Showing papers on "Sleep (system call) published in 2022"

Hyperexcitable arousal circuits drive sleep instability during aging

Abstract: Sleep quality declines with age; however, the underlying mechanisms remain elusive. We found that hyperexcitable hypocretin/orexin (Hcrt/OX) neurons drive sleep fragmentation during aging. In aged mice, Hcrt neurons exhibited more frequent neuronal activity epochs driving wake bouts, and optogenetic activation of Hcrt neurons elicited more prolonged wakefulness. Aged Hcrt neurons showed hyperexcitability with lower KCNQ2 expression and impaired M-current, mediated by KCNQ2/3 channels. Single-nucleus RNA-sequencing revealed adaptive changes to Hcrt neuron loss in the aging brain. Disruption of Kcnq2/3 genes in Hcrt neurons of young mice destabilized sleep, mimicking aging-associated sleep fragmentation, whereas the KCNQ-selective activator flupirtine hyperpolarized Hcrt neurons and rejuvenated sleep architecture in aged mice. Our findings demonstrate a mechanism underlying sleep instability during aging and a strategy to improve sleep continuity. Description Aging and sleep disruption In humans, the deterioration of sleep quality during aging is one of the most prevalent complaints. In an animal model, Li et al. found that aging correlated with enhanced spontaneous activity of wake-promoting brain areas during sleep (see the Perspective by Jacobson and Hoyer). Hypocretin-expressing neurons were more active during sleep, raising the chances of brief arousals and thus causing sleep to be more fragmented. The excitability of hypocretin neurons in aged brain tissue was heightened, possibly because of decreased expression of a subpopulation of potassium channels. Aging-related sleep fragmentation may therefore be due to altered intrinsic excitability of arousal-promoting neurons. —PRS Down-regulation of potassium channels causes hyperexcitability of hypocretin neurons and leads to age related fragmentation of sleep. INTRODUCTION Sleep destabilization is strongly associated with aging and cognitive function decline. Despite sleep fragmentation being central to the most prevalent complaints of sleep problems in elderly populations, the mechanistic underpinnings of sleep instability remain elusive. Fragmented sleep during aging has been observed across species, indicating conserved underlying mechanisms across the phylogenetic tree. Therefore, understanding why the aging brain fails to consolidate sleep may shed light on translational applications for improving the sleep quality of aged individuals. RATIONALE We hypothesized that the decline in sleep quality could be due to malfunction of the neural circuits associated with sleep/wake control. It has been established that hypocretin/orexin (Hcrt/OX) neuronal activity is tightly associated with wakefulness and initiates and maintains the wake state. In this study, we investigated whether the intrinsic excitability of Hcrt neurons is altered, leading to a destabilized control of sleep/wake states during aging. RESULTS Aged mice exhibited sleep fragmentation and a significant loss of Hcrt neurons. Hcrt neurons manifested a more frequent firing pattern, driving wake bouts and disrupting sleep continuity in aged mice. Aged Hcrt neurons were capable of eliciting more prolonged wake bouts upon optogenetic stimulations. These results suggested that hyperexcitability of Hcrt neurons emerges with age. Patch clamp recording in genetically identified Hcrt neurons revealed distinct intrinsic properties between the young and aged groups. Aged Hcrt neurons were hyperexcitable with depolarized membrane potentials (RMPs) and a smaller difference between RMP and the firing threshold. Aged Hcrt neurons expressing ChR2-eYFP were more sensitive to optogenetic stimulations, with a smaller-amplitude attenuation upon repetitive light pulse stimulations. More spikelets were generated in aged Hcrt neurons upon current injections. Recording from non-Hcrt neurons postsynaptic to Hcrt neurons revealed that optogenetic stimulation of Hcrt neurons expressing ChR2-eYFP reliably evoked time-locked postsynaptic currents (PSCs) after optogenetic stimulation more often in the aged group. Aged Hcrt neurons were characterized with a functional impairment of repolarizing M-current mediated by KCNQ2/3 channels and an anatomical loss of KCNQ2, revealed with array tomography at ultrastructural resolution. Single-nucleus RNA-sequencing (snRNA-seq) revealed molecular adaptions, including up-regulated prepro-Hcrt mRNA expression and a smaller fraction of Kcnq family subtypes Kcnq1/2/3/5 in aged Hcrt neurons. CRISPR/SaCas9–mediated disruption of Kcnq2/3 genes selectively in Hcrt neurons was sufficient to recapitulate the aging-associated sleep fragmentation trait in young mice. Pharmacological augmentation of M-current repolarized the RMP, suppressed spontaneous firing activity in aged Hcrt neurons, and consolidated sleep stability in aged mice. Sleep fragmentation in a narcolepsy mouse model with genetic ablation of Hcrt neurons at young ages manifested a mechanism other than hyperexcitable arousal-promoting Hcrt neurons that drives sleep fragmentation during healthy aging. CONCLUSION Our data indicate that emerging hyperexcitability of arousal-promoting Hcrt neurons is strongly associated with fragmented sleep in aged mice, which display a lowered sleep-to-wake transition threshold defined for Hcrt neuronal activity. We have demonstrated that the down-regulation of KCNQ2/3 channels compromising repolarization drives Hcrt neuronal hyperexcitability, which leads to sleep instability during aging. Pharmacological remedy of sleep continuity through targeting KCNQ2/3 channels in aged mice confers a potential translational therapy strategy for improving sleep quality in aged individuals. Hyperexcitable Hcrt neurons drive sleep instability during aging. Elevated excitability of Hcrt neurons with depolarized RMPs and adaptive up-regulation of prepro-Hcrt mRNA expression converge to drive sleep/wake instability in the aged brain with substantial Hcrt neuron loss. Hyperexcitable aged Hcrt neurons express functional impairment of KCNQ2/3 channel–mediated M-current and an anatomical loss of KCNQ2, compromising the neurons to repolarize.

