Biomathematical modeling of fatigue due to sleep inertia.

Biomathematical models of fatigue capture the physiology of sleep/wake regulation and circadian rhythmicity to predict changes in neurobehavioral functioning over time. We used a biomathematical model of fatigue linked to the adenosinergic neuromodulator/receptor system in the brain as a framework to predict sleep inertia, that is, the transient neurobehavioral impairment experienced immediately after awakening. Based on evidence of an adenosinergic basis for sleep inertia, we expanded the biomathematical model with novel differential equations to predict the propensity for sleep inertia during sleep and its manifestation after awakening. Using datasets from large laboratory studies of sleep loss and circadian misalignment, we calibrated the model by fitting just two new parameters and then validated the model's predictions against independent data. The expanded model was found to predict the magnitude and time course of sleep inertia with generally high accuracy. Analysis of the model's dynamics revealed a bifurcation in the predicted manifestation of sleep inertia in sustained sleep restriction paradigms, which reflects the observed escalation of the magnitude of sleep inertia in scenarios with sleep restriction to less than âˆ¼ 4 h per day. Another emergent property of the model involves a rapid increase in the predicted propensity for sleep inertia in the early part of sleep followed by a gradual decline in the later part of the sleep period, which matches what would be expected based on the adenosinergic regulation of non-rapid eye movement (NREM) sleep and its known influence on sleep inertia. These dynamic behaviors provide confidence in the validity of our approach and underscore the predictive potential of the model. The expanded model provides a useful tool for predicting sleep inertia and managing impairment in 24/7 settings where people may need to perform critical tasks immediately after awakening, such as on-demand operations in safety and security, emergency response, and health care.

The dynamic responses of mood and sleep physiology to chronic sleep restriction and subsequent recovery sleep.

Healthy sleep of sufficient duration preserves mood and disturbed sleep is a risk factor for a range of psychiatric disorders. As adults commonly experience chronic sleep restriction (SR), an enhanced understanding of the dynamic relationship between sleep and mood is needed, including whether susceptibility to SR-induced mood disturbance differs between sexes. To address these gaps, data from N=221 healthy adults who completed one of two multi-day laboratory studies with identical 9-day SR protocols were analyzed. Participants randomized to the SR (n=205) condition underwent 5 nights of SR to 4 h time-in-bed and were then randomized to one of seven sleep doses that ranged from 0 h to 12 h in 2 h increments; participants randomized to the control (n=16) condition received 10 h time-in-bed on all study nights. The Profile of Mood States (POMS) was used to assess mood every 2 h during wakefulness and markers of sleep homeostasis (EEG slow-wave activity) were derived via polysomnography. Mood progressively deteriorated across SR with marked disturbances in somatic mood components. Altered sleep physiology contributed to mood disturbance whereby increased EEG slow-wave activity was associated with increased POMS Total Mood Disturbance scores, a finding specific to males. Mood was restored in a dose-response fashion where improvements were greater with longer sleep doses. These findings suggest that when lifestyle and environmental factors are inhibited in the laboratory, the affective consequences of chronic sleep loss are primarily somatic mood disturbances. Altered sleep homeostasis may contribute to mood disturbance, yet sleep-dependent mechanisms may be sex-specific.

Sleep deprivation attenuates neural responses to outcomes from risky decision-making.

Sleep loss impacts a broad range of brain and cognitive functions. However, how sleep deprivation affects risky decision-making remains inconclusive. This study used functional MRI to examine the impact of one night of total sleep deprivation (TSD) on risky decision-making behavior and the underlying brain responses in healthy adults. In this study, we analyzed data from N = 56 participants in a strictly controlled 5-day and 4-night in-laboratory study using a modified Balloon Analogue Risk Task. Participants completed two scan sessions in counter-balanced order, including one scan during rested wakefulness (RW) and another scan after one night of TSD. Results showed no differences in participants' risk-taking propensity and risk-induced activation between RW and TSD. However, participants showed significantly reduced neural activity in the anterior cingulate cortex and bilateral insula for loss outcomes, and in bilateral putamen for win outcomes during TSD compared with RW. Moreover, risk-induced activation in the insula negatively correlated with participants' risk-taking propensity during RW, while no such correlations were observed after TSD. These findings suggest that sleep loss may impact risky decision-making by attenuating neural responses to decision outcomes and impairing brain-behavior associations.

