Abstract

The aim of the present study was to test the hypothesis that afferent mechanoreceptor stimuli from the respiratory muscles contribute to the arousal response to CO2 from both non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. We studied three dogs implanted with electromyographic (EMG) electrodes in the costal diaphragm and transversus abdominis muscles. During sleep, the animals were exposed to supplemental CO2 in O2 to maintain a constant level of end-tidal PCO2 (50 Torr for NREM, 56 Torr for REM) and breathed either spontaneously (SB) or with inspiratory pressure support (IPS). The arousal response was quantified as the time from initiation of CO2 administration to arousal. EMG activity of the costal diaphragm on IPS was decreased to approximately 70% (P < 0.01) of that during SB trials for both NREM and REM, whereas EMG activity of the transversus abdominis muscles did not differ between SB and IPS for either sleep state. The mean time to arousal was increased during NREM from 128.3 +/- 24.7 s (SB) to 216.8 +/- 38.7 s (IPS) (P < 0.025) and was increased during REM from 144.9 +/- 26.1 s (SB) to 219.0 +/- 23.8 s (IPS) (P < 0.001). In summary, in support of our hypothesis, we found that suppression of inspiratory muscle activity, without augmented expiratory muscle activity, delayed the arousal response to hypercapnia during both NREM and REM sleep.

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