Quantitative Evaluation of EEG-Biomarkers for Prediction of Sleep Stages

Abstract: Electroencephalography (EEG) is immediate and sensitive to neurological changes resulting from sleep stages and is considered a computing tool for understanding the association between neurological outcomes and sleep stages. EEG is expected to be an efficient approach for sleep stage prediction outside a highly equipped clinical setting compared with multimodal physiological signal-based polysomnography. This study aims to quantify the neurological EEG-biomarkers and predict five-class sleep stages using sleep EEG data. We investigated the three-channel EEG sleep recordings of 154 individuals (mean age of 53.8 ± 15.4 years) from the Haaglanden Medisch Centrum (HMC, The Hague, The Netherlands) open-access public dataset of PhysioNet. The power of fast-wave alpha, beta, and gamma rhythms decreases; and the power of slow-wave delta and theta oscillations gradually increases as sleep becomes deeper. Delta wave power ratios (DAR, DTR, and DTABR) may be considered biomarkers for their characteristics of attenuation in NREM sleep and subsequent increase in REM sleep. The overall accuracy of the C5.0, Neural Network, and CHAID machine-learning models are 91%, 89%, and 84%, respectively, for multi-class classification of the sleep stages. The EEG-based sleep stage prediction approach is expected to be utilized in a wearable sleep monitoring system.

Memory-enhancing properties of sleep depend on the oscillatory amplitude of norepinephrine

