Effect of exercise on cerebral perfusion in humans at high altitude
Imray CHE., Myers SD., Pattinson KTS., Bradwell AR., Chan CW., Harris S., Collins P., Wright AD.
<jats:p> 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 (rSo<jats:sub>2</jats:sub>%) increased during submaximal exercise from 68.4 (SD 2.1) to 70.9 (SD 3.8) ( P < 0.0001) and at maximal oxygen uptake (V̇o<jats:sub>2 max</jats:sub>) to 69.8 (SD 3.1) ( P < 0.02). In contrast, at each of the high altitudes studied, rSo<jats:sub>2</jats:sub> was reduced during submaximal exercise from 66.2 (SD 2.5) to 62.6 (SD 2.1) at 3,610 m ( P < 0.0001), 63.0 (SD 2.1) to 58.9 (SD 2.1) at 4,750 m ( P < 0.0001), and 62.4 (SD 3.6) to 61.2 (SD 3.9) at 5,260 m ( P < 0.01), and at V̇o<jats:sub>2 max</jats:sub> to 61.2 (SD 3.3) at 3,610 m ( P < 0.0001), to 59.4 (SD 2.6) at 4,750 m ( P < 0.0001), and to 58.0 (SD 3.0) at 5,260 m ( P < 0.0001). Cerebrovascular resistance tended to fall during submaximal exercise ( P = not significant) and rise at V̇o<jats:sub>2 max</jats:sub>, following the changes in arterial oxygen saturation and end-tidal CO<jats:sub>2</jats:sub>. Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at V̇o<jats:sub>2 max</jats:sub>, but at high altitude peaked at 30% of V̇o<jats:sub>2 max</jats:sub> and then fell progressively at higher levels of exercise. The fall in rSo<jats:sub>2</jats:sub> and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and high-altitude cerebral edema. </jats:p>