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

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.

AI snapshot

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.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

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

Cites

262 of 262 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 59 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Chronic sleep restriction can reach levels of deficit equivalent to total sleep loss when the sleep restriction is severe enough (i.e., consecutive days of restricted sleep continue long enough).

    “but the former can reach levels of deficit equivalent to total sleep loss when the sleep restriction is severe enough (i.e., the consecutive days of restricted sleep continue long enough).10,32”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [10] Belenky G Wesensten NJ Thorne DR Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose–response study J Sleep Res 2003 12 1 12 12603781 source

      Not checked in the free run.

    • cites [32] Van Dongen HP Maislin G Mullington JM Dinges DF The cumulative cost of additional wakefulness: dose–response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation Sleep 2003 26 117 126 12683469 source

      Not checked in the free run.

  • Premisecitation

    The two-process model of sleep-wake regulation consists of a homeostatic process (S) and a circadian process (C) that combine to determine the timing of sleep onset and offset.

    “The model consists of a homeostatic process (S) and a circadian process (C), which combine to determine the timing of sleep onset and offset.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [20] Borbély AA A two-process model of sleep regulation Hum Neurobiol 1982 1 195 204 7185792

      Not checked in the free run.

    • cites [21] Daan S Beersma DGM Borbély AA Timing of human sleep: recovery process gated by a circadian pacemaker Am J Physiol 1984 246 R161 R178 6696142

      Not checked in the free run.

    • cites [22] Achermann P Borbély AA Simulation of daytime vigilance by the additive interaction of a homeostatic and a circadian process Biol Cybern 1994 71 115 121 8068773 source

      Not checked in the free run.

  • Premisecitation

    There are large and highly replicable, trait-like individual differences in the magnitude of fatigue, sleepiness, sleep homeostatic, and cognitive performance vulnerability to acute total sleep deprivation and to chronic sleep restriction.

    “We have repeatedly demonstrated that there are large and highly replicable, trait-like individual differences in the magnitude of fatigue, sleepiness, sleep homeostatic, and cognitive performance vulnerability to acute total sleep deprivation170,171 and to chronic sleep restriction.32,148,172,173”
    Quote in the paperSubstantial claim0 of 6 sources checked
    • cites [170] Van Dongen HPA Baynard MD Maislin G Dinges DF Systematic interindividual differences in neurobehavioral impairment from sleep loss: evidence of trait-like differential vulnerability Sleep 2004 27 423 433 15164894

      Not checked in the free run.

    • cites [171] Van Dongen HP Maislin G Dinges DF Dealing with interindividual differences in the temporal dynamics of fatigue and performance: importance and techniques Aviat Space Environ Med 2004 75 A147 A154 15018277

      Not checked in the free run.

    • cites [32] Van Dongen HP Maislin G Mullington JM Dinges DF The cumulative cost of additional wakefulness: dose–response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation Sleep 2003 26 117 126 12683469 source

      Not checked in the free run.

    • cites [148] Goel N Banks S Mignot E Dinges DF PER3 polymorphism predicts cumulative sleep homeostatic but not neurobehavioral changes to chronic partial sleep deprivation PLoS One 2009 4 e5874 19516903 PMC2689932 source

      Not checked in the free run.

    • cites [172] Goel N Banks S Mignot E Dinges DF DQB1*0602 predicts interindividual differences in physiologic sleep, sleepiness and fatigue Neurology 2010 75 1509 1519 20975052 PMC2974463 source

      Not checked in the free run.

    • cites [173] Goel N Banks S Lin L Mignot E Dinges DF Catechol-O-methyltransferase Val158Met polymorphism associates with individual differences in sleep physiologic responses to chronic sleep loss PLoS One 2011 6 e29283 22216231 PMC3246458 source

      Not checked in the free run.

  • Premisecitation

    Morningness-eveningness is estimated to be about 50% heritable.

    “Morningness–eveningness is estimated to be about 50% heritable.129”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [129] Barclay NL Gregory AM Quantitative genetic research on sleep: a review of normal sleep, sleep disturbances and associated emotional, behavioural, and health-related difficulties Sleep Med Rev 2013 17 29 40 22560641 source

      Not checked in the free run.