Abstract: Sleep has a complex micro-architecture, encompassing micro-arousals, sleep spindles and transitions between sleep stages. Fragmented sleep impairs memory consolidation, whereas spindle-rich and delta-rich non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep promote it. However, the relationship between micro-arousals and memory-promoting aspects of sleep remains unclear. In this study, we used fiber photometry in mice to examine how release of the arousal mediator norepinephrine (NE) shapes sleep micro-architecture. Here we show that micro-arousals are generated in a periodic pattern during NREM sleep, riding on the peak of locus-coeruleus-generated infraslow oscillations of extracellular NE, whereas descending phases of NE oscillations drive spindles. The amplitude of NE oscillations is crucial for shaping sleep micro-architecture related to memory performance: prolonged descent of NE promotes spindle-enriched intermediate state and REM sleep but also associates with awakenings, whereas shorter NE descents uphold NREM sleep and micro-arousals. Thus, the NE oscillatory amplitude may be a target for improving sleep in sleep disorders. Kjaerby and Andersen et al. show that norepinephrine (NE) plays profound roles in shaping sleep micro-architecture. NE slowly oscillates during sleep, with NE oscillatory amplitude being a major determinant of spindle-dependent memory consolidation and awakenings.

Rapid eye movement sleep is initiated by basolateral amygdala dopamine signaling in mice

Abstract: The sleep cycle is characterized by alternating non–rapid eye movement (NREM) and rapid eye movement (REM) sleeps. The mechanisms by which this cycle is generated are incompletely understood. We found that a transient increase of dopamine (DA) in the basolateral amygdala (BLA) during NREM sleep terminates NREM sleep and initiates REM sleep. DA acts on dopamine receptor D2 (Drd2)–expressing neurons in the BLA to induce the NREM-to-REM transition. This mechanism also plays a role in cataplectic attacks—a pathological intrusion of REM sleep into wakefulness—in narcoleptics. These results show a critical role of DA signaling in the BLA in initiating REM sleep and provide a neuronal basis for sleep cycle generation. Description Dopamine and the gating of REM sleep Sleep is composed of rapid eye movement (REM) and non-REM sleep, and REM sleep usually appears after periods of non-REM sleep. However, we do not understand the mechanisms by which the brain cycles between those states. Using fiber photometry, Hasegawa et al. found increases in dopamine activation before non-REM to REM transitions but not before non-REM to wake transitions in the basolateral amygdala (see the Perspective by Arrigoni and Fuller). This effect was mediated by dopamine receptor D2-expressing neurons in the amygdala. Artificially activating these neurons induced a transition from non-REM to REM sleep and cataplectic states in awake mice. —PRS Transient dopamine elevation in the amygdala during non-REM sleep plays a role in triggering the non-REM to REM sleep transition.

Effect of Sleep Extension on Objectively Assessed Energy Intake Among Adults With Overweight in Real-life Settings

Abstract: This randomized clinical trial examines the energy intake, energy expenditure, and body weight in adults who slept less than 6.5 hours per night.

The links between sleep duration, obesity and type 2 diabetes mellitus

Abstract: Global rates of obesity and type 2 diabetes mellitus (T2DM) are increasing globally concomitant with a rising prevalence of sleep deprivation and sleep disorders. Understanding the links between sleep, obesity and T2DM might offer an opportunity to develop better prevention and treatment strategies for these epidemics. Experimental studies have shown that sleep restriction is associated with changes in energy homeostasis, insulin resistance and β-cell function. Epidemiological cohort studies established short sleep duration as a risk factor for developing obesity and T2DM. In addition, small studies suggested that short sleep duration was associated with less weight loss following lifestyle interventions or bariatric surgery. In this article, we review the epidemiological evidence linking sleep duration to obesity and T2DM and plausible mechanisms. In addition, we review the impact of changes in sleep duration on obesity and T2DM.

Multi-Modal Physiological Signals Based Squeeze-and-Excitation Network With Domain Adversarial Learning for Sleep Staging