Long-term influence of sleep/wake history on the dynamic neurobehavioural response to sustained sleep restriction.

Chronic sleep restriction, common in today's 24/7 society, causes cumulative neurobehavioural impairment, but the dynamics of the build-up and dissipation of this impairment have not been fully elucidated. We addressed this knowledge gap in a laboratory study involving two, 5-day periods of sleep restriction to 4 hr per day, separated by a 1-day dose-response intervention sleep opportunity. We measured sleep physiological and waking neurobehavioural responses in 70 healthy adults, each randomized to one of seven dose-response intervention sleep doses ranging from 0 to 12 hr, or a non-sleep-restricted control group. As anticipated, sleep physiological markers showed homeostatic dynamics throughout the study, and waking neurobehavioural impairment accumulated across the two sleep restriction periods. Unexpectedly, there was only a slight and short-lived effect of the 1-day dose-response intervention sleep opportunity. Whether the dose-response intervention sleep opportunity involved extension, further restriction or total deprivation of sleep, neurobehavioural functioning during the subsequent second sleep restriction period was dominated by prior sleep-wake history. Our findings revealed a profound and enduring influence of long-term sleep-wake history as a fundamental aspect of the dynamic regulation of the neurobehavioural response to sleep loss.

Antidepressant effects of acute sleep deprivation are reduced in highly controlled environments.

BACKGROUND: Numerous studies summarized in a recent meta-analysis have shown sleep deprivation rapidly improves depressive symptoms in approximately 50 % of individuals with major depressive disorder (MDD), however those studies were typically conducted in clinical settings. Here we investigated the effects of sleep deprivation utilizing a highly controlled experimental approach. METHODS: 36 antidepressant-free individuals with MDD and 10 healthy controls (HC) completed a 5 day/4-night protocol consisting of adaptation, baseline, total sleep deprivation (TSD), and recovery phases. Light was kept consistently dim (≤50 lx), meals were regulated, and activity was restricted. In-the-moment mood was assessed using a modified Hamilton Rating Scale for Depression (HRSD) at screening and each morning following the experimental nights. RESULTS: Day of study had a significant effect on mood in both groups. Post-hoc analyses revealed that significant effects were attributed to mood improvement in the MDD group following study initiation prior to beginning TSD, and in the HC group following recovery sleep, but were not due to mood improvement in the MDD group during TSD. No further improvement in mood occurred during 36 h of TSD. LIMITATIONS: Strict eligibility requirements may limit generalizability. The requirement to be medication free may have biased toward a less severely depressed sample. CONCLUSIONS: Results revealed that individuals with moderate MDD can experience a significant reduction in depressive symptoms upon entering a highly controlled laboratory environment. Environmental effects on mood can be substantial and need to be considered.

The neighborhood environment and sleep health in adolescents.

OBJECTIVE: Neighborhood-level factors, including education, health and environment, and socioeconomic exposures, are important contextual determinants of child health. We explored whether these factors, measured via the Childhood Opportunity Index 2.0, were associated with sleep health in adolescents. METHODS: Actigraphy was used to assess sleep duration, timing, and efficiency among 110 adolescents in eighth (13.9 (0.4)) and ninth (14.9 (0.4)) grade. Home addresses were geocoded and linked to Childhood Opportunity Index 2.0 scores (including 3 subtype scores and the 29 individual factor Z-scores). Mixed-effects linear regression was used to determine associations between the Childhood Opportunity Index 2.0 scores and the sleep outcomes, adjusting for sex, race, parent education, household income, school grade and weeknight status. Interactions were also tested by school grade, weeknight status, sex, and race. RESULTS: No associations were observed between overall or subtype scores with sleep outcomes in adolescents. However, we detected associations between select individual Childhood Opportunity Index 2.0 Z-scores, spanning health & environment and education domains, and sleep outcomes. For example, greater fine particulate matter was associated with later timing of sleep onset and offset; ozone concentration was associated with earlier sleep onset and offset; greater exposure to extreme temperature was associated with later sleep onset and offset and increased odds of optimal sleep efficiency. CONCLUSIONS: Specific neighborhood factors indexed by the Childhood Opportunity Index 2.0 were associated with sleep health among adolescents. In particular, neighborhood air quality measures were associated with sleep timing and efficiency, warranting further investigation.

