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University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, United Kingdom
Received 11 October 1995; accepted in final form 24 September 1996.
Liang, Pei-Ji, Daphne A. Bascom, and Peter A. Robbins.
Extended models of the ventilatory response to sustained isocapnic hypoxia in humans. J. Appl. Physiol. 82(2): 667-677, 1997.
The purpose of this study was to examine extensions of a model
of hypoxic ventilatory decline (HVD) in humans. In the original model (model I) devised by R. Painter, S. Khamnei, and P. Robbins
(J. Appl. Physiol. 74: 2007-2015, 1993), HVD is modeled
entirely by a modulation of peripheral chemoreflex sensitivity. In the
first extension (model II), a more complicated dynamic is used
for the change in peripheral chemoreflex sensitivity. In the second
extension (model III), HVD is modeled as a combination of
both the mechanism of Painter et al. and a component that is
independent of peripheral chemoreflex sensitivity. In all cases, a
parallel noise structure was incorporated to describe the stochastic
properties of the ventilatory behavior to remove the correlation of the
residuals. Data came from six subjects from a study by D. A. Bascom, J. J. Pandit, I. D. Clement, and P. A. Robbins (Respir. Physiol.
88: 299-312, 1992). For model II, there was a significant
improvement in fit for two out of six subjects. The reasons for this
were not entirely clear. For model III, the fit was again
significantly improved in two subjects, but in this case the subjects
were those who had the most marked undershoot and recovery of
ventilation at the relief of hypoxia. In these two subjects, the
chemoreflex-independent component contributed ~50% to total HVD.
In the other four subjects, the chemoreflex-independent component
contributed ~10% to total HVD. It is concluded that in some
subjects, but not in others, there may be a component of HVD that
is independent of peripheral chemoreflex sensitivity.
sustained isocapnic hypoxia; hypoxic ventilatory decline; peripheral chemoreflex sensitivity
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