Baseline Night Research Articles

0292 Baseline Pro-Inflammatory Cytokine and Cortisol Levels Differentially Predict Mood Disturbance and Working Memory Deficits Induced by Chronic Sleep Restriction

Abstract Introduction Sleep restriction disturbs mood, impairs neurocognitive performance, and elevates proinflammatory cytokine levels. However, whether basal inflammation influences mood and neurocognitive performance across sleep restriction is unknown. This study examines whether baseline IL-6, cortisol, and TNF-α levels predict the deterioration of mood and working memory performance across sleep restriction. Methods N=124 healthy participants (52% female; n=64), 22–45 years of age, had valid protein, mood, and working memory data. The study included two baseline nights (8h time in bed [TIB]) followed by five nights of 4h TIB. Venous blood was collected on the second baseline day and IL-6, cortisol, and TNF-α levels were measured via commercially available ELISA assays. The profile of mood states (POMS) and the digit span test (DST) were completed every 2h during wakefulness and daily averages were computed. Mixed-effects multi-level models, adjusted for baseline, evaluated the main effect of IL-6, cortisol, and TNF-α levels on the POMS and DST independently and examined the trajectory of POMS and DST by the interaction of protein levels and day of sleep restriction. Results At baseline, IL-6, cortisol, and TNF-α levels were not associated with POMS or DST. There was a main effect of IL-6, but not cortisol or TNF-α, levels on mood disturbance (β=3.811; P=0.015); IL-6 levels did not predict the trajectory of mood across sleep restriction (β=0.187; P=0.57). Higher baseline cortisol levels predicted increasing mood disturbance across days (β=-1.329; P<0.0001). Higher baseline TNF-α levels predicted degrading DST performance across days (β=-0.313; P=0.020). Higher IL-6 (β=-0.246; P=0.010) and lower cortisol (β=0.185; P=0.037) levels also predicted degrading DST performance across days. Conclusion The study findings suggest that basal inflammatory cytokine and cortisol levels are implicated in the individual risk of mood disturbance and working memory deficits resulting from chronic sleep restriction and highlight the need to consider biological processes and phenotypes together. Support This work was supported by National Institute of Health NIH R01NR004281 and National Space and Biomedical Research Institute NSRBI NCC 5–98.

0265 Cortisol and C-Reactive Protein Fail to Predict Individual Differences in Neurobehavioral Performance Responses to Total Sleep Deprivation and Psychological Stress

Abstract Introduction Individuals show marked differential vulnerability in neurobehavioral deficits from psychosocial stress and sleep deprivation. Although changes in salivary cortisol and C-reactive protein (CRP) typically occur across total sleep deprivation (TSD) and recovery sleep, whether these biological markers during fully rested conditions predict individual differences in cognitive performance during TSD and stress remains unknown. Methods Thirty-one healthy adults (ages 27–53; mean ± SD, 35.4 ± 7.1y; 14 females) participated in a five-day experiment consisting of two 8h time-in-bed (TIB) baseline nights, followed by 39h TSD, and two 8h-10h TIB recovery nights. A modified Trier Social Stress Test (TSST) was conducted on the day of TSD to induce psychological stress. Salivary cortisol and CRP from blood were obtained at six time points during the study (pre-study, baseline, during TSD, during TSD after the TSST, after recovery, and post-study). A median split of TSD performance [total lapses (>500 ms response time) and errors] on the 10-minute Psychomotor Vigilance Test (PVT) defined cognitively resilient (n=15) and cognitively vulnerable (n=16) groups. Repeated measures ANOVA and post-hoc comparisons corrected for multiple testing, examined cortisol and CRP across time points between groups. Results In both cognitively resilient and vulnerable individuals, cortisol increased with TSD compared to baseline in the morning and decreased with TSD + psychological stress in the afternoon compared to TSD alone. By contrast, there were no significant changes in CRP levels throughout the experiment. In addition, there were no significant time*group interactions in cortisol or CRP levels. Conclusion Salivary cortisol increased with TSD compared to baseline and showed a time-of-day effect with stress during TSD. Notably, cortisol and CRP did not differ between cognitively resilient and vulnerable individuals across TSD, psychological stress or recovery sleep and thus are not reliable biomarkers for predicting performance under these conditions. Support NASA NNX14AN49G.