Enhanced amygdala-cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation.

Sleep loss robustly disrupts mood and emotion regulation in healthy individuals but can have a transient antidepressant effect in a subset of patients with depression. The neural mechanisms underlying this paradoxical effect remain unclear. Previous studies suggest that the amygdala and dorsal nexus (DN) play key roles in depressive mood regulation. Here, we used functional MRI to examine associations between amygdala- and DN-related resting-state connectivity alterations and mood changes after one night of total sleep deprivation (TSD) in both healthy adults and patients with major depressive disorder using strictly controlled in-laboratory studies. Behavioral data showed that TSD increased negative mood in healthy participants but reduced depressive symptoms in 43% of patients. Imaging data showed that TSD enhanced both amygdala- and DN-related connectivity in healthy participants. Moreover, enhanced amygdala connectivity to the anterior cingulate cortex (ACC) after TSD associated with better mood in healthy participants and antidepressant effects in depressed patients. These findings support the key role of the amygdala-cingulate circuit in mood regulation in both healthy and depressed populations and suggest that rapid antidepressant treatment may target the enhancement of amygdala-ACC connectivity.

Associations of bedroom PM2.5, CO2, temperature, humidity, and noise with sleep: An observational actigraphy study.

OBJECTIVE: Climate change and urbanization increasingly cause extreme conditions hazardous to health. The bedroom environment plays a key role for high-quality sleep. Studies objectively assessing multiple descriptors of the bedroom environment as well as sleep are scarce. METHODS: Particulate matter with a particle size <2.5 µm (PM2.5), temperature, humidity, carbon dioxide (CO2), barometric pressure, and noise levels were continuously measured for 14 consecutive days in the bedroom of 62 participants (62.9% female, mean ± SD age: 47.7 ± 13.2 years) who wore a wrist actigraph and completed daily morning surveys and sleep logs. RESULTS: In a hierarchical mixed effect model that included all environmental variables and adjusted for elapsed sleep time and multiple demographic and behavioral variables, sleep efficiency calculated for consecutive 1-hour periods decreased in a dose-dependent manner with increasing levels of PM2.5, temperature, CO2, and noise. Sleep efficiency in the highest exposure quintiles was 3.2% (PM2.5, p < .05), 3.4% (temperature, p < .05), 4.0% (CO2, p < .01), and 4.7% (noise, p < .0001) lower compared to the lowest exposure quintiles (all p-values adjusted for multiple testing). Barometric pressure and humidity were not associated with sleep efficiency. Bedroom humidity was associated with subjectively assessed sleepiness and poor sleep quality (both p < .05), but otherwise environmental variables were not statistically significantly associated with actigraphically assessed total sleep time and wake after sleep onset or with subjectively assessed sleep onset latency, sleep quality, and sleepiness. Assessments of bedroom comfort suggest subjective habituation irrespective of exposure levels. CONCLUSIONS: These findings add to a growing body of evidence highlighting the importance of the bedroom environment-beyond the mattress-for high-quality sleep.

Promoting Sleep Duration in the Pediatric Setting Using a Mobile Health Platform: A Randomized Optimization Trial.

Objective: Determine the optimal combination of digital health intervention component settings that increase average sleep duration by ≥30 minutes per weeknight. Methods: Optimization trial using a 25 factorial design. The trial included 2 week run-in, 7 week intervention, and 2 week follow-up periods. Typically developing children aged 9-12y, with weeknight sleep duration <8.5 hours were enrolled (N=97). All received sleep monitoring and performance feedback. The five candidate intervention components (with their settings to which participants were randomized) were: 1) sleep goal (guideline-based or personalized); 2) screen time reduction messaging (inactive or active); 3) daily routine establishing messaging (inactive or active); 4) child-directed loss-framed financial incentive (inactive or active); and 5) caregiver-directed loss-framed financial incentive (inactive or active). The primary outcome was weeknight sleep duration (hours per night). The optimization criterion was: ≥30 minutes average increase in sleep duration on weeknights. Results: Average baseline sleep duration was 7.7 hours per night. The highest ranked combination included the core intervention plus the following intervention components: sleep goal (either setting was effective), caregiver-directed loss-framed incentive, messaging to reduce screen time, and messaging to establish daily routines. This combination increased weeknight sleep duration by an average of 39.6 (95% CI: 36.0, 43.1) minutes during the intervention period and by 33.2 (95% CI: 28.9, 37.4) minutes during the follow-up period. Conclusions: Optimal combinations of digital health intervention component settings were identified that effectively increased weeknight sleep duration. This could be a valuable remote patient monitoring approach to treat insufficient sleep in the pediatric setting.

