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1 Physiology & Biophysics, University of Calgary, Calgary, Alberta, Canada
2 Physiology & Biophysics, University of Calgary, Calgary, Alberta, Canada; Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada; Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada
* To whom correspondence should be addressed. E-mail: poulin{at}ucalgary.ca.
This study examined the effect of high, normal and uncontrolled end-tidal PCO2 (PETCO2) on the ventilatory, peak middle cerebral artery blood flow velocity (VP) and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, 3 hypoxic protocols (PETO2 was held at 8 steps between 300-45 Torr) in conditions of hypercapnia, isocapnia or poikilocapnia (PETCO2 +7.5, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure VP. The slopes of the linear regressions of ventilation, VP, and MAP with SaO2 were significantly greater in hypercapnia than in both isocapnia and poikilocapnic (P < 0.05). Strong significant correlations were observed between ventilation, VP and MAP with each PETCO2 condition. These data suggest: 1) a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses (AHRCBF) during poikilocapnic hypoxia, due to hypocapnic-incuded cerebral vasoconstriction; 2) in hypercapnic hypoxia, a high AHVR is associated with a high AHRCBF demonstrating linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of PETCO2 and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in VP and MAP responses to hypoxia. Individuals with a high AHVR are also found to have high VP and MAP responses to hypoxia.
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