Cited by 400Sleep and Work-Related FatigueCircadian rhythm and melatoninSleep and Wakefulness Research

The DOI matches its Crossref record; 261 of the 284 references it cites were found in a registry or an index; 11 of the 59 sources its claims cite were checked for support.

Circadian Rhythms, Sleep Deprivation, and Human Performance

Open access
Goel, Namni, Basner, Mathias, Rao, Hengyi, Dinges, David F.·2013·Progress in Molecular Biology and Translational Science

Abstract

Much of the current science on, and mathematical modeling of, dynamic changes in human performance within and between days is dominated by the two-process model of sleep–wake regulation, which posits a neurobiological drive for sleep that varies homeostatically (increasing as a saturating exponential during wakefulness and decreasing in a like manner during sleep), and a circadian process that neurobiologically modulates both the homeostatic drive for sleep and waking alertness and performance. Endogenous circadian rhythms in neurobehavioral functions, including physiological alertness and cognitive performance, have been demonstrated using special laboratory protocols that reveal the interaction of the biological clock with the sleep homeostatic drive. Individual differences in circadian rhythms and genetic and other components underlying such differences also influence waking neurobehavioral functions. Both acute total sleep deprivation and chronic sleep restriction increase homeostatic sleep drive and degrade waking neurobehavioral functions as reflected in sleepiness, attention, cognitive speed, and memory. Recent evidence indicating a high degree of stability in neurobehavioral responses to sleep loss suggests that these trait-like individual differences are phenotypic and likely involve genetic components, including circadian genes. Recent experiments have revealed both sleep homeostatic and circadian effects on brain metabolism and neural activation. Investigation of the neural and genetic mechanisms underlying the dynamically complex interaction between sleep homeostasis and circadian systems is beginning. A key goal of this work is to identify biomarkers that accurately predict human performance in situations in which the circadian and sleep homeostatic systems are perturbed.

Overview

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Written from the paper’s full text.

TL;DR

This review synthesizes evidence on how circadian rhythms, sleep homeostasis, and masking factors jointly shape human alertness and cognitive performance, with particular attention to the two-process model and its limits under chronic sleep restriction. It also reviews interindividual differences, genetic markers, and neuroimaging findings, concluding that biomarkers predicting performance under circadian/sleep perturbation remain a high priority.

Key findings

  • The two-process model (homeostatic process S plus circadian process C) explains acute total sleep deprivation but fails to predict escalating vigilant-attention declines under chronic sleep restriction; forced desynchrony studies show the interaction is nonlinear and nonadditive.
  • Chronic sleep loss is common: 35–40% of the adult US population report sleeping less than 7 h on weekday nights; shift work affects approximately one out of five working Americans, with 15% of full-time salaried workers usually working shifts that include nights; the International Agency for Research on Cancer concluded in 2007 that shift work involving circadian disruption is probably carcinogenic to humans.
  • The McCauley et al. model predicts a critical daily wake duration of 20.2 h; daily wake above ca. 15.8 h but below 20.2 h (total sleep time 3.8–8.2 h) converges to stable performance deficits, whereas above 20.2 h performance impairments escalate; a single night of recovery sleep is predicted and experimentally confirmed to be inadequate after prolonged sleep restriction.
  • Trait-like individual differences are large: intraclass correlation coefficients account for 50–90% of the variance in neurobehavioral measures after acute total sleep deprivation; in monozygotic twins, 56.2% of total variance was due to between-pair variance versus 14.5% in dizygotic twins; morningness–eveningness is estimated to be about 50% heritable.

Methods

  • The paper is a narrative review; it does not report a systematic search strategy, inclusion criteria, or meta-analysis.
  • It synthesizes human laboratory protocols (constant routine, forced desynchrony), acute total and chronic partial sleep deprivation/restriction studies, chronotype and clock-gene association studies, and neuroimaging methods including PET, BOLD fMRI, arterial spin-labeled perfusion fMRI, and resting-state functional connectivity fMRI.
  • The main analysis is a qualitative integration of findings around the two-process model, interindividual variability, and neural/genetic mechanisms.

Limitations

  • Stated: the two-process model fails to adequately predict chronic sleep-restriction effects; the circadian and homeostatic interaction is nonlinear/nonadditive, making relative contributions difficult or impossible to quantify and variable across conditions and subjects.
  • Stated: task-related BOLD fMRI measures only relative signal changes, lacks absolute quantification, and cannot easily dissociate sleep loss, time-of-day, or circadian effects on brain function from behavioral performance confounds; few neuroimaging studies have examined chronic partial sleep loss and recovery.
  • Stated: genetic associations (e.g., CLOCK 3111C, PER3 VNTR) are inconsistent and need replication, and in vitro fibroblast rhythms do not necessarily correlate with in vivo physiological rhythms. Evident from the text: as a narrative review, no systematic methods or risk-of-bias assessment are reported.

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Integrity signals

Registry

Crossref · 10.1016/b978-0-12-396971-2.00007-5

Cites

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Claims the paper makes

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Show all 26 claims

  • It may state two separate claims as one. 14
  • Probably not a substantial claim. 3
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  • The paper relies on this without support.

    The biological clock that modulates the timing of sleep and wakefulness is located in the suprachiasmatic nuclei of the anterior hypothalamus.

    “The endogenous circadian regulating system (i.e., biological clock) that modulates the timing of both sleep and wakefulness is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus.”
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Citations

Cites

Research works printed but not linked: 2

  1. Hockey, 1972, Diurnal variation in human performance: a review, 1
  2. Rao, 2011, Differential effects of total sleep deprivation on regional cortical activity at rest and during Psychomotor Vigilance Test performance, Sleep, 34, A97

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Metadata

Authors
Goel, N., Basner, M., Rao, H., & Dinges, D. F.
Affiliations
University of Pennsylvania (US)
Venue
Progress in Molecular Biology and Translational Science
Publisher
Elsevier
Published
2013
Volume
119
Pages
155-190
ISSN
1877-1173 (ISSN-L)
OpenAlex
W1902549
Cited by
400
References
284
Citations by year
2026: 19 · 2025: 30 · 2024: 32 · 2023: 44 · 2022: 40 · 2021: 36 · 2020: 37 · 2019: 39 · 2018: 37 · 2017: 19 · 2016: 23 · 2015: 26 · 2014: 15 · 2013: 2
FWCI
79.39
Type
book chapter
Language
en
Open access
Locations
  • Progress in molecular biology and translational science (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL102119, HL102119)
  • National Institute of Nursing Research (NR004281, R01NR004281)
Topics
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
Keywords
circadian rhythm, sleep deprivation, human performance, two-process model, sleep homeostasis, circadian genes, individual differences, sleepiness, cognitive performance, attention, memory, brain metabolism, neuronal activation, biomarkers
MeSH terms
Circadian Rhythm, Humans, Sleep Deprivation, Task Performance and Analysis

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