Dynamic ensemble prediction of cognitive performance in spaceflight.

During spaceflight, astronauts face a unique set of stressors, including microgravity, isolation, and confinement, as well as environmental and operational hazards. These factors can negatively impact sleep, alertness, and neurobehavioral performance, all of which are critical to mission success. In this paper, we predict neurobehavioral performance over the course of a 6-month mission aboard the International Space Station (ISS), using ISS environmental data as well as self-reported and cognitive data collected longitudinally from 24 astronauts. Neurobehavioral performance was repeatedly assessed via a 3-min Psychomotor Vigilance Test (PVT-B) that is highly sensitive to the effects of sleep deprivation. To relate PVT-B performance to time-varying and discordantly-measured environmental, operational, and psychological covariates, we propose an ensemble prediction model comprising of linear mixed effects, random forest, and functional concurrent models. An extensive cross-validation procedure reveals that this ensemble outperforms any one of its components alone. We also identify the most important predictors of PVT-B performance, which include an individual's previous PVT-B performance, reported fatigue and stress, and temperature and radiation dose. This method is broadly applicable to settings where the main goal is accurate, individualized prediction of human behavior involving a mixture of person-level traits and irregularly measured time series.

Sleep deficiency in spaceflight is associated with degraded neurobehavioral functions and elevated stress in astronauts on six-month missions aboard the International Space Station.

Astronauts are required to maintain optimal neurobehavioral functioning despite chronic exposure to the stressors and challenges of spaceflight. Sleep of adequate quality and duration is fundamental to neurobehavioral functioning, however astronauts commonly experience short sleep durations in spaceflight (<6 h). As humans embark on long-duration space exploration missions, there is an outstanding need to identify the consequences of sleep deficiency in spaceflight on neurobehavioral functions. Therefore, we conducted a longitudinal study that examined the sleep-wake behaviors, neurobehavioral functions, and ratings of stress and workload of N = 24 astronauts before, during, and after 6-month missions aboard the International Space Station (ISS). The computerized, Reaction SelfTest (RST), gathered astronaut report of sleep-wake behaviors, stress, workload, and somatic behavioral states; the RST also objectively assessed vigilant attention (i.e. Psychomotor Vigilance Test-Brief). Data collection began 180 days before launch, continued every 4 days in-flight aboard the ISS, and up to 90 days post-landing, which produced N = 2,856 RSTs. Consistent with previous ISS studies, astronauts reported sleeping ~6.5 h in-flight. The adverse consequences of short sleep were observed across neurobehavioral functions, where sleep durations <6 h were associated with significant reductions in psychomotor response speed, elevated stress, and higher workload. Sleep durations <5 h were associated with elevated negative somatic behavioral states. Furthermore, longer sleep durations had beneficial effects on astronaut neurobehavioral functions. Taken together, our findings highlight the importance of sleep for the maintenance of neurobehavioral functioning and as with humans on Earth, astronauts would likely benefit from interventions that promote sleep duration and quality.

Predictors of interindividual differences in vulnerability to neurobehavioral consequences of chronic partial sleep restriction.

Interindividual differences in the neurobehavioral response to sleep loss are largely unexplained and phenotypic in nature. Numerous factors have been examined as predictors of differential response to sleep loss, but none have yielded a comprehensive view of the phenomenon. The present study examines the impact of baseline factors, habitual sleep-wake patterns, and homeostatic response to sleep loss on accrued deficits in psychomotor vigilance during chronic partial sleep restriction (SR), in a total of 306 healthy adults that participated in one of three independent laboratory studies. Findings indicate no significant impact of personality, academic intelligence, subjective reports of chronotype, sleepiness and fatigue, performance on working memory, and demographic factors such as sex, ethnicity, and body mass index, on neurobehavioral vulnerability to the negative effects of sleep loss. Only superior baseline performance on the psychomotor vigilance test and ability to sustain wakefulness on the maintenance of wakefulness test were associated with relative resilience to decrements in vigilant attention during SR. Interindividual differences in vulnerability to the effects of sleep loss were not accounted for by prior sleep history, habitual sleep patterns outside of the laboratory, baseline sleep architecture, or homeostatic sleep response during chronic partial SR. A recent theoretical model proposed that sleep-wake modulation may be influenced by competing internal and external demands which may promote wakefulness despite homeostatic and circadian signals for sleep under the right circumstances. Further research is warranted to examine the possibility of interindividual differences in the ability to prioritize external demands for wakefulness in the face of mounting pressure to sleep.

