Effect of different levels of hyperoxia on breathing in healthy subjects

Abstract

Becker, Heinrich F., Olli Polo, Stephen G. McNamara, Michael Berthon-Jones, and Colin E. Sullivan. Effect of different levels of hyperoxia on breathing in healthy subjects. J. Appl. Physiol. 81(4): 1683–1690, 1996.—We have recently shown that breathing 50% O2 markedly stimulates ventilation in healthy subjects if end-tidal [Formula: see text]([Formula: see text]) is maintained. The aim of this study was to investigate a possible dose-dependent stimulation of ventilation by O2 and to examine possible mechanisms of hyperoxic hyperventilation. In eight normal subjects ventilation was measured while they were breathing 30 and 75% O2 for 30 min, with[Formula: see text] being held constant. Acute hypercapnic ventilatory responses were also tested in these subjects. The 75% O2 experiment was repeated without controlling[Formula: see text] in 14 subjects, and in 6 subjects arterial blood gases were taken at baseline and at the end of the hyperoxia period. Minute ventilation (V˙i) increased by 21 and 115% with 30 and 75% isocapnic hyperoxia, respectively. The 75% O2 without any control on[Formula: see text] led to a 16% increase inV˙i, but[Formula: see text] decreased by 3.6 Torr (9%). There was a linear correlation ( r = 0.83) between the hypercapnic and the hyperoxic ventilatory response. In conclusion, isocapnic hyperoxia stimulates ventilation in a dose-dependent way, withV˙i more than doubling after 30 min of 75% O2. If isocapnia is not maintained, hyperventilation is attenuated by a decrease in arterial[Formula: see text]. There is a correlation between hyperoxic and hypercapnic ventilatory responses. On the basis of data from the literature, we concluded that the Haldane effect seems to be the major cause of hyperventilation during both isocapnic and poikilocapnic hyperoxia.