Acute Sleep Loss Research Articles

Erratum to: Identifying and validating blood mRNA biomarkers for acute and chronic insufficient sleep in humans: a machine learning approach.

Acute and chronic insufficient sleep are associated with adverse health outcomes and risk of accidents. There is therefore a need for biomarkers to monitor sleep debt status. None are currently available. We applied Elastic-net and Ridge regression to entire and pre-filtered transcriptome samples collected in healthy young adults during acute total sleep deprivation and following 1 week of either chronic insufficient (< 6 h) or sufficient sleep (~8.6 h) to identify panels of mRNA biomarkers of sleep debt status. The size of identified panels ranged from 9-74 biomarkers. Panel performance, assessed by leave-one-subject-out cross-validation and independent validation, varied between sleep debt conditions. Using between-subject assessments based on one blood sample, the accuracy of classifying ‘Acute sleep loss’ was 92%, but only 57% for classifying ‘Chronic sleep insufficiency’. A reasonable accuracy for classifying ‘chronic sleep insufficiency’ could only be achieved by a within-subject comparison of blood samples. Biomarkers for sleep debt status showed little overlap with previously identified biomarkers for circadian phase. Biomarkers for acute and chronic sleep loss also showed little overlap but were associated with common functions related to the cellular stress response, such as heat shock protein activity, the unfolded protein response, protein ubiquitination and endoplasmic reticulum associated protein degradation, and apoptosis. This characteristic response of whole blood to sleep loss can further aid our understanding of how sleep insufficiencies negatively affect health. Further development of these novel biomarkers for research and clinical practice requires validation in other protocols and age groups.

Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men.

ObjectiveDisrupted sleep increases CSF levels of tau and β-amyloid (Aβ) and is associated with an increased risk of Alzheimer disease (AD). Our aim was to determine whether acute sleep loss alters diurnal profiles of plasma-based AD-associated biomarkers.MethodsIn a 2-condition crossover study, 15 healthy young men participated in 2 standardized sedentary in-laboratory conditions in randomized order: normal sleep vs overnight sleep loss. Plasma levels of total tau (t-tau), Aβ40, Aβ42, neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) were assessed using ultrasensitive single molecule array assays or ELISAs, in the fasted state in the evening prior to, and in the morning after, each intervention.ResultsIn response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau (p = 0.035). No changes between the sleep conditions were seen for levels of Aβ40, Aβ42, NfL, or GFAP (all p > 0.10). The AD risk genotype rs4420638 did not significantly interact with sleep loss–related diurnal changes in plasma levels of Aβ40 or Aβ42 (p > 0.10). Plasma levels of Aβ42 (−17.1%) and GFAP (−12.1%) exhibited an evening to morning decrease across conditions (p < 0.05).ConclusionsOur exploratory study suggests that acute sleep loss results in increased blood levels of t-tau. These changes provide further evidence that sleep loss may have detrimental effects on brain health even in younger individuals. Larger cohorts are warranted to delineate sleep vs circadian mechanisms, implications for long-term recurrent conditions (e.g., in shift workers), as well as interactions with other lifestyle and genetic factors.

Adverse insulin sensitivity profile associated with the observed increase in circulating hormone FGF-21 levels and altered peripheral tissue promoter dna methylation following acute sleep loss in humans

Adverse insulin sensitivity profile associated with the observed increase in circulating hormone FGF-21 levels and altered peripheral tissue promoter dna methylation following acute sleep loss in humans

Impact of acute sleep deprivation on dynamic functional connectivity states.

Sleep deprivation (SD) could amplify the temporal fluctuation of spontaneous brain activities that reflect different arousal levels using a dynamic functional connectivity (dFC) approach. Therefore, we intended to evaluate the test–retest reliability of dFC characteristics during rested wakefulness (RW), and to explore how the properties of these dynamic connectivity states were affected by extended durations of acute sleep loss (28/52 hr). We acquired resting‐state fMRI and neuropsychological datasets in two independent studies: (a) twice during RW and once after 28 hr of SD (n = 15) and (b) after 52 hr of SD and after 14 hr of recovery sleep (RS; n = 14). Sliding‐window correlations approach was applied to estimate their covariance matrices and corresponding three connectivity states were generated. The test–retest reliability of dFC properties demonstrated mean dwell time and fraction of connectivity states were reliable. After SD, the mean dwell time of a specific state, featured by strong subcortical–cortical anticorrelations, was significantly increased. Conversely, another globally hypoconnected state was significantly decreased. Subjective sleepiness and objective performances were separately positive and negative correlated with the increased and decreased state. Two brain connectivity states and their alterations might be sufficiently sensitive to reflect changes in the dynamics of brain mental activities after sleep loss.