1100 Self-Monitoring Of PVT Performance In Healthy Adults And Individuals With MDD

Abstract Introduction Negativity bias in depression has been repeatedly demonstrated in the judgment and decision-making literature. Research investigating the impact of sleep deprivation on self-evaluation of performance in healthy or depressed populations is limited. We examined 1) whether individuals with Major Depressive Disorder (MDD) exhibit a negativity bias in subjective ratings of performance on the Psychomotor Vigilance Task (PVT) as compared with healthy adults, and 2) the impact of total sleep deprivation (TSD) on these ratings. Methods N=33 individuals with MDD and n=9 healthy adults completed a 5-day study protocol including two baseline nights (B1-B2, 9h TIB), 36 hours of TSD, and one night of recovery sleep opportunity (Rec). The PVT was administered every 2-4 hours. A brief questionnaire was administered immediately prior to (PRE) and following (POST) the PVT, asking participants to estimate their average reaction time (RT) using a 9-point Likert-type scale. Mixed-effects models examined the impact of group (MDD, Control), protocol day (B1, B2, SD, Rec), and their interaction on objective PVT performance (mean RT) and subjective performance estimates (PRE and POST ratings). Results Mean RT was significantly slower during TSD (p<0.001) for all participants. Individuals with MDD and healthy adults did not differ in objective PVT performance (p=0.25) across days. There was no significant interaction between group and protocol day (p=0.96). Both groups predicted slower RTs during TSD as compared with baseline or recovery days (PRE-PVT, p=0.006). Individuals with MDD anticipated slower RTs as compared with healthy adults (p=0.001). On POST-PVT estimates, all participants reported subjective poorer performance during TSD (p<0.008). Individuals with MDD reported slower RTs as compared with healthy adults (p=0.002). Interaction effects between group and protocol day on PRE- and POST- performance ratings were not significant. Conclusion This project is the first to investigate subjective estimates of PVT performance in healthy and depressed individuals. Individuals with MDD subjectively reported slower response times as compared with control participants, despite similar objective performance. Depressive symptoms may be a potential confounder of subjective, but not objective, PVT performance. Support 5R01MH107571

0041 Heart Rate Variability Differs in Resilient vs. Vulnerable Adults from Total Sleep Deprivation and Psychological Stress and Predicts Cognitive Performance

Abstract Introduction There are substantial individual differences (resilience and vulnerability) in neurobehavioral performance from psychosocial stress and sleep loss. However, the time course of heart rate variability (HRV) across baseline, total sleep deprivation (TSD), the combination of TSD + psychological stress, and recovery has not been investigated; in addition, it remains unknown whether HRV and blood pressure (BP) differ in resilient vs. vulnerable individuals and predict individual differences in cognitive performance. Methods Thirty-one healthy adults (ages 27–53; mean±SD, 35.4±7.1y; 14 females) participated in a five-day experiment consisting of two 8h time-in-bed (TIB) baseline nights, 39h TSD, and two 8h-10h TIB recovery nights. A modified Trier Social Stress Test (TSST) induced psychological stress on the TSD day. Systolic and diastolic BP and HRV (derived from echocardiographic R-R interval) were obtained at six time points (pre-study, baseline, during TSD, during TSD after the TSST, after recovery, and post-study). Cognitively resilient (n=15) and vulnerable (n=16) groups were defined by a median split on 10-minute Psychomotor Vigilance Test (PVT) TSD performance [total lapses (>500ms response time) and errors]. Repeated measures ANOVA and post-hoc comparisons corrected for multiple testing, examined BP and HRV across time points between groups. Results HRV showed a significant time*group interaction: while resilient individuals had significantly lower HRV at pre-study compared to vulnerable individuals, their HRV increased above that of vulnerable individuals with TSD and with TSD + psychological stress. By contrast, systolic and diastolic BP did not show significant time*group interactions and did not predict cognitive vulnerability during TSD. Conclusion HRV differed between resilient and vulnerable individuals across TSD, psychological stress and recovery sleep and predicted individual differences in cognitive performance, whereby lower HRV during full-rested conditions predicted resilience to TSD and TSD + psychological stress. HRV, but not BP, is a reliable biomarker of sleep deprivation, psychological stress, and neurobehavioral vulnerability. Support NASA NNX14AN49G.

0280 Change in Sleep Depth Across the Night as a Measure of Sleep Adequacy

Abstract Introduction It is well known that sleep becomes lighter towards the end of the night reflecting the reduction in homeostatic sleep pressure. We hypothesized that more adequate nocturnal sleep (i.e. sufficient quantity and quality for the individual) would result in a greater reduction in sleep depth across the night and would be reflected in decreased next-day sleep tendency. Methods In a secondary analysis of data from a study in which sleep depth was altered by sleep restriction combined with either placebo or gaboxadol (a delta-promoting drug) we correlated change across the night in two measures of sleep depth with next-day Multiple Sleep Latency Test (MSLT) latencies. Forty-one healthy subjects underwent 8 consecutive sleep studies; two baseline, four sleep restriction (5 hours) and two recovery nights. MSLT was performed following each baseline night and the last two restriction nights. Sleep depth in the first and last hours of NREM sleep was determined by two methods 1) Log delta spectral power; 2) The odds-ratio-product (ORP), a recently introduced continuous measure of sleep depth. The difference between initial and final values was calculated (ΔDelta, ΔORP). Post-restriction MSLT latency was correlated with baseline MSLT latency, ΔDelta, ΔORP, log delta power and ORP in the last hour, lost total sleep time and lost REM time. Results ΔDelta was -0.27 ±0.13 and ΔORP was 0.17 ±0.13, both changes reflecting lightening of sleep across the night. In both univariate and multivariate analysis only baseline MSLT latency (p &lt 0.001) and ΔORP (p &lt 0.01) were significantly and positively correlated with post-restriction MSLT latency. Conclusion The reduction in sleep depth across the night as measured by ORP, but not by delta power, is significantly correlated with reduced objective sleepiness following sleep restriction. ΔORP may be a useful index that reflects sleep adequacy during the night. Support None

