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1 Zoology, University of Latrobe, Melbourne, Australia
2 Physiology, University of Otago, Dunedin, New Zealand
3 Physiology, University of Otago, New Zealand
* To whom correspondence should be addressed. E-mail: philip.ainslie{at}stonebow.otago.ac.nz.
We hypothesised that in healthy subjects without pharmacological intervention, an overnight reduction in cerebrovascular CO2 reactivity would be associated with an elevated hypercapnic ventilatory (VE) responsiveness and a reduction in cerebral oxygenation. In 20 healthy male individuals with no sleep-related disorders, continuous recordings of blood velocity in the middle cerebral artery (MCAv), arterial blood pressure, VE, end-tidal gases and frontal cortical oxygenation using near infrared spectroscopy were monitored during hypercapnia (inspired CO2, 5%), hypoxia [arterial O2 saturation (SaO2) ~84%], and during a 20-s breath-hold to investigate the related responses to hypercapnia, hypoxia and apnea, respectively. Measurements were conducted in the evening (6-8PM) and in the early morning (6-8AM). From evening to morning, the cerebrovascular reactivity to hypercapnia was reduced [5.3±0.6 vs. 4.6±1.1 (%/Torr); P<0.05], and was associated with a reduced increase in cerebral oxygenation (r=0.39; P<0.05) and an elevated morning hypercapnic VE response (r=0.54; P<0.05). Whilst there were no overnight changes in cerebrovascular reactivity or VE response to hypoxia, there was greater cerebral desaturation for a given SaO2 in the morning (AM; -0.45±0.14 vs. PM; -0.35±0.14 %/ SaO2; P<0.05). Following the 20-s breath-hold, in morning, there was a smaller surge MCAv and cerebral oxygenation (P<0.05 vs. PM). These data indicate that normal diurnal changes in the cerebrovascular response to CO2 influence the hypercapnic ventilatory response as well as the level of cerebral oxygenation during changes in arterial PCO2; this may be a contributing factor for diurnal changes in breathing stability and the high incidence of stroke in the morning.
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