Abstract: Sleep staging is the basis of sleep medicine for diagnosing psychiatric and neurodegenerative diseases. However, the existing sleep staging methods ignore the fact that multi-modal physiological signals are heterogeneous, and different modalities contribute to sleep staging with distinct impacts on specific stages. Therefore, how to model the heterogeneity of multi-modal signals and adaptively utilize the multi-modal signals for sleep staging remains challenging. Moreover, existing methods suffer from the individual variance of physiological signals. How to generalize the sleep staging model for the variance among subjects is also challenging. To address the above challenges, we propose the multi-modal physiological signals based Squeeze-and-Excitation Network with Domain Adversarial Learning (SEN-DAL) to capture the features of electroencephalogram (EEG) and electrooculogram (EOG) for sleep staging. The SEN-DAL is made up of two independent feature extraction networks for modeling the heterogeneity, a Multi-modal Squeeze-and-Excitation feature fusion module for adaptively utilizing the multi-modal signals, and a Domain Adversarial Learning module to extract subject-invariant sleep feature. Experiments demonstrate that the SEN-DAL is superior to the baseline models on a public sleep staging dataset, reaching an F1-Score of 82.1%, which is similar to human experts. Through the ablation experiments, we found that the proposed mechanisms, including modal-independent feature extraction, adaptive utilization of multi-modal signals, and domain adversarial learning, are effective for sleep staging tasks. The code of SEN-DAL is available at https://github.com/xiyangcai/SEN-DAL.

Light exposure during sleep impairs cardiometabolic function

Abstract: Significance Ambient nighttime light exposure is implicated as a risk factor for adverse health outcomes, including cardiometabolic disease. However, the effects of nighttime light exposure during sleep on cardiometabolic outcomes and the related mechanisms are unclear. This laboratory study shows that, in healthy adults, one night of moderate (100 lx) light exposure during sleep increases nighttime heart rate, decreases heart rate variability (higher sympathovagal balance), and increases next-morning insulin resistance when compared to sleep in a dimly lit (<3 lx) environment. Moreover, a positive relationship between higher sympathovagal balance and insulin levels suggests that sympathetic activation may play a role in the observed light-induced changes in insulin sensitivity.

Sleep Quality: A Narrative Review on Nutrition, Stimulants, and Physical Activity as Important Factors

Abstract: Sleep is a cyclically occurring, transient, and functional state that is controlled primarily by neurobiological processes. Sleep disorders and insomnia are increasingly being diagnosed at all ages. These are risk factors for depression, mental disorders, coronary heart disease, metabolic syndrome, and/or high blood pressure. A number of factors can negatively affect sleep quality, including the use of stimulants, stress, anxiety, and the use of electronic devices before sleep. A growing body of evidence suggests that nutrition, physical activity, and sleep hygiene can significantly affect the quality of sleep. The aim of this review was to discuss the factors that can affect sleep quality, such as nutrition, stimulants, and physical activity.

The two‐process model of sleep regulation: Beginnings and outlook

Abstract: The two‐process model serves as a major conceptual framework in sleep science. Although dating back more than four decades, it has not lost its relevance for research today. Retracing its origins, I describe how animal experiments aimed at exploring the oscillators driving the circadian sleep–wake rhythm led to the recognition of gradients of sleep states within the daily sleep period. Advances in signal analysis revealed that the level of slow‐wave activity in non‐rapid eye movement sleep electroencephalogram is high at the beginning of the 12‐light period and then declines. After sleep deprivation, the level of slow‐wave activity is enhanced. By scheduling recovery sleep to the animal's activity period, the conflict between the sleep–wake‐dependent and the circadian influence resulted in a two‐stage recovery pattern. These experiments provided the basis for the first version of the two‐process model. Sleep deprivation experiments in humans showed that the decline of slow‐wave activity during sleep is exponential. The two‐process model posits that a sleep–wake‐dependent homeostatic process (Process S) interacts with a process controlled by the circadian pacemaker (Process C). At present, homeostatic and circadian facets of sleep regulation are being investigated at the synaptic level as well as in the transcriptome and proteome domains. The notion of sleep has been extended from a global phenomenon to local representations, while the master circadian pacemaker has been supplemented by multiple peripheral oscillators. The original interpretation that the emergence of sleep may be viewed as an escape from the rigid control imposed by the circadian pacemaker is still upheld.