Sleep and Alertness Among Interns in Intensive Care Compared to General Medicine Rotations: A Secondary Analysis of the iCOMPARE Trial.

BACKGROUND: Medical interns are at risk for sleep deprivation from long and often rotating work schedules. However, the effects of specific rotations on sleep are less clear. OBJECTIVE: To examine differences in sleep duration and alertness among internal medicine interns during inpatient intensive care unit (ICU) compared to general medicine (GM) rotations. METHODS: This secondary analysis compared interns during a GM or ICU rotation from a randomized trial (2015-2016) of 12 internal medicine residency programs assigned to different work hour limit policies (standard 16-hour shifts or no shift-length limits). The primary outcome was sleep duration/24-hour using continuous wrist actigraphy over a 13-day period. Secondary outcomes assessed each morning during the concomitant actigraphy period were sleepiness (Karolinska Sleepiness Scale [KSS]), alertness (number of Brief Psychomotor Vigilance Test [PVT-B] lapses), and self-report of excessive sleepiness over past 24 hours. Linear mixed-effect models with random program intercept determined associations between each outcome by rotation, controlling for age, sex, and work hour policy followed. RESULTS: Of 398 interns, 386 were included (n = 261 GM, n = 125 ICU). Average sleep duration was 7.00±0.08h and 6.84±0.10h, and number of PVT lapses were 5.5±0.5 and 5.7±0.7 for GM and ICU, respectively (all P > .05). KSS was 4.8±0.1 for both rotations. Compared to GM, ICU interns reported more days of excessive sleepiness from 12am-6am (2.6 vs 1.7, P < .001) and 6am-12pm (2.6 vs 1.9, P = .013) and had higher percent of days with sleep duration < 6 hours (27.6% vs 23.4%, P < .001). GM interns reported more days with no excessive sleepiness (5.3 vs 3.7, P < .001). CONCLUSIONS: Despite ICU interns reporting more excessive sleepiness in morning hours and more days of insufficient sleep (<6 hours), overall sleep duration and alertness did not significantly differ between rotations.

Impaired Vigilant Attention Partly Accounts for Inhibition Control Deficits After Total Sleep Deprivation and Partial Sleep Restriction.

PURPOSE: Sleep loss impairs a range of neurobehavioral functions, particularly vigilant attention and arousal. However, the detrimental effects of sleep deprivation on inhibition control and its relationship to vigilant attention impairments remain unclear. This study examined the extent to which vigilant attention deficits contribute to inhibition control performance after one night of total sleep deprivation (TSD) and two nights of partial sleep restriction (PSR). PARTICIPANTS AND METHODS: We analyzed data from N = 49 participants in a one-night of TSD experiment, N=16 participants in a control experiment without sleep loss, and N = 16 participants in a two-nights of PSR experiment (time in bed, TIB = 6 h for each night). Throughout waking periods in each condition, participants completed the psychomotor vigilance test (PVT), which measures vigilant attention, and the Go/No-Go task, which measures inhibition control. RESULTS: After TSD and PSR, participants displayed significantly slower reaction times (RT) and more lapses in PVT performance, as well as slower Go RT and more errors of omission during the Go/No-Go task. PVT deficits accounted for 18.0% of the change in Go RT and 12.4% of the change in errors of omission in the TSD study, and 23.7% of the change in Go RT and 20.3% of the change in errors of omission in the PSR study. CONCLUSION: Both TSD and PSR impaired inhibition control during the Go/No-Go task, which can be partly accounted for by vigilant attention deficits during the PVT. These findings support the key role of vigilant attention in maintaining overall neurobehavioral function after sleep loss.

Fatigue risk management based on self-reported fatigue: Expanding a biomathematical model of fatigue-related performance deficits to also predict subjective sleepiness.

