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Spontaneous movements in both stage 2 and REM steep are preceded by similar heart rate increase, beginning approximately 8 sec before onset the movement. It is suggested that the HR acceleration before spontaneous movement in sleep is not a gradual response to vascular congestion but, rather, may be triggered by internal arousal stimuli which, like movements, have sleep‐stage‐specific rules of occurrence.

Electrophysiological and self‐report data were obtained from 10 and 20 Ss, respectively, during 15 days of baseline, 30 days of 24‐hr per day exposure to a 660 msec, 3.5K Hz tone pulse with a 22 sec interstimulus interval (10 days each at 80, 85, and 90 dB), and during a 10‐day post‐exposure period. A self‐reported increase in difficulty falling asleep was not substantiated by objective sleep latency measures. Changes in total hours of sleep, number of awakenings, and percent time for sleep stages were of small magnitude and not consistently related to stimulus intensity. All 10 monitored Ss gave clear EEG and autonomic responses to the stimulus, with no evidence of response extinction over the 30‐day exposure period. There was no change in average all‐night heart rate. Total number of body movements during the night did not change. However, the movements that did occur, tended to be triggered by the stimulus, with most movements closely following the tone pulse. The youth and good health of the Ss, and the 24‐hr per day exposure, favoring rapid adaptation to the stimulus, are suggested to account for the lack of disruption of sleep.