic CA and MCAv during sleep at HA may promote the pathogenesis of breathing instability.
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