Biomathematical models of fatigue can be used to predict neurobehavioral deficits during sleep/wake or work/rest schedules. Current models make predictions for objective performance deficits and/or subjective sleepiness, but known differences in the temporal dynamics of objective versus subjective outcomes have not been addressed. We expanded a biomathematical model of fatigue previously developed to predict objective performance deficits as measured on the Psychomotor Vigilance Test (PVT) to also predict subjective sleepiness as self-reported on the Karolinska Sleepiness Scale (KSS). Four model parameters were re-estimated to capture the distinct dynamics of the KSS and account for the scale difference between KSS and PVT. Two separate ensembles of datasets - drawn from laboratory studies of sleep deprivation, sleep restriction, simulated night work, napping, and recovery sleep - were used for calibration and subsequent validation of the model for subjective sleepiness. The expanded model was found to exhibit high prediction accuracy for subjective sleepiness, while retaining high prediction accuracy for objective performance deficits. Application of the validated model to an example scenario based on cargo aviation operations revealed divergence between predictions for objective and subjective outcomes, with subjective sleepiness substantially underestimating accumulating objective impairment, which has important real-world implications. In safety-sensitive operations such as commercial aviation, where self-ratings of sleepiness are used as part of fatigue risk management, the systematic differences in the temporal dynamics of objective versus subjective measures of functional impairment point to a potentially significant risk evaluation sensitivity gap. The expanded biomathematical model of fatigue presented here provides a useful quantitative tool to bridge this previously unrecognized gap.

Serum micronutrient status, sleep quality and neurobehavioural function among early adolescents.

OBJECTIVE: To examine associations between serum micronutrients and neurobehavioural function and the mediating role of sleep quality in early adolescents. DESIGN: In this cross-sectional study, peripheral blood samples were analysed for Fe and Zn levels. The Pittsburgh Sleep Quality Index and Penn Computerized Neurocognitive Battery were used to assess sleep quality and neurobehavioural function, respectively. The logistic/linear regressions and generalised structural equation modelling were performed to estimate the associations. SETTING: Jintan, China. PARTICIPANTS: In total, 226 adolescents (106 females) from the Jintan Child Cohort study. RESULTS: Adolescents with low Fe (<75 µg/dl) (OR = 1·29, P = 0·04) and low Zn (<70 µg/dl) (OR = 1·58, P < 0·001) were associated with increased odds for poor sleep quality. Adolescents with low Fe and Zn were associated with fast (Fe: ß = -1353·71, P = 0·002, Zn: ß = -2262·01, P = 0·02) but less-accurate (Fe: ß = -0·97, P = 0·04; Zn: ß = -1·76, P = 0·04) performance on non-verbal reasoning task and poor sleep quality partially mediated the associations between low Fe/Zn and non-verbal reasoning (P < 0·05). Additionally, low Fe was associated with a slower reaction on spatial processing task (ß = 276·94, P = 0·04), and low Zn was associated with fast (ß = -1781·83, P = 0·03), but error-prone performance (ß = -1·79, P = 0·04) on spatial processing ability and slower reaction speed (ß = 12·82, P = 0·03) on the attention task. We observed similar trends using a cut-off point of 75 µg/dl for low serum Zn, except for the association with attention task speed (P > 0·05). CONCLUSION: Fe and Zn deficiencies may possibly be associated with poor sleep and neurobehavioural function among early adolescents. Poor sleep may partially mediate the relationship between micronutrients and neurobehavioural function.

Engineering a mobile platform to promote sleep in the pediatric primary care setting.

STUDY OBJECTIVES: Pediatricians lack tools to support families at home for the promotion of childhood sleep. We are using the Multiphase Optimization Strategy (MOST) framework to guide the development of a mobile health platform for childhood sleep promotion. The objective of this study is to demonstrate feasibility of a mobile health platform towards treating children with insufficient sleep. METHODS: Children aged 10-12 years were enrolled (Study #1: N = 30; Study #2: N = 43). Participants wore a sleep tracker to measure sleep duration. Data were retrieved by a mobile health platform, programmed to send introductory messages during run-in (2 weeks) and goal achievement messages during intervention (7 weeks) periods. In study #1, participants were randomized to control, gain-framed incentive or loss-framed incentive arms. In study #2, participants were randomized to control, loss-framed incentive, normative feedback or loss-framed incentive plus normative feedback arms. RESULTS: In study #1, 1514 nights of data were captured (69%) and sleep duration during the intervention was higher by an average of 21 (95% CI: -8, 51) and 34 (95% CI: 7, 61) minutes per night for the gain-framed and loss-framed arms, respectively, compared to controls. In study #2, 2,689 nights of data were captured (81%), with no major differences in average sleep duration between the control and the loss-framed or normative feedback arms. CONCLUSIONS: We have developed and deployed a mobile health platform that can capture sleep data and remotely communicate with families. Promising candidate intervention components will be further investigated under the optimization phase of the MOST framework. CLINICAL TRIALS: Both studies included in this manuscript were registered at clinicaltrials.gov:-Study #1: NCT03263338-Study #2: NCT03426644.