A Validation of Six Wearable Devices for Estimating Sleep, Heart Rate and Heart Rate Variability in Healthy Adults

Abstract: The primary aim of this study was to examine the validity of six commonly used wearable devices, i.e., Apple Watch S6, Garmin Forerunner 245 Music, Polar Vantage V, Oura Ring Generation 2, WHOOP 3.0 and Somfit, for assessing sleep. The secondary aim was to examine the validity of the six devices for assessing heart rate and heart rate variability during, or just prior to, night-time sleep. Fifty-three adults (26 F, 27 M, aged 25.4 ± 5.9 years) spent a single night in a sleep laboratory with 9 h in bed (23:00–08:00 h). Participants were fitted with all six wearable devices—and with polysomnography and electrocardiography for gold-standard assessment of sleep and heart rate, respectively. Compared with polysomnography, agreement (and Cohen’s kappa) for two-state categorisation of sleep periods (as sleep or wake) was 88% (κ = 0.30) for Apple Watch; 89% (κ = 0.35) for Garmin; 87% (κ = 0.44) for Polar; 89% (κ = 0.51) for Oura; 86% (κ = 0.44) for WHOOP and 87% (κ = 0.48) for Somfit. Compared with polysomnography, agreement (and Cohen’s kappa) for multi-state categorisation of sleep periods (as a specific sleep stage or wake) was 53% (κ = 0.20) for Apple Watch; 50% (κ = 0.25) for Garmin; 51% (κ = 0.28) for Polar; 61% (κ = 0.43) for Oura; 60% (κ = 0.44) for WHOOP and 65% (κ = 0.52) for Somfit. Analyses regarding the two-state categorisation of sleep indicate that all six devices are valid for the field-based assessment of the timing and duration of sleep. However, analyses regarding the multi-state categorisation of sleep indicate that all six devices require improvement for the assessment of specific sleep stages. As the use of wearable devices that are valid for the assessment of sleep increases in the general community, so too does the potential to answer research questions that were previously impractical or impossible to address—in some way, we could consider that the whole world is becoming a sleep laboratory.

Rising temperatures erode human sleep globally

Abstract: •Warmer temperatures reduce sleep globally, amplifying the risk of insufficient sleep •The elderly, women, and residents of lower-income countries are impacted most •Those living in warmer climates lose more sleep per degree of temperature rise •Climate change is projected to unequally erode sleep, widening global inequalities Ambient temperatures are rising worldwide, with the greatest increases recorded at night. Concurrently, the prevalence of insufficient sleep is rising in many populations. Yet it remains unclear whether warmer-than-average temperatures causally impact objective measures of sleep globally. Here, we link billions of repeated sleep measurements from sleep-tracking wristbands comprising over 7 million sleep records (n = 47,628) across 68 countries to local daily meteorological data. Controlling for individual, seasonal, and time-varying confounds, increased temperature shortens sleep primarily through delayed onset, increasing the probability of insufficient sleep. The temperature effect on sleep loss is substantially larger for residents from lower-income countries and older adults, and females are affected more than males. Those in hotter regions experience comparably more sleep loss per degree of warming, suggesting limited adaptation. By 2099, suboptimal temperatures may erode 50–58 h of sleep per person-year, with climate change producing geographic inequalities that scale with future emissions. Ambient temperatures are rising worldwide, with the greatest increases recorded at night. Concurrently, the prevalence of insufficient sleep is rising in many populations. Yet it remains unclear whether warmer-than-average temperatures causally impact objective measures of sleep globally. Here, we link billions of repeated sleep measurements from sleep-tracking wristbands comprising over 7 million sleep records (n = 47,628) across 68 countries to local daily meteorological data. Controlling for individual, seasonal, and time-varying confounds, increased temperature shortens sleep primarily through delayed onset, increasing the probability of insufficient sleep. The temperature effect on sleep loss is substantially larger for residents from lower-income countries and older adults, and females are affected more than males. Those in hotter regions experience comparably more sleep loss per degree of warming, suggesting limited adaptation. By 2099, suboptimal temperatures may erode 50–58 h of sleep per person-year, with climate change producing geographic inequalities that scale with future emissions.

