Rist K E, Daubenspeck J A, McGovern J F
Respir Physiol. 1986 Feb;63(2):241-56. doi: 10.1016/0034-5687(86)90117-9.
We observed that ventilation fell and end-tidal CO2 rose in the change from wakefulness to non-REM (NREM) sleep in 4 normal human subjects studied on two nights each. We hypothesized that the observed ventilatory depression was due to effects of sleep both upon the central respiratory neural output and upon the mechanical respiratory pump. Both the central controller response to CO2, as measured by diaphragmatic and intercostal EMG activity, and the ability of the respiratory pump in effecting ventilation in response to diaphragmatic or intercostal activation, as measured by the relationship between the EMG activities and minute ventilation, are reduced in NREM sleep. We describe a general method of apportioning the separate effects of sleep, or other factors, upon the central respiratory controller, the respiratory mechanical pump, and the metabolic rate, in determining the total observed increase in end-tidal CO2.