NEURAL-MECHANICAL COUPLING OF BREATHING IN REM-SLEEP

During rapid-eye-movement (REM) sleep the ventilatory response to airw ay occlusion is reduced. Possible mechanisms are reduced chemosensitiv ity, mechanical impairment of the chest wall secondary to the atonia o f REM sleep, or phasic REM events that interrupt or fraction ate ongoi ng diaphragm electromyogram (EMG) activity. To differentiate between t hese possibilities, we studied three chronically instrumented dogs bef ore, during, and after 15-20 s of airway occlusion during non-REM (NRE M) and phasic REM sleep. We found that 1) for a given inspiratory time the integrated diaphragm EMG (integral Di) was similar or reduced in REM sleep relative to NREM sleep; 2) for a given integral Di in respon se to airway occlusion and the hyperpnea following occlusion, the mech anical output (flow or pressure) was similar or reduced during REM sle ep relative to NREM sleep; 3) for comparable durations of airway occlu sion the integral Di and integrated inspiratory tracheal pressure tend ed to be smaller and more variable in REM than in NREM sleep, and 4) s ignificant fractionations (caused visible changes in tracheal pressure ) of the diaphragm EMG during airway occlusion in REM sleep occurred i n similar to 40% of breathing efforts. Thus reduced and/or erratic mec hanical output during and after airway occlusion in REM sleep in terms of flow rate, tidal volume, and/or pressure generation is attributabl e largely to reduced neural activity of the diaphragm, which in turn i s 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 ai rway occlusion when ventilatory drive is highest.