SLEEP-RELATED CHANGES IN HUMAN MUSCLE AND SKIN SYMPATHETIC-NERVE ACTIVITIES

To characterize the features of sympathetic nerve activity during non-REM sleep, we measured the muscle and skin sympathetic nerve activities (MSNA and SSNA, respectively) using a double recording microneurographic technique. Eight healthy volunteers were monitored by polysomnography (including EEG, EGG, EMG, and ECG) and received acoustic stimuli (880 Hz, 125 ms) during sleep stage 2. The specific discharge properties of MSNA during wakefulness included pulse-synchronicity, short burst duration and a non-responsiveness to arousal stimuli. These were considered to be generated by an inhibitory input from the baroreceptors to the cardiovascular center. In contrast, SSNA lacked pulse-synchronicity, had longer bursts, and was responsive to a variety of stimuli. Burst rates of MSNA and SSNA were reduced during sleep stages 1 and 2 (light sleep) us. during a wakefulness. Both MSNA and SSNA appeared to be related to spontaneously occurring K-complexes. The baroreflex latency (from the ECG R-wave to the integrated MSNA burst peak) was constant at approximately 1.20 s during sleep, suggesting that pulse-synchronicity was maintained. The MSNA burst evolution time (interval between initiation of the burst and its peak) became longer with a transition to deeper non-REM sleep stages, whereas the SSNA burst evolution times remained constant. K-complexes induced by acoustic stimuli were frequently accompanied by MSNA and/or SSNA. MSNA responded to acoustic stimuli during light sleep, but some bursts lacked a close relation in time to cardiac rhythm. We concluded that: (1) both SSNA and MSNA were centrally suppressed during light sleep; (2) MSNA, SSNA, or both MSNA and SSNA, frequently accompanied spontaneous and arousal stimuli-induced K-complexes; (3) The burst properties of MSNA resembled those of SSNA during light sleep; and (4) SSNA and MSNA may share a common origin in the central nervous system.