Wakefulness/sleep architecture and electroencephalographic activity in mice lacking the translational repressor 4E-BP1 or 4E-BP2.

Sleep and sleep loss are affecting protein synthesis in the brain, but the contribution of translational control to wakefulness and sleep regulation remains poorly understood. Here, we studied the role of two suppressors of protein synthesis, the eukaryotic translation initiation factor 4E-binding proteins 1 and 2 (4E-BP1 and 4E-BP2), in sleep architecture and electroencephalographic (EEG) activity as well as in the EEG and molecular responses to acute sleep loss. The EEG of mice mutant for the genes encoding 4E-BP1 or 4E-BP2 (Eif4ebp1 and Eif4ebp2 knockout [KO] mice) was recorded under undisturbed conditions and following a 6-hour sleep deprivation (SD). The effect of SD on the expression of genes known to respond to SD was also measured in the prefrontal cortex of Eif4ebp1 and Eif4ebp2 KO mice. Eif4ebp1 KO mice differed from wild-type mice in parameters of wakefulness and sleep quantity and quality, and more subtly in the gene expression response to SD. For instance, Eif4ebp1 KO mice spent more time in slow-wave sleep (SWS) and showed altered baseline 24-h time courses of SWS delta (1-4 Hz) activity and sigma (10-13 Hz) activity. Eif4ebp2 KO mice differed from wild-type mice only for wakefulness and sleep quality, expressing changes in EEG spectral activity generally revealed during and after SD. These findings suggest different roles of effectors of translational control in the regulation of wakefulness and sleep and of synchronized cortical activity.

Distinct pattern of oculomotor impairment associated with acute sleep loss and circadian misalignment.

Key points Inadequate sleep and irregular work schedules have not only adverse consequences for individual health and well‐being, but also enormous economic and safety implications for society as a whole.This study demonstrates that visual motion processing and coordinated eye movements are significantly impaired when performed after sleep loss and during the biological night, and thus may be contributing to human error and accidents.Because affected individuals are often unaware of their sensorimotor and cognitive deficits, there is a critical need for non‐invasive, objective indicators of mild, yet potentially unsafe, impairment due to disrupted sleep or biological rhythms.Our findings show that a set of eye‐movement measures can be used to provide sensitive and reliable indicators of such mild neural impairments. Sleep loss and circadian misalignment have long been known to impair human cognitive and motor performance with significant societal and health consequences. It is well known that human reaction time to a visual cue is impaired following sleep loss and circadian misalignment, but it has remained unclear how more complex visuomotor control behaviour is altered under these conditions. In this study, we measured 14 parameters of the voluntary ocular tracking response of 12 human participants (six females) to systematically examine the effects of sleep loss and circadian misalignment using a constant routine 24‐h acute sleep‐deprivation paradigm. The combination of state‐of‐the‐art oculometric and sleep‐research methodologies allowed us to document, for the first time, large changes in many components of pursuit, saccades and visual motion processing as a function of time awake and circadian phase. Further, we observed a pattern of impairment across our set of oculometric measures that is qualitatively different from that observed previously with other mild neural impairments. We conclude that dynamic vision and visuomotor control exhibit a distinct pattern of impairment linked with time awake and circadian phase. Therefore, a sufficiently broad set of oculometric measures could provide a sensitive and specific behavioural biomarker of acute sleep loss and circadian misalignment. We foresee potential applications of such oculometric biomarkers assisting in the assessment of readiness‐to‐perform higher risk tasks and in the characterization of sub‐clinical neural impairment in the face of a multiplicity of potential risk factors, including disrupted sleep and circadian rhythms.

Somatostatin+/nNOS+ neurons are involved in delta electroencephalogram activity and cortical-dependent recognition memory.

Slow-wave activity (SWA) is an oscillatory neocortical activity occurring in the electroencephalogram delta (δ) frequency range (~0.5-4 Hz) during nonrapid eye movement sleep. SWA is a reliable indicator of sleep homeostasis after acute sleep loss and is involved in memory processes. Evidence suggests that cortical neuronal nitric oxide synthase (nNOS) expressing neurons that coexpress somatostatin (SST) play a key role in regulating SWA. However, previous studies lacked selectivity in targeting specific types of neurons that coexpress nNOS-cells which are activated in the cortex after sleep loss. We produced a mouse model that knocks out nNOS expression in neurons that coexpress SST throughout the cortex. Mice lacking nNOS expression in SST positive neurons exhibited significant impairments in both homeostatic low-δ frequency range SWA production and a recognition memory task that relies on cortical input. These results highlight that SST+/nNOS+ neurons are involved in the SWA homeostatic response and cortex-dependent recognition memory.

