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.

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.