Continuous and Intermittent Artificial Gravity as a Countermeasure to the Cognitive Effects of 60 Days of Head-Down Tilt Bed Rest.

Environmental and psychological stressors can adversely affect astronaut cognitive performance in space. This study used a 6° head-down tilt bed rest (HDBR) paradigm to simulate some of the physiologic changes induced by microgravity. Twenty-four participants (mean ± SD age 33.3 ± 9.2 years, N = 16 men) spent 60 consecutive days in strict HDBR. They were studied in three groups of eight subjects each. One group served as Control, whereas the other two groups received either a continuous or intermittent artificial gravity (AG) countermeasure of 30 min centrifugation daily (1 g acceleration at the center of mass and 2 g at the feet). Participants performed all 10 tests of NASA's Cognition battery and a brief alertness and mood survey repeatedly before, during, and after the HDBR period. Test scores were adjusted for practice and stimulus set difficulty effects. A modest but statistically significant slowing across a range of cognitive domains was found in all three groups during HDBR compared to baseline, most consistently for sensorimotor speed, whereas accuracy was unaffected. These changes were observed early during HDBR and did not further worsen or improve with increasing time in HDBR, except for emotion recognition performance. With increasing time spent in HDBR, participants required longer time to decide which facial emotion was expressed. They were also more likely to select categories with negative valence over categories with neutral or positive valence. Except for workload, which was rated lower in the Control group, continuous or intermittent AG did not modify the effect of HDBR on cognitive performance or subjective responses. Participants expressed several negative survey responses during HDBR relative to baseline, and some of the responses further deteriorated during recovery, which highlights the importance of adequate medical and psychological support during extended duration HDBR studies. In conclusion, 60 days of HDBR were associated with moderate cognitive slowing and changes in emotion recognition performance, but these effects were not mitigated by either continuous or intermittent exposure to AG for 30 min daily.

Effects of six weeks of chronic sleep restriction with weekend recovery on cognitive performance and wellbeing in high-performing adults.

Chronic sleep loss is associated with escalating declines in vigilant attention across days of sleep restriction. However, studies exceeding 2 weeks of chronic sleep loss are scarce, and the cognitive performance outcomes assessed are limited. We assessed the effects of 6 weeks of chronic sleep restriction on a range of cognitive domains in 15 high-performing individuals (38.5 ± 8.2 years, 6 women) confined to small space in groups of 4. Sleep opportunities were limited to 5 h on weekdays and 8 h on weekends. Individual sleep-wake patterns were recorded with actigraphy. Neurobehavioral performance was assessed in evenings with Cognition, a computerized battery of ten tests assessing a range of cognitive domains. There were some small to moderate effects of increasing sleep debt relative to pre-mission baseline, with decreases in accuracy across cognitive domains (standardized ß = -0.121, p = 0.001), specifically on tests of spatial orientation (ß = -0.289, p = 0.011) and vigilant attention (ß = -0.688, p < 0.001), which were not restored by two nights of weekend recovery sleep. Cognitive and subjective decrements occurred despite occasional daytime napping in breach of study protocol, evening testing around the circadian peak, and access to caffeine before 14:00. Sensorimotor speed, spatial learning and memory, working memory, abstraction and mental flexibility, emotion identification, abstract reasoning, cognitive throughput, and risk decision making were not significantly affected by sleep debt. Taken together with modest lower subjective ratings of happiness and healthiness, these findings underline the importance of sufficient sleep, on both an acute and chronic basis, for performance in selected cognitive domains and subjective wellbeing in operationally relevant environments.