The Effects of Caffeine Intake on Cardiovascular Parameters in Sleep Deprived Medical Residents

Physicians and medical residents are particularly affected by sleep deprivation are, especially in East European countries. The aim of our study is to analyze the effect of caffeine intake on cardiovascular functions in sleep deprived residents (clinicians in-training) after continuous 24h on-call duty. 26 medical residents aged between 22-33 years old, 12 men and 14 women, who began their activity at 2 pm were included. Each subject consumed coffee or caffeinated drinks such as Coca cola during this period, after 2 am, expressed in caffeine units. We have evaluated their cardiovascular function using impedance cardiography (ICG-M501) and blood pressure measurement using the manometric method, before (at 7 pm) and after caffeine consumption (at 7 am), during one night of on-call duty. Surprisingly, after caffeine consumption, all subjects have had a decrease of the heart rate after one night of sleep deprivation (from mean: 83 b/min before to 69.73 b/min after, p = 0.000), also the mean arterial blood pressure is lower after the overnight call (from mean: 95.3 mmHg before to 88.9 mmHg after). Moreover, cardiac output, stroke volume and cardiac index decreases along with an increase of peripheral vascular resistance. Caffeine intake exerts a paradoxical effect on sleep deprived subjects; acute sleep loss, due to continuously, intense on-call work, modifies several cardiovascular parameters, such as heart rate, blood pressures, stroke volume and cardiac output.

0118 Increased Circulating Levels and Peripheral Tissue Promoter DNA Methylation of the Hormone FGF-21 Following Acute Sleep Loss in Humans

0118 Increased Circulating Levels and Peripheral Tissue Promoter DNA Methylation of the Hormone FGF-21 Following Acute Sleep Loss in Humans

Time-of-day and days-on-shift predict increased fatigue over two-week offshore day-shifts

ObjectivesThe purpose of this study was to investigate the accumulation of fatigue over a two-week offshore period. In particular, the effects of (1) time-of-day and days-on-shift as well as (2) acute and chronic sleep loss on the rate at which fatigue accumulates were investigated. Methods42 day-shift offshore workers were examined. Fatigue was measured using pre- and post-shift scores on the Karolinska Sleepiness Scale (KSS). Total sleep time was measured using actigraphy (Motionwatch8, Camntech). Data was analyzed using a linear mixed model analyses. ResultsAverage sleep loss per night was 92 min (95%CI: 89.6–94.0; p < .001). Mean cumulative sleep loss across the study was 21:20hrs (SD = 08:10hrs) over the 14 days. Chronic sleep loss was significantly related to a modest increase in sleepiness (KSS) across the shift (95%CI: 0.01–0.17; p = .020) and in post-shift scores (95%CI:.07–0.19; p < .001). Time-of-day (95%CI: 0.63 to −0.01; p = .042) and days-on-shift (95%CI: 0.03–0.08; p < .001) as well as their interaction (95%CI: 0.08 to −0.00; p = .027) influenced the rate at which fatigue accumulated over a two-week offshore period. ConclusionsPre- and post-shift fatigue accumulate in different ways over the two-week offshore period. The accumulation of post-shift fatigue scores was positively related to successive days-on-shift and chronic sleep loss. Our results suggest that prolonging offshore periods will likely result in elevated fatigue risk. Accumulating fatigue and sleep loss over two-week offshore periods should be considered in fatigue risk management plans and systems.

Acute sleep loss induces signs of visual discomfort in young men.

Acute sleep loss influences visual processes in humans, such as recognizing facial emotions. However, to the best of our knowledge, no study till date has examined whether acute sleep loss alters visual comfort when looking at images. One image statistic that can be used to investigate the level of visual comfort experienced under visual encoding is the slope of the amplitude spectrum, also referred to as the slope constant. The slope constant describes the spatial distribution of pixel intensities and deviations from the natural slope constant can induce visual discomfort. In the present counterbalanced crossover design study, 11 young men with normal or corrected‐to‐normal vision participated in two experimental conditions: one night of sleep loss and one night of sleep. In the morning after each intervention, subjects performed a computerized psychophysics task. Specifically, they were required to adjust the slope constant of images depicting natural landscapes and close‐ups with a randomly chosen initial slope constant until they perceived each image as most natural looking. Subjects also rated the pleasantness of each selected image. Our analysis showed that following sleep loss, higher slope constants were perceived as most natural looking when viewing images of natural landscapes. Images with a higher slope constant are generally perceived as blurrier. The selected images were also rated as less pleasant after sleep loss. No such differences between the experimental conditions were noted for images of close‐ups. The results suggest that sleep loss induces signs of visual discomfort in young men. Possible implications of these findings are discussed.

