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Neurobehavioral task performance is modulated by the circadian and homeostatic processes of sleep/wake regulation. Biomathematical modeling of the temporal dynamics of these processes and their interaction allows for prospective prediction of performance impairment in shift-workers and provides a basis for fatigue risk management in 24/7 operations. It has been reported, however, that the impact of the circadian rhythm—and in particular its timing—is inherently task-dependent, which would have profound implications for our understanding of the temporal dynamics of neurobehavioral functioning and the accuracy of biomathematical model predictions. We investigated this issue in a laboratory study designed to unambiguously dissociate the influences of the circadian and homeostatic processes on neurobehavioral performance, as measured during a constant routine protocol preceded by three days on either a simulated night shift or a simulated day shift schedule. Neurobehavioral functions were measured every 3 h using three functionally distinct assays: a digit symbol substitution test, a psychomotor vigilance test, and the Karolinska Sleepiness Scale. After dissociating the circadian and homeostatic influences and accounting for inter-individual variability, peak circadian performance occurred in the late biological afternoon (in the “wake maintenance zone”) for all three neurobehavioral assays. Our results are incongruent with the idea of inherent task-dependent differences in the endogenous circadian impact on performance. Rather, our results suggest that neurobehavioral functions are under top-down circadian control, consistent with the way they are accounted for in extant biomathematical models.

Introduction Changes in waking neurobehavioral functioning (NF) over time are governed by homeostatic and circadian processes. It has been reported that peak circadian timing varies inherently between tasks, such that the optimal timing for NF would be task-dependent. Here we investigated this idea with a simulated shift work study protocol followed by a 24h constant routine (CR) protocol to experimentally and statistically separate the circadian from the homeostatic process. Methods N=13 healthy adults (ages 25.5±3.2y; 9 men) completed a 7-day/6-night in-laboratory study. They were randomized to a 3-day simulated day shift condition (n=7) with nighttime sleep (22:00–06:00) or a 3-day simulated night shift condition (n=6) with daytime sleep (10:00–18:00). They then underwent a 24h CR protocol, during which they stayed awake under constant behavioral and environmental conditions and blood was collected at 1–3h intervals for the assessment of dim light melatonin onset (DLMO). During scheduled wakefulness, subjects completed three functionally distinct NF tasks at ~2h intervals: the Karolinska Sleepiness Scale (KSS), Digit Symbol Substitution Test (DSST), and Psychomotor Vigilance Test (PVT). Data from these tasks taken during the CR protocol were analyzed with non-linear mixed-effects regression to separate endogenous circadian effects from the homeostatic process. Results Following simulated night shift, compared to simulated day shift, on average there was a modest, 1.4h (±0.8h SE) delay in DLMO (F1,11=3.68, p=0.082). As such, the simulated night shift condition produced a 10.6h shift in alignment of the homeostatic process relative to the circadian process. Regardless of prior shift condition, the peak of the circadian rhythm effect on NF occurred post-DLMO by 16.8h (±1.0h) for KSS, 15.9h (±1.4h) for DSST, and 18.6h (±1.0h) for PVT, which was not significantly different (F2,9=1.55, p=0.26). Conclusion As proof of principle, we studied three distinct NF assays, and found only small, non-significant differences between them in the timing of underlying circadian rhythmicity. While a larger sample could have yielded statistical significance in our comparison of circadian peak times, the small magnitude of the observed difference does not support the idea of inherent task-dependent differences in the timing of the endogenous circadian rhythm’s influence on NF. Support (If Any) CDMRP W81XWH-16-1-0319 and W81XWH-20-1-0442