Neural-mechanical coupling of breathing in REM sleep.

During rapid-eye-movement (REM) sleep the ventilatory response to airway occlusion is reduced. Possible mechanisms are reduced chemosensitivity, mechanical impairment of the chest wall secondary to the atonia of REM sleep, or phasic REM events that interrupt or fractionate ongoing diaphragm electromyogram (EMG) activity. To differentiate between these possibilities, we studied three chronically instrumented dogs before, during, and after 15-20 s of airway occlusion during non-REM (NREM) and phasic REM sleep. We found that 1) for a given inspiratory time the integrated diaphragm EMG (Di) was similar or reduced in REM sleep relative to NREM sleep; 2) for a given Di in response to airway occlusion and the hyperpnea following occlusion, the mechanical output (flow or pressure) was similar or reduced during REM sleep relative to NREM sleep; 3) for comparable durations of airway occlusion the Di and integrated inspiratory tracheal pressure tended to be smaller and more variable in REM than in NREM sleep, and 4) significant fractionations (caused visible changes in tracheal pressure) of the diaphragm EMG during airway occlusion in REM sleep occurred in approximately 40% of breathing efforts. Thus reduced and/or erratic mechanical output during and after airway occlusion in REM sleep in terms of flow rate, tidal volume, and/or pressure generation is attributable largely to reduced neural activity of the diaphragm, which in turn is likely attributable to REM effects, causing reduced chemosensitivity at the level of the peripheral chemoreceptors or, more likely, at the central integrator. Chest wall distortion secondary to the atonia of REM sleep may contribute to the reduced mechanical output following airway occlusion when ventilatory drive is highest.