Sleep Loss Disrupts Morning-to-Evening Differences in Human White Adipose Tissue Transcriptome.

Chronodisruption, as caused by such conditions as perturbations of 24-hour rhythms of physiology and behavior, may promote the development of metabolic diseases. To assess the acute effects of sleep curtailment on circadian regulation (i.e., morning-to-evening differences) of white adipose tissue (WAT) transcriptome in normal-weight men. Fifteen healthy men aged 18 to 30 years (mean ± SEM, 24.0 ± 0.9years) were studied. In randomized, balanced order they underwent three separate nights with regular sleep duration (8 hours of sleep between 11:00 pm and 7:00 am), sleep restriction (4 hours of sleep between 3:00 am and 7:00 am), and sleep deprivation (no sleep at all). Sleep was polysomnographically evaluated. WAT biopsy samples were taken twice at 9:00 pm and 7:00 am to assess morning-to-evening differences. WAT transcriptome profile was assessed by RNA sequencing, and expression of relevant circadian core clock genes were analyzed. Glucose homeostasis, lipid profile, and adipokines were assessed. Sleep restriction dramatically blunted morning-to-evening transcriptome variations with further dampening after sleep deprivation. Although most core clock genes remained stably rhythmic, morning-to-evening regulated pathways of carbohydrate and lipid metabolism were highly sensitive to sleep loss. In particular, genes associated with carbohydrate breakdown lost rhythmicity after sleep deprivation, with an overall trend toward an upregulation in the morning. In line with specific transcriptional changes in WAT, retinol-binding-protein 4 was increased and β-cell secretory capacity was diminished. Acute sleep loss induces a profound restructuring of morning-to-evening WAT transcriptome with uncoupling from the local clock machinery, resulting in increased WAT carbohydrate turnover and impaired glucose homeostasis. Our data support an optimization of sleep duration and timing to prevent metabolic disorders such as obesity and type 2 diabetes.

Sustained vigilance is negatively affected by mild and acute sleep loss reflected by reduced capacity for decision making, motor preparation, and execution.

The behavioral and cognitive consequences of severe sleep deprivation are well understood. Surprisingly, relatively little is known about the neural correlates of mild and acute sleep restriction on tasks that require sustained vigilance for prolonged periods of time during the day. Event-related potential (ERP) paradigms can reveal insight into the neural correlates underlying visual processing and behavioral responding that is impaired with reduced alertness, as a consequence of sleep loss. Here, we investigated the impact of reduced vigilance following at-home mild sleep restriction to better understand the associated behavioral consequences and changes in information processing revealed by ERPs. As expected, vigilance was reduced (e.g. increased lapses and response slowing) that increased over the course of the experiment in the "sleep restricted" (5 hr sleep) compared with the "sleep-extension" (9 hr sleep) condition. Corresponding to these lapses, we found decreased positivity of visually evoked potentials in the Sleep Restriction vs. Sleep Extension condition emerging from 316 to 449 ms, maximal over parietal/occipital cortex. We also investigated electrophysiological signs of motor-related processing by comparing lateralized readiness potentials (LRPs) and found reduced positivity of LRPs in the Sleep Restriction vs. Sleep Extension condition at 70-40 ms before, and 115-158 ms after a response was made. These results suggest that even a single night of mild sleep restriction can negatively affect vigilance, reflected by reduced processing capacity for decision making, and dulls motor preparation and execution.

Identifying and validating blood mRNA biomarkers for acute and chronic insufficient sleep in humans: a machine learning approach.

