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This study was designed to examine the effects of brief naps taken after lunch on alertness, performance, and autonomic balance. Three groups each comprising ten healthy subjects, who had slept normally at home the previous night, were randomly assigned to groups taking one of three 'lengths of nap (0, 15, and 45 min) after lunch. The P300, an event-related potential which is a neurophysiological correlate of cognitive function, subjective sleepiness (visual analogue scale), and electrocardiogram were measured before, 30 min after, and 3 h after the naps. Each measurement was followed by an English transcription task lasting 90 min. The P300 latency was significantly shorter after the 15-min than after the 45-min nap, or after no nap had been taken, while its amplitude was not affected by the length of nap. Subjective sleepiness was lower after both naps than after no nap. The task performance was significantly better during the second half of the last task session after the 15-min nap than after no nap. The high-frequency component of the R-R interval spectrum increased significantly during the 45-min nap, showing a temporary shift to a predominance of the parasympathetic nervous system. Mean total sleep times during the 15- and 45-min naps were 7.3 and 30.1 min, respectively. These results would indicate that the 15-min nap may serve to shorten the stimulus evaluation time, reducing subjective sleepiness, and slightly improving task performance. Our data demonstrated that in our subjects a brief nap after lunch was effective for enhancing subsequent alertness and performance after normal sleep the previous night.

The effects on sympathic-parasympathetic nervous system balance of single exposure and repeated exposures to a cognitively demanding task were examined by power spectrum analysis of cardiac R-R intervals. In the single task experiment, 32 healthy subjects engaged in a 90-min English language transcription task and in 90-min reading as a nontask control. In the repeated task experiment, 14 subjects experienced either intermittent exposure to the transcription task until late at night, or daytime exposure to the transcription task followed by relax wakefulness until sleep onset. The single task exposure significantly increased the normalized low frequency component (%LF; 0.05-0.15 Hz) of the R-R interval spectrum compared with the nontask control, but there was no significant task difference in the normalized high frequency component (0.15-0.50 Hz). The increased %LF values immediately returned to control levels after cessation of the task. Repeated exposure to the cognitive task until late at night produced a significantly greater %LF during the first nonrapid eye movement sleep period when compared to relaxed wakefulness. These results would suggest that a single exposure to a cognitive task may produce a shift to sympathetic nervous system dominance only during the period of the task, whereas repeated exposures to a cognitive task until late at night may produce a shift to sympathetic nervous system dominance which lasts into the subsequent sleep period.

The effects of a prolonged cognitive task prior to sleep onset on subsequent sleep patterns were examined in 14 healthy subjects who were randomly assigned to two conditions. Those assigned to a working condition were asked to engage in a prolonged cognitive task until close to bedtime (0200 hours), whereas those assigned to a relaxing condition were instructed to perform the same task during the daytime and then to stay awake in a relaxed state until the same bedtime as the work group. Visual scoring of sleep stages showed no significant differences in the amounts of stage 4 and slow wave sleep (stage 3+4) between the two conditions. Power spectrum analysis of sleep electroencephalogram (EEG) revealed that the EEG delta (0.5-4.0 Hz) power density in the first non-rapid eye movement (REM)-REM sleep cycle was significantly lower following the prolonged cognitive task prior to sleep onset than following the relaxed wakefulness and that the decreased EEG delta power density in the first sleep cycle was not compensated for during the later part of the sleep. These findings would indicate that the prolonged cognitive task prior to sleep onset may suppress EEG delta power density during subsequent sleep, suggesting that such a task may interfere with the development of deep non-REM sleep.