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J Appl Physiol 89: 291-296, 2000;
8750-7587/00 $5.00
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Vol. 89, Issue 1, 291-296, July 2000

Peripheral chemoreflex function in hyperoxia following ventilatory acclimatization to altitude

Michala E. F. Pedersen1, Paul Robach2, Jean-Paul Richalet3, and Peter A. Robbins1

1 University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, United Kingdom; 2 Ecole National de Ski et d'Alpinisme, 74401 Chamonix cedex; and 3 Association pour la Recherche en Physiologie de l'Environnement, Laboratoire Réponses Cellulaires et Fonctionelles à l'Hypoxie, Université Paris XIII, 93017 Bobigny cedex, France

After a period of ventilatory acclimatization to high altitude (VAH), a degree of hyperventilation persists after relief of the hypoxic stimulus. This is likely, in part, to reflect the altered acid-base status, but it may also arise, in part, from the development during VAH of a component of carotid body (CB) activity that cannot be entirely suppressed by hyperoxia. To test this hypothesis, eight volunteers undergoing a simulated ascent of Mount Everest in a hypobaric chamber were acutely exposed to 30 min of hyperoxia at various stages of acclimatization. For the second 10 min of this exposure, the subjects were given an infusion of the CB inhibitor, dopamine (3 µg · kg-1 · min-1). Although there was both a significant rise in ventilation (P < 0.001) and a fall in end-tidal PCO2 (P < 0.001) with VAH, there was no progressive effect of dopamine infusion on these variables with VAH. These results do not support a role for CB in generating the persistent hyperventilation that remains in hyperoxia after VAH.

hypobaric hypoxia; dopamine; carotid body; human


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