Abstract:

The circadian rhythm is an endogenous timing system adapted to Earth’s rotation, and its stability is vital for health and cognition. Circadian disruption impairs cognitive performance, which fluctuates diurnally—typically troughing from early morning to late morning and recovering from late afternoon to night. Further studies show that circadian regulation is domain-specific: different cognitive functions have distinct peak phases and sensitivities, suggesting different neural mechanisms. However, existing research has three major limitations. First, the conceptual definition and underlying mechanisms of circadian effects remain unclear. Second, studies have largely focused on attentional vigilance and working memory, lacking systematic cross-domain comparisons, especially under differentiated intrinsic mechanisms. Third, neural evidence remains fragmented and limited. Thus, systematically clarifying how circadian rhythms differentially regulate cognitive functions through distinct intrinsic mechanisms is a key scientific question.
The classic two-process model of sleep-wake regulation posits that cognitive performance during wakefulness is governed jointly by the homeostatic process (Process S) and the circadian process (Process C). During early daytime wakefulness, Process C counteracts the accumulating effect of Process S, maintaining cognitive performance; during the biological night, the wake-promoting effect of Process C diminishes, and cognitive performance reaches its nadir; it recovers the next day as Process C strengthens. However, different experimental paradigms vary considerably in their control over confounding factors, leading to divergent interpretations of the mechanisms involved. Physiologically, the circadian rhythm depends on a multilevel network involving molecular clocks, the central clock, and the endocrine system. The suprachiasmatic nucleus regulates subcortical arousal systems through neural projections and modulates the rhythmic secretion of hormones such as melatonin and cortisol, thereby broadly conveying temporal signals to different brain regions. This framework provides a neurophysiological basis for distinguishing between broad and narrow circadian effects.
To systematically investigate the effects of the circadian rhythm on cognitive functions and their temporal distribution, this review included 73 studies, covering subjective sleepiness, attentional vigilance, complex executive function, working memory, risk decision-making, and moral behavior. Analyses of broad circadian effects revealed that subjective sleepiness, attentional vigilance, and complex executive function exhibited a robust pattern of lower levels in the morning and higher levels in the evening, suggesting they may be subject to general regulation by global arousal levels. In contrast, results for working memory and risk decision-making showed high heterogeneity, while moral behavior did not display a stable rhythmic pattern. These differences may arise from methodological factors, such as incomplete coverage of measurement times, and also suggest that the neural circuits underlying different cognitive functions may respond to circadian regulation in functionally specific ways. For narrow circadian effects, researchers typically use post-hoc analyses based on the two-process model or its derivatives to isolate the cognitive fluctuations driven purely by Process C. The results showed that subjective sleepiness, attentional vigilance, and complex executive function still followed a consistent pattern of lower levels in the morning and higher levels in the evening, indicating that narrow circadian effects may exert general regulation on cognitive functions by modulating common arousal mechanisms. At the same time, significant differences in peak phases were observed across cognitive functions, suggesting that the endogenous circadian clock may provide specific temporal regulation to distinct brain regions or networks via differentiated neural or endocrine pathways. Taken together, the behavioral evidence suggests that circadian rhythms influence cognitive functions through both a general regulatory mechanism based on global arousal and differentiated regulatory mechanisms relying on distinct neural circuits.
Integrating evidence from functional magnetic resonance imaging and electroencephalography studies, circadian rhythms may influence cognitive functions through two mechanisms. First, they exert general regulation by modulating global arousal levels. The circadian rhythm regulates arousal-related structures such as the hypothalamus, thalamus, and locus coeruleus, as well as their ascending drive to cortical states, dynamically shaping time windows such as the circadian trough and the wake maintenance zone, thereby exerting relatively non-specific effects on a broad range of cognitive functions. Second, they exert specific regulation by modulating activity in task-relevant brain regions or functional networks. Broad circadian effects differentially modulate specific cortical networks and their information processing over time, selectively influencing the efficiency and peak phases of different cognitive functions.
Finally, this review outlines directions for future research. Future research should integrate multimodal neural data with computational models, combine targeted neuromodulation techniques to establish causal relationships, and explore precision light-based intervention strategies based on specific time windows, thereby providing precise cognitive protection for individuals with circadian rhythm disorders.
By distinguishing circadian effects driven by different intrinsic mechanisms and integrating behavioral and neural evidence, this review aims to construct a clear framework for how circadian rhythms influence cognitive functions and to provide mechanistic explanations for their effects on human cognition.

Key words: circadian rhythm, two-process model of sleep-wake regulation, cognitive function