Once ventilatory acclimatization begins in sea level residents sojourning at high altitude, abrupt restoration of normal oxygen tensions will not restore ventilation to normal. We have investigated the role of cerebrospinal fluid (CSF) [H+] in this sustained hyperventilation by measuring CSF acid-base status in seven men (lumbar) and five ponies (cisternal) in normoxia, first at sea level and then periodically over 13-24 h of “deacclimatization” after 3-5 d in hypoxia (PB = 440 mm Hg). After 1 h deacclimatization, hyperventilation continued at a level only slightly less than that obtained in chronic hypoxia (+1−2 mm Hg PaCO2), whereas CSF pH was either equal (in man) or alkaline (in pony, +0.02, P < 0.01) to sea level values. Between 1 and 12-13 h deacclimatization in all humans and ponies Va fell progressively (PaCO2 increased 4-7 mm Hg) and CSF pH became increasingly more acid (−0.02 to −0.05, P < 0.01). Between 12 and 24 h of normoxic deacclimatization in ponies, PaCO2 rose further toward normal, coincident with an increasing acidity in CSF (−0.02 pH). Similar negative correlations were found between changes in arterial pH and Va throughout normoxic deacclimatization. We conclude that [H+] in the lumbar or cisternal CSF is not the mediator of the continued hyperventilation and its gradual dissipation with time during normoxic deacclimatization from chronic hypoxia. These negative relationships of Va to CSF [H+] in normoxia are analogous to those previously shown during acclimatization to hypoxia.
J. A. Dempsey, H. V. Forster, G. E. Bisgard, L. W. Chosy, P. G. Hanson, A. L. Kiorpes, D. A. Pelligrino