EXTENDED MODELS OF THE VENTILATORY RESPONSE TO SUSTAINED ISOCAPNIC HYPOXIA IN HUMANS

The purpose of this study was to examine extensions of a model of hypo xic ventilatory decline (HVD) in humans. In the original model (model I) devised by Il. Painter, S. Khamnei, and P. Robbins (J. Appl. Physio l. 74: 2007-2015, 1993), HVD is modeled entirely by a modulation of pe ripheral chemoreflex sensitivity. In the first extension (model II), a more complicated dynamic is used for the change in peripheral chemore flex sensitivity. In the second extension (model III), HVD is modeled as a combination of both the mechanism of Painter et al. and a compone nt that is independent of peripheral chemoreflex sensitivity. In all c ases, a parallel noise structure was incorporated to describe the stoc hastic properties of the ventilatory behavior to remove the correlatio n 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. Physio l. 88: 299-312, 1992). For model II, there was a significant improveme nt in fit for two out of six subjects. The reasons for this were not e ntirely 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 h ypoxia. In these two subjects, the chemoreflex-independent component c ontributed similar to 50% to total HVD. In the other four subjects, th e chemoreflex-independent component contributed similar to 10% to tota l HVD. It is concluded that in some subjects, but not in others, there may be a component of HVD that is independent of peripheral chemorefl ex sensitivity.