To investigate the role of the circadian pacemaker in autonomic modulation of base rate cardiac activity, 29 healthy subjects participated in a constant routine protocol. They were randomly divided into two groups in order to manipulate prior wakefulness. Group 1 started at 0900 hours immediately after a monitored sleep period, while group 2 started 12 h later. Measures of interbeat intervals (IBIs), respiratory sinus arrhythmia (RSA, an estimate of parasympathetic activity), pre-ejection period (PEP, an estimate of sympathetic activity), and core body temperature (CBT) were recorded continuously. Multilevel regression analyses (across-subjects) revealed significant 24- and/or 12-h sinusoidal circadian variation for CBT, IBI, and RSA, but not for PEP. Subject-specific 24+12 h sinusoidal fits demonstrated a convergence of phase distribution for IBI and RSA of group 1 similar to CBT, while PEP showed a relatively large (i.e. random) distribution of phase. In group 2, all cardiac measures showed large distributions of phase. Unexpected results in the cardiac measures were found in group 2, probably caused by group differences in prior activation. Also, effects of sleep deprivation were observed for IBI and RSA in group 2. Consequently, all cardiac measures revealed significant sinusoidal x group interactions, a result not shown in CBT. These findings were interpreted as an indication for circadian endogenous parasympathetic modulation of cardiac activity that is mainly confounded by prior wakefulness that extends 24 h, while the sympathetic modulation is relatively uncoupled from the endogenous circadian drive and mainly influenced by prior activation.

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.

Time course in task performance has been studied extensively. In particular, the investigation of circadian rhythmicity in task performance that varied in complexity. However, these studies disclosed heterogeneous outcomes. This could be the result of confounding exogenous factors, the use of diverse tasks, as well as accumulating sleepiness interfering with the underlying circadian drive. The present study varied task demands systematically within a single task and a dual task, using a constant routine protocol to examine the unmasked influence of the endogenous circadian oscillator on the periodicity of performance. Moreover, the subjects were divided into an early-start and a late-start group to estimate the potential interaction of circadian rhythmicity with the duration of prior wakefulness. The results revealed a distinct congruence in the circadian rhythms of all performance measures, with which prior wakefulness (< 40 h) did not interact. Also, single-task as well as dual-task complexity did not interfere with circadian rhythmicity. In conclusion, when sufficiently controlled for masking exogenous factors, task complexity is removed from the underlying circadian rhythms.

To investigate the role of the circadian pacemaker in cortisol reactivity to a cold pressor challenge, 26 diurnally subjects participated in a constant-routine protocol and were divided into two groups. Group 1 started immediately after a monitored sleep period at 09:00 h, while group 2 started 12 h later. After 2 h of adaptation, a cold pressor test was presented every 3 h. The cortisol response was assessed by means of saliva samples that were taken before and after the test. The pretest samples were considered to be base-rate measures and base-rate values as subtracted from post-test values were considered as reactivity measures. Both measures showed distinct Time-of-Day variations (respectively: F(7,168) = 16.92, p < 0.001, epsilon = 0.383; and F(7,175) = 8.01, p < 0.001, epsilon = 0.523). These findings are interpreted as evidence for the existence of an endogenous circadian periodicity underlying the sensitivity of the hypothalamus-pituitary-adrenal (HPA)-axis to acute stress.

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