0042 Stroke Volume and Cardiac Index are Differentially Altered by Total Sleep Deprivation and Psychological Stress in Resilient vs. Vulnerable Individuals and Predict Cognitive Performance

Abstract Introduction Individuals show robust resilience and vulnerability in neurobehavioral performance to sleep loss and stress. For the first time, we investigated the time course of two cardiovascular measurements, stroke volume (SV) and cardiac index (CI), both derived from echocardiography, across baseline, total sleep deprivation (TSD), the combination of TSD+psychological stress, and recovery. We also determined whether these variables differ in resilient vs. vulnerable individuals and whether they predict differential vulnerability in cognitive performance. Methods Thirty-one healthy adults (ages 27–53; mean±SD, 35.4±7.1y; 14 females) participated in a five-day experiment consisting of two 8h time-in-bed (TIB) baseline nights, 39h TSD, and two 8h-10h TIB recovery nights. A modified Trier Social Stress Test (TSST) was conducted on the TSD day to induce psychological stress. Echocardiographic measures of SV and CI were obtained at six time points (pre-study, baseline, during TSD, during TSD after the TSST, after recovery, and post-study). A median split of TSD performance [total lapses (>500 ms response time) and errors] on the 10-minute Psychomotor Vigilance Test (PVT), defined cognitively resilient (n=15) and vulnerable (n=16) groups. Repeated measures ANOVA and post-hoc comparisons corrected for multiple testing, examined SV and CI across time points between groups. Results There was a significant time*group interaction for SV: cognitively resilient individuals had greater SV during the five-day experiment. In addition, in both resilient and vulnerable individuals, SV increased with TSD and with TSD+psychological stress compared with baseline. Like SV, there was a significant time*group interaction for CI: resilient individuals had greater CI at all points of the experiment. Conclusion SV and CI differed between resilient and vulnerable individuals across TSD, psychological stress and recovery sleep. Greater SV and greater CI at baseline predicted resilience to TSD and TSD+psychological stress. CI and SV are novel physiological biomarkers of sleep loss, stress, and individual differences in cognitive performance. Support NASA NNX14AN49G.

0105 Working Memory Impairment Due to Chronic Sleep Restriction, Dose Response to Recovery and Re-Exposure

Abstract Introduction Chronic sleep restriction negatively effects working memory. Recovery sleep following sleep restriction partially restores working memory performance. This study examines the impact of chronic sleep restriction and subsequent recovery sleep dose on the N-Back Task (N-Back), a valid measure of working memory. Methods N=223 participants (29.9±6.9 years; 48.4% female), completed two baseline nights of 8h time in bed (TIB), followed by five nights of 4h TIB, and were then randomized to a sleep dose of 0, 2, 4, 6, 8, 10, or 12 h TIB. A subset of participants (n=73) were re-exposed to another five nights of 4h TIB. Participants completed the three versions of the N-Back (i.e. 1-Back, 2-Back, and B-back) every two hours during wakefulness and daily averages were computed. Mixed effects and linear regression models were used to assess the impact of sleep restriction and the sleep dose response on percent correct on the N-Back corrected for baseline. Results N=219 participants had valid working memory data. The 2-Back (β =-4.5%; P<0.0001) and the 3-Back (β =-12.5%; P<0.0001) were more difficult than the 1-Back. Working memory performance declined across days of sleep restriction for all N-Backs: 1-Back (β =-1.10%; P<0.0001), 2-Back (β =-0.99%; P<0.0001), and 3-Back (β =-1.10%; P<0.0001). The sleep dose analysis revealed a positive association with N-Back performance for all N-Back versions, 1-Back (β =0.99%; P=0.0002), 2-Back (β =1.46%; P<0.0001), and 3-Back (β =1.43%; P<0.0001). Re-exposure to only one night of 4h TIB following recovery sleep resulted in performance decrements equal to performance prior to recovery sleep for all N-Back versions (Ps>0.41). Conclusion These data indicate that working memory is adversely impacted by sleep restriction, and that sufficient recovery sleep, possibly across consecutive days, is necessary to maintain optimal working memory performance. Support Funded by National Institute of Health NIH R01NR004281 and National Space and Biomedical Research Institute NSRBI NCC 5–98