Acute and chronic insufficient sleep are associated with adverse health outcomes and risk of accidents. There is therefore a need for biomarkers to monitor sleep debt status. None are currently available. We applied elastic net and ridge regression to transcriptome samples collected in 36 healthy young adults during acute total sleep deprivation and following 1 week of either chronic insufficient (<6 hr) or sufficient sleep (~8.6 hr) to identify panels of mRNA biomarkers of sleep debt status. The size of identified panels ranged from 9 to 74 biomarkers. Panel performance, assessed by leave-one-subject-out cross-validation and independent validation, varied between sleep debt conditions. Using between-subject assessments based on one blood sample, the accuracy of classifying “acute sleep loss” was 92%, but only 57% for classifying “chronic sleep insufficiency.” A reasonable accuracy for classifying “chronic sleep insufficiency” could only be achieved by a within-subject comparison of blood samples. Biomarkers for sleep debt status showed little overlap with previously identified biomarkers for circadian phase. Biomarkers for acute and chronic sleep loss also showed little overlap but were associated with common functions related to the cellular stress response, such as heat shock protein activity, the unfolded protein response, protein ubiquitination and endoplasmic reticulum-associated protein degradation, and apoptosis. This characteristic response of whole blood to sleep loss can further aid our understanding of how sleep insufficiencies negatively affect health. Further development of these novel biomarkers for research and clinical practice requires validation in other protocols and age groups.

Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans.

Curtailed sleep promotes weight gain and loss of lean mass in humans, although the underlying molecular mechanisms are poorly understood. We investigated the genomic and physiological impact of acute sleep loss in peripheral tissues by obtaining adipose tissue and skeletal muscle after one night of sleep loss and after one full night of sleep. We find that acute sleep loss alters genome-wide DNA methylation in adipose tissue, and unbiased transcriptome-, protein-, and metabolite-level analyses also reveal highly tissue-specific changes that are partially reflected by altered metabolite levels in blood. We observe transcriptomic signatures of inflammation in both tissues following acute sleep loss, but changes involving the circadian clock are evident only in skeletal muscle, and we uncover molecular signatures suggestive of muscle breakdown that contrast with an anabolic adipose tissue signature. Our findings provide insight into how disruption of sleep and circadian rhythms may promote weight gain and sarcopenia.

Cognitive impairments by alcohol and sleep deprivation indicate trait characteristics and a potential role for adenosine A1 receptors

Trait-like differences in cognitive performance after sleep loss put some individuals more at risk than others, the basis of such disparities remaining largely unknown. Similarly, interindividual differences in impairment in response to alcohol intake have been observed. We tested whether performance impairments due to either acute or chronic sleep loss can be predicted by an individual's vulnerability to acute alcohol intake. Also, we used positron emission tomography (PET) to test whether acute alcohol infusion results in an up-regulation of cerebral A1 adenosine receptors (A1ARs), similar to the changes previously observed following sleep deprivation. Sustained attention in the psychomotor vigilance task (PVT) was tested in 49 healthy volunteers (26 ± 5 SD years; 15 females) (i) under baseline conditions: (ii) after ethanol intake, and after either (iii) total sleep deprivation (TSD; 35 hours awake; n = 35) or (iv) partial sleep deprivation (PSD; four nights with 5 hours scheduled sleep; n = 14). Ethanol- versus placebo-induced changes in cerebral A1AR availability were measured in 10 healthy male volunteers (31 ± 9 years) with [18F]8-cyclopentyl-3-(3-fluoropropyl)-1-propylxanthine (CPFPX) PET. Highly significant correlations between the performance impairments induced by ethanol and sleep deprivation were found for various PVT parameters, including mean speed (TSD, r = 0.62; PSD, r = 0.84). A1AR availability increased up to 26% in several brain regions with ethanol infusion. Our studies revealed individual trait characteristics for being either vulnerable or resilient to both alcohol and to sleep deprivation. Both interventions induce gradual increases in cerebral A1AR availability, pointing to a potential common molecular response mechanism.

Plasticity and Susceptibility of Brain Morphometry Alterations to Insufficient Sleep.

