Figure 5. Previous and revised models to explain the transient hyperpnoea at wake onset from sleep.

A, previous model used to explain the surge in ventilation upon awakening from sleep and revisions based on the results of the present study. Points a and b indicate the changes in P_a,CO2 and ventilation between wakefulness and non-REM sleep, respectively, and the dashed and continuous lines represent the ventilatory responses to CO₂ in these two states. Upon awakening from sleep (at point b), the prevailing P_a,CO2 is initially hypercapnic for the levels normally encountered in wakefulness, and this discrepancy drives ventilation in accordance with the waking hypercapnic ventilatory response (point c). The results of the present study show that this sleeping CO₂ level actually contributes < 50 % of the total ventilation elicited at wake onset from sleep (point d). B and C show alternative, but not mutually exclusive, conceptual models further illustrating the modifications to the current model to explain the transient hyperpnoea at awakening from sleep. In B, it is the difference in physiological control mechanisms between sleep and wakefulness, with an inappropriate level of CO₂ at wake onset that produces the surge in ventilation at wake onset. In this scheme, the stimulatory effect of wakefulness (i.e. the wakefulness stimulus) is the same at wake onset compared with subsequent wakefulness. In C, it is the property of the awake state at wake onset that importantly contributes to respiratory activation by providing a transiently increased wakefulness stimulus. See text for further discussion. The magnitude and time constant of the depicted changes are arbitrary, and were chosen simply to highlight the differences between the two models.