When the Locus Coeruleus Speaks Up in Sleep: Recent Insights, Emerging Perspectives

Abstract: For decades, numerous seminal studies have built our understanding of the locus coeruleus (LC), the vertebrate brain’s principal noradrenergic system. Containing a numerically small but broadly efferent cell population, the LC provides brain-wide noradrenergic modulation that optimizes network function in the context of attentive and flexible interaction with the sensory environment. This review turns attention to the LC’s roles during sleep. We show that these roles go beyond down-scaled versions of the ones in wakefulness. Novel dynamic assessments of noradrenaline signaling and LC activity uncover a rich diversity of activity patterns that establish the LC as an integral portion of sleep regulation and function. The LC could be involved in beneficial functions for the sleeping brain, and even minute alterations in its functionality may prove quintessential in sleep disorders.

Sleep apnoea and ischaemic stroke: current knowledge and future directions

Abstract: Sleep apnoea, one of the most common chronic diseases, is a risk factor for ischaemic stroke, stroke recurrence, and poor functional recovery after stroke. More than half of stroke survivors present with sleep apnoea during the acute phase after stroke, with obstructive sleep apnoea being the most common subtype. Following a stroke, sleep apnoea frequency and severity might decrease over time, but moderate to severe sleep apnoea is nevertheless present in up to a third of patients in the chronic phase after an ischaemic stroke. Over the past few decades evidence suggests that treatment for sleep apnoea is feasible during the acute phase of stroke and might favourably affect recovery and long-term outcomes. Nevertheless, sleep apnoea still remains underdiagnosed and untreated in many cases, due to challenges in the detection and prediction of post-stroke sleep apnoea, uncertainty as to the optimal timing for its diagnosis, and a scarcity of clear treatment guidelines (ie, uncertainty on when to treat and the optimal treatment strategy). Moreover, the pathophysiology of sleep apnoea associated with stroke, the proportion of stroke survivors with obstructive and central sleep apnoea, and the temporal evolution of sleep apnoea subtypes following stroke remain to be clarified. To address these shortcomings, the management of sleep apnoea associated with stroke should be integrated into a multidisciplinary diagnostic, treatment, and follow-up strategy.

The brain structure and genetic mechanisms underlying the nonlinear association between sleep duration, cognition and mental health

Abstract: Sleep duration, psychiatric disorders and dementias are closely interconnected in older adults. However, the underlying genetic mechanisms and brain structural changes are unknown. Using data from the UK Biobank for participants primarily of European ancestry aged 38–73 years, including 94% white people, we identified a nonlinear association between sleep, with approximately 7 h as the optimal sleep duration, and genetic and cognitive factors, brain structure, and mental health as key measures. The brain regions most significantly underlying this interconnection included the precentral cortex, the lateral orbitofrontal cortex and the hippocampus. Longitudinal analysis revealed that both insufficient and excessive sleep duration were significantly associated with a decline in cognition on follow up. Furthermore, mediation analysis and structural equation modeling identified a unified model incorporating polygenic risk score (PRS), sleep, brain structure, cognition and mental health. This indicates that possible genetic mechanisms and brain structural changes may underlie the nonlinear relationship between sleep duration and cognition and mental health. Change in sleep patterns is an important feature of the aging process. This study shows that sleep duration is nonlinearly associated with mental health and cognition measures in the 38- to 73-year-old population, with underlying brain and genetic mechanisms.