  • Premisecitation

    Forced desynchrony protocols reveal the variance in neurobehavioral functions attributable primarily to endogenous circadian control and the variance attributable primarily to the sleep homeostatic drive.

    “Recent forced desynchrony protocols, which serve to experimentally reveal the variance in neurobehavioral functions attributable primarily to endogenous circadian control and the variance attributable primarily to the sleep homeostatic drive, have revealed that circadian dynamics can expose large neurobehavioral vulnerability during chronic sleep restriction.26,27”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [26] Cohen DA Wang W Wyatt JK Uncovering residual effects of chronic sleep loss on human performance Sci Transl Med 2010 2 14ra13 PMC2892834 20371466 source

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    • cites [27] Zhou X Ferguson SA Matthews RW Sleep, wake and phase dependent changes in neurobehavioral function under forced desynchrony Sleep 2011 34 931 941 21731143 PMC3119835

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  • May combine two claims. 14
  • Classified as probably not a substantial claim. 3
  • May combine two claims.

    Premisecitation

    Circadian variation in performance is most evident when sleep loss is present, and sleep loss has its largest effects on attention, working memory, and cognitive throughput.

    “Circadian variation in performance is most evident when sleep loss is present, and sleep loss has its largest effects on attention, working memory, and cognitive throughput.39”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [39] Lim J Dinges DF A meta-analysis of the impact of short-term sleep deprivation on cognitive variables Psychol Bull 2010 136 375 389 20438143 PMC3290659 source

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  • May combine two claims.

    Premisenone given

    The homeostatic process represents a drive for sleep that increases as a saturating exponential during wakefulness and decreases as a saturating exponential during sleep.

    “The homeostatic process represents the drive for sleep that increases as a saturating exponential during wakefulness (as can be observed when wakefulness is maintained beyond habitual bedtime into the night and subsequent day) and decreases as a saturating exponential during sleep (which represents recuperation obtained from sleep).”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Premisecitation

    Sleep deprivation affects a wide range of cognitive domains (including attention, working memory, abstraction, and decision making) and results in decreases in both the encoding of new information and memory consolidation.

    “Sleep deprivation affects a wide range of cognitive domains (including attention, working memory, abstraction, and decision making) and results in decreases in both the encoding of new information and memory consolidation.165”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [165] Diekelmann S Born J The memory function of sleep Nat Rev Neurosci 2010 11 114 126 20046194 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Healthy adults show interindividual differences in the free-running circadian period (tau), which shows robust stability within individuals.

    “Healthy adults show interindividual differences in the free-running circadian period (tau),94–98 which shows robust stability within individuals.97”
    Quote in the paperNot a substantial claim0 of 5 sources checked
    • cites [94] Czeisler CA Duffy JF Shanahan TL Stability, precision, and near-24-hour period of the human circadian pacemaker Science 1999 284 2177 2181 10381883 source

      Not checked in the free run.

    • cites [95] Smith MR Burgess HJ Fogg LF Eastman CI Racial differences in the human endogenous circadian period PLoS One 2009 4 e6014 19564915 PMC2699031 source

      Not checked in the free run.

    • cites [96] Lázár AS Santhi N Hasan S Circadian period and the timing of melatonin onset in men and women: predictors of sleep during the weekend and in the laboratory J Sleep Res 2013 22 155 159 23216995 source

      Not checked in the free run.

    • cites [97] Hasan S Santhi N Lázár AS Assessment of circadian rhythms in humans: comparison of real-time fibroblast reporter imaging with plasma melatonin FASEB J 2012 26 2414 2423 22371527 PMC3360144 source

      Not checked in the free run.

    • cites [98] Chang AM Buch AM Bradstreet DS Klements DJ Duffy JF Human diurnal preference and circadian rhythmicity are not associated with the CLOCK 3111C/T gene polymorphism J Biol Rhythms 2011 26 276 279 21628555 PMC3689429 source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisereasoning

    The circadian process represents daily oscillatory modulation of the threshold levels for sleep and wakefulness.