Background: Insufficient sleep is common in daily life and can lead to cognitive impairment. Sleep disturbance also exists in neuropsychiatric diseases. However, whether and how acute and chronic sleep loss affect brain morphology remain largely unknown.Methods: We used voxel-based morphology method to study the brain structural changes during sleep deprivation (SD) at six time points of rested wakefulness, 20, 24, 32, 36 h SD, and after one night sleep in 22 healthy subjects, and in 39 patients with chronic primary insomnia relative to 39 status-matched good sleepers. Attention network and spatial memory tests were performed at each SD time point in the SD Procedure. The longitudinal data were analyzed using one-way repeated measures ANOVA, and post-hoc analysis was used to determine the between-group differences.Results: Acute SD is associated with widespread gray matter volume (GMV) changes in the thalamus, cerebellum, insula and parietal cortex. Insomnia is associated with increased GMV in temporal cortex, insula and cerebellum. Acute SD is associated with brain atrophy and as SD hours prolong more areas show reduced GMV, and after one night sleep the brain atrophy is restored and replaced by increased GMV in brain areas. SD has accumulative negative effects on attention and working memory.Conclusions: Acute SD and insomnia exhibit distinct morphological changes of GMV. SD has accumulative negative effects on brain morphology and advanced cognitive function. The altered GMV may provide neurobiological basis for attention and memory impairments following sleep loss.Statement of significanceSleep is less frequently studied using imaging techniques than neurological and psychiatric disorders. Whether and how acute and chronic sleep loss affect brain morphology remain largely unknown. We used voxel-based morphology method to study brain structural changes in healthy subjects over multiple time points during sleep deprivation (SD) status and in patients with chronic insomnia. We found that prolonged acute SD together with one night sleep recovery exhibits accumulative atrophic effect and recovering plasticity on brain morphology, in line with behavioral changes on attentional tasks. Furthermore, acute SD and chronic insomnia exhibit distinct morphological changes of gray matter volume (GMV) but they also share overlapping GMV changes. The altered GMV may provide structural basis for attention and memory impairments following sleep loss.

0230 Mild and Acute Sleep Loss Negatively Impacts Vigilance Reflected by Reduced Neural Sensory Processing, Motor Preparation and Execution

0230 Mild and Acute Sleep Loss Negatively Impacts Vigilance Reflected by Reduced Neural Sensory Processing, Motor Preparation and Execution

Low-grade neuroinflammation due to chronic sleep deprivation results in anxiety and learning and memory impairments.

Chronic sleep loss/fragmentation prevalent in the current 24/7 society is associated with irreversible consequences on health and overall wellbeing. Various studies have well documented the ill effects of acute sleep loss on cognitive functions of individuals; however, the underlying mechanism behind the chronic sleep loss is yet to be explored. The present study was aimed to investigate whether chronic sleep deprivation (CSD) triggers anxiety-like behaviour and memory decline in male Wistar rats. Rats were sleep deprived by placing them over slowly rotating drum (2rpm) for 18h (between 4pm and 10 am) followed by 6h of recovery sleep for 21 consecutive days. Post CSD regimen, rats were subjected to behavioural tests such as elevated plus maze (EPM), Novel Object Recognition (NOR) and Rotarod performance testand then sacrificed to remove brain for further molecular studies. The study demonstrated that CSD rats showed anxiogenic behaviour along with recognition memory decline compared to control rats. CSD rats further showed elevated levels of inflammatory cytokines (TNFα, IL-1β) along with activation of NFκB and AP1 transcription factors in hippocampus and piriform cortex (PC) regions of brain. These observations were also accompanied by enhanced expression of GFAP and Iba1 in the two brain regions. The data suggest that CSD triggered low-grade neuroinflammation which caused anxiogenic response and recognition memory impairment. The study provides preliminary leads to further explore the role of astrocytes/microglial cells and inflammatory cytokines in mediating these neurobehavioural consequences of chronic sleep loss and to develop effective interventions to combat them.

A single night of sleep loss impairs objective but not subjective working memory performance in a sex-dependent manner.

SummaryAcute sleep deprivation can lead to judgement errors and thereby increases the risk of accidents, possibly due to an impaired working memory. However, whether the adverse effects of acute sleep loss on working memory are modulated by auditory distraction in women and men are not known. Additionally, it is unknown whether sleep loss alters the way in which men and women perceive their working memory performance. Thus, 24 young adults (12 women using oral contraceptives at the time of investigation) participated in two experimental conditions: nocturnal sleep (scheduled between 22:30 and 06:30 hours) versus one night of total sleep loss. Participants were administered a digital working memory test in which eight‐digit sequences were learned and retrieved in the morning after each condition. Learning of digital sequences was accompanied by either silence or auditory distraction (equal distribution among trials). After sequence retrieval, each trial ended with a question regarding how certain participants were of the correctness of their response, as a self‐estimate of working memory performance. We found that sleep loss impaired objective but not self‐estimated working memory performance in women. In contrast, both measures remained unaffected by sleep loss in men. Auditory distraction impaired working memory performance, without modulation by sleep loss or sex. Being unaware of cognitive limitations when sleep‐deprived, as seen in our study, could lead to undesirable consequences in, for example, an occupational context. Our findings suggest that sleep‐deprived young women are at particular risk for overestimating their working memory performance.