Sleep function: an evolutionary perspective

Abstract: Prospective epidemiological studies in industrial societies indicate that 7 h of sleep per night in people aged 18 years or older is optimum, with higher and lower amounts of sleep predicting a shorter lifespan. Humans living a hunter-gatherer lifestyle (eg, tribal groups) sleep for 6-8 h per night, with the longest sleep durations in winter. The prevalence of insomnia in hunter-gatherer populations is low (around 2%) compared with the prevalence of insomnia in industrial societies (around 10-30%). Sleep deprivation studies, which are done to gain insights into sleep function, are often confounded by the effects of stress. Consideration of the duration of spontaneous daily sleep across species of mammals, which ranges from 2 h to 20 h, can provide important insights into sleep function without the stress of deprivation. Sleep duration is not related to brain size or cognitive ability. Rather, sleep duration across species is associated with their ecological niche and feeding requirements, indicating a role for wake-sleep balance in food acquisition and energy conservation. Brain temperature drops from waking levels during non-rapid eye movement (non-REM) sleep and rises during REM sleep. Average daily REM sleep time of homeotherm orders is negatively correlated with average body and brain temperature, with the largest amount of REM sleep in egg laying (monotreme) mammals, moderate amounts in pouched (marsupial) mammals, lower amounts in placental mammals, and the lowest amounts in birds. REM sleep might, therefore, have a key role in the regulation of temperature and metabolism of the brain during sleep and in the facilitation of alert awakening.

Automatic sleep staging of EEG signals: recent development, challenges, and future directions

Abstract: Abstract Modern deep learning holds a great potential to transform clinical studies of human sleep. Teaching a machine to carry out routine tasks would be a tremendous reduction in workload for clinicians. Sleep staging, a fundamental step in sleep practice, is a suitable task for this and will be the focus in this article. Recently, automatic sleep-staging systems have been trained to mimic manual scoring, leading to similar performance to human sleep experts, at least on scoring of healthy subjects. Despite tremendous progress, we have not seen automatic sleep scoring adopted widely in clinical environments. This review aims to provide the shared view of the authors on the most recent state-of-the-art developments in automatic sleep staging, the challenges that still need to be addressed, and the future directions needed for automatic sleep scoring to achieve clinical value.

Performance of Four Commercial Wearable Sleep-Tracking Devices Tested Under Unrestricted Conditions at Home in Healthy Young Adults

Abstract: Commercial wearable sleep-tracking devices are growing in popularity and in recent studies have performed well against gold standard sleep measurement techniques. However, most studies were conducted in controlled laboratory conditions. We therefore aimed to test the performance of devices under naturalistic unrestricted home sleep conditions.Healthy young adults (n = 21; 12 women, 9 men; 29.0 ± 5.0 years, mean ± SD) slept at home under unrestricted conditions for 1 week using a set of commercial wearable sleep-tracking devices and completed daily sleep diaries. Devices included the Fatigue Science Readiband, Fitbit Inspire HR, Oura ring, and Polar Vantage V Titan. Participants also wore a research-grade actigraphy watch (Philips Respironics Actiwatch 2) for comparison. To assess performance, all devices were compared with a high performing mobile sleep electroencephalography headband device (Dreem 2). Analyses included epoch-by-epoch and sleep summary agreement comparisons.Devices accurately tracked sleep-wake summary metrics (ie, time in bed, total sleep time, sleep efficiency, sleep latency, wake after sleep onset) on most nights but performed best on nights with higher sleep efficiency. Epoch-by-epoch sensitivity (for sleep) and specificity (for wake), respectively, were as follows: Actiwatch (0.95, 0.35), Fatigue Science (0.94, 0.40), Fitbit (0.93, 0.45), Oura (0.94, 0.41), and Polar (0.96, 0.35). Sleep stage-tracking performance was mixed, with high variability.As in previous studies, all devices were better at detecting sleep than wake, and most devices compared favorably to actigraphy in wake detection. Devices performed best on nights with more consolidated sleep patterns. Unrestricted sleep TIB differences were accurately tracked on most nights. High variability in sleep stage-tracking performance suggests that these devices, in their current form, are still best utilized for tracking sleep-wake outcomes and not sleep stages. Most commercial wearables exhibited promising performance for tracking sleep-wake in real-world conditions, further supporting their consideration as an alternative to actigraphy.