    “The circadian process represents daily oscillatory modulation of these threshold levels.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationreasoning

    The two-process model has been very successful in explaining changes in neurobehavioral performance in acute total sleep deprivation paradigms, but it fails to adequately predict the escalating declines in vigilant attention observed under chronic sleep-restriction conditions.

    “Thus, while the two-process model has been very successful in explaining changes in neurobehavioral performance in acute total sleep deprivation paradigms, it fails to adequately predict the escalating declines in vigilant attention observed under chronic sleep-restriction conditions.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Premisecitation

    Some individuals are highly vulnerable to neurobehavioral performance deficits when sleep deprived, others demonstrate remarkable neurobehavioral resistance to sleep loss, and others show intermediate responses.

    “Some individuals are highly vulnerable to neurobehavioral performance deficits when sleep deprived, others demonstrate remarkable levels of neurobehavioral resistance to sleep loss, and others show intermediate responses.171,174”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [171] Van Dongen HP Maislin G Dinges DF Dealing with interindividual differences in the temporal dynamics of fatigue and performance: importance and techniques Aviat Space Environ Med 2004 75 A147 A154 15018277

      Not checked in the free run.

    • cites [174] Goel N Dinges DF Behavioral and genetic markers of sleepiness J Clin Sleep Med 2011 7 S19 S21 22003324 PMC3190416 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Varying the amount of baseline nightly sleep prior to chronic sleep restriction affects both the rate at which alertness is degraded and the rate at which deficits are reversed by repeated nights of recovery sleep.

    “who varied the amount of baseline nightly sleep prior to chronic sleep restriction and found that it affected both the rate at which alertness was degraded and the rate at which deficits were reversed by repeated nights of recovery sleep.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [169] Rupp TL Wesensten NJ Bliese PD Balkin TJ Banking sleep: realization of benefits during subsequent sleep restriction and recovery Sleep 2009 32 311 321 19294951 PMC2647785 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Individuals cognitively vulnerable to sleep deprivation showed reduced frontoparietal activation, while resilient individuals showed increased parietal activation associated with lapses of attention during total sleep deprivation.

    “Individuals cognitively vulnerable to sleep deprivation showed reduced frontoparietal activation, while resilient individuals showed increased parietal activation associated with lapses of attention during total sleep deprivation201”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [201] Chee MWL Tan JC Lapsing when sleep deprived: neural activation characteristics of resistant and vulnerable individuals Neuroimage 2010 51 835 843 20171288 source

      Not checked in the free run.

  • May combine two claims.

    Premiseown data

    The PER3 VNTR polymorphism related to individual differences in sleep homeostatic responses, but not cognitive performance responses, to chronic sleep restriction.

    “We showed that this polymorphism related to individual differences in sleep homeostatic responses, but not cognitive performance responses to chronic sleep restriction.148”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [148] Goel N Banks S Mignot E Dinges DF PER3 polymorphism predicts cumulative sleep homeostatic but not neurobehavioral changes to chronic partial sleep deprivation PLoS One 2009 4 e5874 19516903 PMC2689932 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    It remains unclear whether the same individuals vulnerable to the adverse neurobehavioral effects of chronic sleep restriction are also vulnerable to acute total sleep deprivation.

    “It remains unclear, however, whether the same individuals vulnerable to the adverse neurobehavioral effects of chronic sleep restriction are also vulnerable to acute total sleep deprivation.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationreasoning

    Interindividual differences in circadian parameters, especially phase, and differential vulnerability to sleep loss also markedly affect neurobehavioral responses, suggesting genetic underpinnings.

    “Moreover, interindividual differences in circadian parameters, especially phase, and differential vulnerability to sleep loss also markedly affect neurobehavioral responses, suggesting genetic underpinnings.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationnone given

    The reasons for differential neurobehavioral vulnerabilities to sleep loss are unknown and have not been accounted for by demographic factors, IQ, or sleep need.

    “The reasons for differential neurobehavioral vulnerabilities to sleep loss are unknown, and thus far have not been accounted for by demographic factors, IQ, or sleep need.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationreasoning

    Studies that systematically examined the same subjects in both chronic sleep restriction and acute total sleep deprivation reported inconsistent results, likely due to small sample sizes, different populations, varying doses of sleep restriction, and different outcome measures.

