STUDY OBJECTIVES: Recent work indicates that cardiac sympathetic activity is not influenced by the circadian system and instead decreases after sleep onset. However, little is known about the pattern of change in cardiac sympathetic activity during NREM/REM sleep cycles and whether this is associated with alterations in slow-wave activity (SWA). To address these questions, we examined SWA, cardiac sympathetic activity, heart rate and rectal and foot temperatures during the first three NREM/REM sleep cycles and during transitions between NREM and REM sleep.
DESIGN: Subjects were required to maintain a constant sleep-wake cycle for at least a week and have at least one adaptation night, before their night of recording.
SETTING: Individual temperature controlled bedrooms.
PARTICIPANTS: 10 young healthy males and females.
INTERVENTIONS: NA.
MEASUREMENTS AND RESULTS: All variables showed the greatest change in the first NREM cycle. Specifically, SWA, sympathetic activity, heart rate and foot temperature increased while rectal temperature decreased. After the initial increase, cardiac sympathetic activity decreased across the sleep phase, in association with a decrease in heart rate. Cardiac sympathetic activity did not significantly alter across NREM-REM cycles.
CONCLUSIONS: The results suggest that increases in heart rate and cardiac sympathetic activity early in the sleep period are, in part, a compensatory reaction to the concomitant thermoregulatory changes observed. These results also indicate that the effect of time asleep on cardiac sympathetic activity may be greater than the influence of sleep cycles. These results are discussed with reference to the recuperative value of naps.

Melatonin has a functional role in the nocturnal regulation of sleep and thermoregulation. In addition to its action on peripheral receptors, melatonin may act by altering autonomic activity. To determine the effect of melatonin on cardiac autonomic activity, 5 mg of melatonin or placebo was orally administered to 12 young subjects at 14:00 hr, in a repeated measures design. Melatonin decreased sleep onset latency to Stage 2 sleep by 4.92+/-1.81 min (measured by Multiple Sleep Latency Tests), rectal temperature by 0.19+/-0.05 degrees C, and increased foot temperature by 0.74+/-0.45 degrees C (all P<0.05). Melatonin decreased heart rate by 3.66+/-1.68 beats/min (P<0.05) and pre-ejection period (measure of cardiac sympathetic activity) by 16.48+/-4.28 ms (P<0.05), but had no effect on respiratory sinus arrhythmia (measure of cardiac parasympathetic activity) (P>0.05). As the decrease in pre-ejection period is likely to have resulted from a decrease in blood pressure, these results do not confirm an effect of melatonin on cardiac sympathetic activity. However, the results do clearly indicate that melatonin is unlikely to drive the previously observed presleep increase in cardiac parasympathetic activity.

STUDY OBJECTIVES: It has been hypothesized that general hyperarousal, present during both sleep and wakefulness, may underlie chronic insomnia. The present study explored, under strictly controlled conditions, whether chronic insomnia is associated with altered physiologic markers of arousal, both in absolute levels and in terms of circadian rhythmicity, relative to controls.
DESIGN: A 24-hour constant-routine protocol was implemented to assess physiologic measures.
SETTING: The study was conducted in an isolated, temperature- and light-controlled, sound-attenuated sleep laboratory.
PARTICIPANTS: Eleven subjects with clinically diagnosed chronic insomnia were compared with 13 healthy matched controls.
INTERVENTIONS: The subjects underwent physiologic parameter recordings and cognitive performance testing during 24 hours of total sleep deprivation under strictly controlled circumstances.
MEASUREMENTS AND RESULTS: Cardiovascular parameters, free cortisol, and body temperature were subjected to mixed-model analysis of variance and mixed-model harmonic regression. Overall, no differences were found in either the absolute level or the circadian parameters (amplitude, phase) of these variables between the insomniacs and the control subjects.
CONCLUSIONS: Although physiologic indexes of arousal were slightly elevated in the insomnia group relative to the controls, the differences between the groups were not statistically significant. This could have been due to a lack of statistical power or could reflect the actual absence of arousal in our sample of chronic insomniacs. Systematic interindividual level differences overwhelmed any differences between the 2 groups, making it unlikely that general hyperarousal was a critical underlying factor in our sample. Earlier findings of hyperarousal in insomnia during studies that allowed sleep may have been specifically related to the sleep state.