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1 Coventry & Watwickshire Vascular Unit, University Hospitals Coventry & Warwickshire NHS Trust, Coventry, West Midlands, United Kingdom
2 Qinetiq, Farnborough, Hampshire, United Kingdom
3 Nuffield Department of Anaesthetics, John Radcliffe Hospital, Headington, Oxford, United Kingdom
4 The Medical School, University of Birmingham, Birmingham, West Midlands, United Kingdom
5 ScanMed Medical Instruments, Moreton-in-the-Marsh, Gloucestershire, United Kingdom
* To whom correspondence should be addressed. E-mail: chrisimray{at}aol.com.
The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable, recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m mean (SD) cerebral oxygenation (rSO2 %) increased during submaximal exercise from 68.4 (2.1) to 70.9 (3.8) (P<0.0001) and at VO2max to 69.8 (3.1) (P<0.02). In contrast, at each of the high altitudes studied, rSO2 was reduced during submaximal exercise from 66.2 (2.5) to 62.6 (2.1) at 3,610 m (P< 0.0001), 63.0 (2.1) to 58.9 (2.1) at 4,750 m (P<0.0001) and 62.4 (3.6) to 61.2 (3.9) at 5,260 m (P< 0.01) and at VO2max to 61.2 (3.3) at 3,610 m (P< 0.0001), to 59.4 (2.6) at 4,750 m (P<0.0001) and to 58.0 (3.0) at 5,260 m (P<0.0001). Cerebrovascular resistance tended to fall during submaximal exercise (NS) and rise at VO2max, following the changes in arterial oxygen saturation and end-tidal CO2. Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a non-significant fall at VO2max, but at high altitude peaked at 30% of VO2max and then fell progressively at higher levels of exercise. The fall in rSO2 and oxygen delivery during exercise may limit exercise at altitude and are likely contribute to the problems of acute mountain sickness and high altitude cerebral edema.
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