    “These studies reported inconsistent results, likely due to small sample sizes, different populations, varying doses of sleep restriction, and different outcome measures.”
    Quote in the paperNot a substantial claim0 of 5 sources checked
    • cites [167] Lo JC Groeger JA Santhi N Effects of partial and acute total sleep deprivation on performance across cognitive domains, individuals and circadian phase PLoS One 2012 7 e45987 23029352 PMC3454374 source

      Not checked in the free run.

    • cites [175] Rupp TL Wesensten NJ Balkin TJ Trait-like vulnerability to total and partial sleep loss Sleep 2012 35 1163 1172 22851812 PMC3397820 source

      Not checked in the free run.

    • cites [178] Tassi P Schimchowitsch S Rohmer O Effects of acute and chronic sleep deprivation on daytime alertness and cognitive performance of healthy snorers and non-snorers Sleep Med 2012 13 29 35 22177345 source

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    • cites [179] Philip P Sagaspe P Prague M Acute versus chronic partial sleep deprivation in middle-aged people: differential effect on performance and sleepiness Sleep 2012 35 997 1002 22754046 PMC3369235 source

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    • cites [180] Drake CL Roehrs TA Burduvali E Bonahoom A Rosekind M Roth T Effects of rapid versus slow accumulation of eight hours of sleep loss Psychophysiology 2001 38 979 987 12240674 source

      Not checked in the free run.

  • May combine two claims.

    Interpretationnone given

    The sleep homeostat and neurobehavioral performance are affected by acute total sleep deprivation and chronic sleep restriction, although the two forms of sleep loss likely differentially affect neural and behavioral responses.

    “The sleep homeostat and neurobehavioral performance are affected by acute total sleep deprivation and chronic sleep restriction, although the two forms of sleep loss likely differentially affect neural and behavioral responses.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisecitation

    In monozygotic and dizygotic twin pairs, 56.2% of the total variance in monozygotic twins was due to variance between pairs whereas only 14.5% of the total variance in dizygotic twins was due to variance between pairs.

    “56.2% of the total variance in the monozygotic twins was due to variance between pairs whereas only 14.5% of the total variance in dizygotic twins was due to variance between pairs (Fig. 7.3)”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [182] Kuna ST Maislin G Pack FM Heritability of performance deficit accumulation during acute sleep deprivation in twins Sleep 2012 35 1223 1233 22942500 PMC3413799

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    The circadian drive for wakefulness, the homeostatic drive for sleep, and masking factors simultaneously interact to affect neurobehavioral functioning.

    “The circadian drive for wakefulness, the homeostatic drive for sleep, and masking factors simultaneously interact to affect neurobehavioral functioning.”
    Quote in the paperNot a substantial claim
17 of 17
  • 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.”
1 of 1

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Sleep deprivation leads to cognitive impairment and reduced attention.

    “sleep deprivation leads to cognitive impairment and reduced attention(43-46).”
  • Genetic variants may underlie some interindividual and interethnic differences in the period of the endogenous circadian cycle that manifest as differences in chronotype.

    “Such genetic variants may underlie some of the interindividual (44) and interethnic differences (45) in the period (or τ) of the endogenous circadian cycle that manifest themselves as differences in chronotype.”
  • Sleep is a vital biological function that directly impacts physical and mental health.

    “Sleep is a vital biological function that directly impacts physical and mental health [14,15].”

    From Mental Health of Canadian Firefighters: The Impact of Sleep (2021) · cites this paper as [14]

  • Insufficient sleep (e.g., less than 4-6 h per night) increases the risk of death by suicide, mortality, cardiovascular disease, depression, diabetes, decreases immune system functioning, and has a negative impact on cognition.

    “Insufficient sleep (e.g., less than 4–6 h per night) increases the risk of death by suicide [7,17], mortality, cardiovascular disease, depression, diabetes, decreases immune system functioning, and has a negative impact on cognition [14,18].”

    From Mental Health of Canadian Firefighters: The Impact of Sleep (2021) · cites this paper as [14]

Cites

Flagged first, then by citations

22 of the 284 references couldn’t be matched to a known paper.

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

Cited by

Sorted by citations

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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