Effects of slow wave sleep on ventilatory compensation to inspiratory elastic loading.
We determined the effects of slow wave sleep on ventilatory compensation to inspiratory elastic loads (18 cm H2O/L). Multiple loading trials of variable duration were applied in three healthy adult humans in wakefulness and during NREM sleep. During wakefulness, ventilatory response over 5 loaded breaths were highly variable. Tidal volume (VT), mean inspiratory flow (VT/TI), and minute ventilation (VE) were preserved or increased in 2 of the 3 subjects in whom mouth occlusion pressure (P0.1) was augmented in the immediate (second breath) response to the load. In the third subject who showed no change in P0.1, VE was not preserved during loading. During NREM sleep, the loading response was highly consistent in all trials and in all 3 subjects. P0.1 on the second loaded breath was not increased; thus VE, VT and VT/TI were reduced over five loaded breaths. This absence of immediate load compensation during NREM sleep was similar during normoxia, hyperoxia, and hypercapnia. During sustained loading in NREM sleep VE and VT returned toward control levels coincident with an increase in end tidal CO2. We conclude that augmentation of inspiratory neural drive sufficient for immediate compensation to elastic loads requires wakefulness. Compensatory responses to loading do not occur during NREM sleep until inspiratory effort is augmented by chemical stimuli.
D000328:Adult; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D008297:Male; D010100:Oxygen / Q000494:pharmacology; D012119:Respiration; D012890:Sleep / Q000502:physiology*; D013990:Tidal Volume; D014851:Wakefulness / Q000502:physiology
D010100:Oxygen