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.

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.

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.