In this study characteristics of cardiac functioning were investigated in nine subjects during their nocturnal sleep. The pre-ejection period and the high frequency component of heart rate variability were used as indices of cardiac sympathetic and parasympathetic activity of the autonomic nervous system respectively. Heart rate and the autonomic indices were assessed across physiological determined sleep stages and consecutive temporal sleep cycles. Repeated measures ANOVA analyses indicated a significant pattern of heart rate as a function of sleep stages, which was mirrored by parasympathetic activity. Further, a significant decrease of heart rate as a function of sleep cycles was mirrored by an increase of sympathetic activity. Moreover, non-REM/REM differences revealed a dominant role of parasympathetic activity during sleep stages as well as sleep cycles. These findings demonstrate that sympathetic activity is influenced by time asleep, whereas parasympathetic activity is influenced by the depth of sleep.

The role of endogenous circadian rhythmicity in autonomic cardiac reactivity to different stressors was investigated. A constant routine protocol was used with repeated exposure to a dual task and a cold pressor test. The 29 subjects were randomly divided into two groups in order to manipulate prior wakefulness. Group 1 started at 09:00 h immediately after a monitored sleep period, whereas group 2 started 12 h later. Measures of interbeat intervals (IBI), respiratory sinus arrythmia (RSA, a measure of parasympathetic activity), pre-ejection period (PEP, a measure of sympathetic activity), as well as core body temperature (CBT) were recorded continuously. Multilevel regression analyses (across-subjects) revealed significant (mainly 24 h) sinusoidal circadian variation in the response to both stressors for IBI and RSA, but not for PEP. Individual 24 + 12 h cosine fits demonstrated a relatively large interindividual variation of the phases of the IBI and RSA rhythms, as compared to that of the CBT rhythm. Sinusoidal by group interactions were found for IBI and PEP, but not for RSA. These findings were interpreted as an indication for endogenous circadian and exogenous parasympathetic (vagal) modulation of cardiac reactivity, while sympathetic reactivity is relatively unaffected by the endogenous circadian drive and mainly influenced by exogenous factors.

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.