This study investigated the effects of variations in sleep pressure on cardiac autonomic activity and body temperature. In a counterbalanced design, 12 healthy, young subjects (6 men and 6 women) remained recumbent during 30 h of wakefulness (high sleep pressure) and 6 h of wakefulness (low sleep pressure). Both periods of wakefulness were immediately followed by a sleep opportunity, and the first 2 h of sleep were analyzed. During extended hours of wakefulness, a reduction in heart rate was mediated by a decline in cardiac sympathetic activity (measured via preejection period) and the maintenance of cardiac parasympathetic activity (measured via respiratory sinus arrhythmia). In subsequent high-pressure sleep, parasympathetic activity was amplified and sympathetic activity was negatively associated with electroencephalographic slow-wave activity. Sleep deprivation had no impact on foot temperature, but it did alter the pattern of change in core body temperature. A downregulation of cardiac autonomic activity during both extended hours of wakefulness and subsequent sleep may respectively provide “protection” and “recovery” from the temporal extension of cardiac demand.

Melatonin increases sleepiness, decreases core temperature, and increases peripheral temperature in humans. Melatonin may produce these effects by activating peripheral receptors or altering autonomic activity. The latter hypothesis was investigated in 16 supine subjects. Three conditions were created by using bright light and exogenous melatonin: normal endogenous, suppressed, and pharmacological melatonin levels. Data during wakefulness from 1.5 h before to 2.5 h after each subject’s estimated melatonin onset (wake time + 14 h) were analyzed. Respiratory sinus arrhythmia (cardiac parasympathetic activity) and preejection period (cardiac sympathetic activity) did not vary among conditions. Pharmacological melatonin levels significantly decreased systolic blood pressure [5.75 ± 1.65 (SE) mmHg] but did not significantly change heart rate. Suppressed melatonin significantly increased rectal temperature (0.27 ± 0.06°C), decreased foot temperature (1.98 ± 0.70°C), and increased sleep onset latency (5.53 ± 1.87 min). Thus melatonin does not significantly alter cardiac autonomic activity and instead may bind to peripheral receptors in the vasculature and heart. Furthermore, increases in cardiac parasympathetic activity before normal nighttime sleep cannot be attributed to the concomitant increase in endogenous melatonin.

Objective: To compare noninvasive measures of cardiac autonomic activity during sleep. Methods: The absolute and normalized (n.u.) high and low frequency peaks from the spectral analysis of R-R intervals (HF, LF, HFn.u., LFn.u.), LF/HF ratio, pre-ejection period (PEP) from impedance cardiography, and the autocorrelation coefficient (rRR) as illustrated in Poincaré plots were measured during night-time sleep in 9 young healthy subjects. Heart rate and blood pressure were also recorded. Results: Heart rate was significantly associated with cardiac sympathetic activity (PEP, average r=−0.46), but not with cardiac parasympathetic activity (HF, average r=−0.17). rRR was significantly associated with heart rate (average r=0.41), and LF/HF (average r=0.69), but not with PEP or HF. From NREM to REM sleep, heart rate, LFn.u., LF and rRR significantly increased, HFn.u. significantly decreased, LF/HF showed an increasing trend (P=0.07) and PEP showed a decreasing trend (P=0.06). Blood pressure and HF were highly variable without significant changes from NREM to REM sleep. Conclusions: Cardiac parasympathetic activity (HF) does not vary greatly between sleep stages. Cardiac sympathetic activity (PEP) decreases linearly during sleep. rRR and LF/HF can track sympathovagal changes during sleep, but cannot differentiate between changes in cardiac parasympathetic and sympathetic activity. The relative advantages and disadvantages of the different measures are discussed.