Endogenous circadian rhythm in human motor activity uncoupled from circadian influences on cardiac dynamics

Abstract

The endogenous circadian pacemaker influences key physiologic functions, such as body temperature and heart rate, and is normally synchronized with the sleep/wake cycle. Epidemiological studies demonstrate a 24-h pattern in adverse cardiovascular events with a peak at Ϸ10 a.m. It is unknown whether this pattern in cardiac risk is caused by a day/night pattern of behaviors, including activity level and/or influences from the internal circadian pacemaker. We recently found that a scaling index of cardiac vulnerability has an endogenous circadian peak at the circadian phase corresponding to Ϸ10 a.m., which conceivably could contribute to the morning peak in cardiac risk. Here, we test whether this endogenous circadian influence on cardiac dynamics is caused by circadian-mediated changes in motor activity or whether activity and heart rate dynamics are decoupled across the circadian cycle. We analyze high-frequency recordings of motion from young healthy subjects during two complementary protocols that decouple the sleep/wake cycle from the circadian cycle while controlling scheduled behaviors. We find that static activity properties (mean and standard deviation) exhibit significant circadian rhythms with a peak at the circadian phase corresponding to 5-9 p.m. (Ϸ9 h later than the peak in the scale-invariant index of heartbeat fluctuations). In contrast, dynamic characteristics of the temporal scale-invariant organization of activity fluctuations (long-range correlations) do not exhibit a circadian rhythm. These findings suggest that endogenous circadian-mediated activity variations are not responsible for the endogenous circadian rhythm in the scale-invariant structure of heartbeat fluctuations and likely do not contribute to the increase in cardiac risk at Ϸ10 a.m.cardiac vulnerability ͉ circadian pacemaker ͉ locomotor activity ͉ scale invariance E pidemiological studies demonstrate that myocardial infarction (1-4), stroke (5, 6), and sudden cardiac death (7) have a 24-h daily pattern with a broad peak at 9-11 a.m. This 24-h pattern is widely assumed to be due to day/night patterns in behaviors that affect cardiovascular variables, such as autonomic balance, blood pressure, and platelet aggregability, in vulnerable individuals (8). However, endogenous influences from the circadian pacemaker [suprachiasmatic nuclei of the hypothalamus (SCN)], independent from external behavioral effects, may also contribute to this daily pattern of adverse cardiovascular events. These circadian influences could occur via hormonal effects, direct neuronal links between the SCN and the sympathetic system (9) and through circadian modulation of the sympathovagal balance (10). Recently, we demonstrated (11) that dynamical scale-invariant features of heartbeat fluctuations [related to underlying mechanisms of cardiac control (12-17)], exhibit a significant endogenous circadian rhythm, independent from extrinsic scheduled behaviors and the sleep/wake cycle. These dynamical features of heartbeat fluctuations move closer to the features ob...

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