0291 Recovery Sleep Alleviates Mood Disturbance Following Chronic Sleep Restriction, Albeit Transiently and in a Dose-Dependent Manner

Abstract Introduction Fatigue is one contributor to mood disturbance observed following sleep restriction; however, the contribution of other factors remains unclear. This study examined contributions to mood disturbance resulting from sleep restriction beyond that of fatigue, evaluated the benefit of recovery sleep, and assessed whether recovery sleep buffered the re-emergence of mood disturbance upon re-exposure to sleep restriction. Methods N=223 healthy participants (48% female; n=108) approximately 30-years-old (SD=6.89, range=22–45 years) completed two baseline nights of 8h time in bed (TIB), followed by five nights of 4h TIB, and were then then randomized to one of 7 sleep recovery opportunities (i.e., 0, 2, 4, 6, 8, 10, or 12 hours TIB). Following the sleep period, a subset of participants (n=72) were re-exposed to five consecutive nights of 4h TIB. The profile of mood states (POMS) was completed every 2h during wakefulness and daily averages were calculated. The POMS total mood disturbance (TMD) score without the fatigue subscale (i.e., mood disturbance = TMD - fatigue) was the primary outcome to isolate changes in mood disturbance beyond fatigue. Individual growth curve models were applied to the trajectory of mood disturbance. General linear models were used to evaluate the dose-response function of mood disturbance after recovery sleep. Results Mood disturbance (absent the POMS fatigue scale) increased with each day of sleep restriction (β=1.550 per day; P<0.0001), and decreased with longer recovery sleep durations in a dose-dependent manner (β=-1.614 for every 2h increase; P<0.0001). The benefits of recovery sleep were abated by the second night of 4h sleep during re-exposure, where mood disturbance was slightly higher than that observed before recovery, but this difference was not statistically significant (β=0.046; P=0.85). Conclusion The study findings suggest that fatigue is not the only contributor to mood disturbance following sleep restriction. Recovery sleep attenuates mood disturbance in a dose-dependent manner, albeit transiently. Candidate pathways linking sleep restriction and mood include the immune system and the dynamics of sleep physiology. Support This work was funded by National Institute of Health NIH R01NR004281 and National Space and Biomedical Research Institute NSRBI NCC 5–98.

Spending the night next to a router - Results from the first human experimental study investigating the impact of Wi-Fi exposure on sleep.

The use of wireless telecommunication systems such as wireless fidelity (Wi-Fi)-enabled devices has steadily increased in recent years. There are persistent concerns that radiofrequency electromagnetic field (RF-EMF) exposure might affect health. Possible effects of RF-EMF exposure on human sleep were examined with regard to mobile phones and base stations, but not with regard to Wi-Fi exposure. The present double-blind, sham-controlled, randomized, fully counterbalanced cross-over study addressed for the first time the question whether a whole night Wi-Fi exposure has an effect on sleep. Thirty-four healthy young male subjects (mean±SD: 24.1±2.9 years) spent five nights in the sleep laboratory. A screening and adaptation night was followed by two experimental nights. Each of the experimental nights was preceded by a baseline night. Sleep was evaluated at the subjective level by a questionnaire and at the objective level (macro- and microstructure) by polysomnography. Either 2.45GHz Wi-Fi (max psSAR10g of 6.4mW/kg) or sham signals were delivered by a newly developed head exposure facility. Results showed no statistically significant acute effects of a whole-night Wi-Fi exposure on subjective sleep parameters as well as on parameters characterizing the macrostructure of sleep. Analyses of the microstructure of sleep revealed a reduction in global EEG power in the alpha frequency band (8.00-11.75Hz) during NREM sleep under acute Wi-Fi exposure compared to sham. The results of the present human experimental study are well in line with several other neurophysiological studies showing that acute RF-EMF exposure has no effect on the macrostructure of sleep. The slight physiological changes in EEG power observed under Wi-Fi exposure are neither reflected in the subjective assessment of sleep nor at the level of objective measurements. The present results are not indicative of a sleep disturbing effect of Wi-Fi exposure.

Acute Pressor Responses in Mice Exposed to Early Life Stress

Exposure to adverse childhood experiences, also known as early life stress, is an independent risk factor for the development of cardiovascular disease in adulthood. Previous studies have indicated ELS in rodents may induce impaired blood pressure regulation in response to various pro‐hypertensive stimuli. In the current study, we used maternal separation and early weaning (MSEW), a mouse model of early life stress, to determine the effects of acute behavioral stress on blood pressure regulation (n = 9/group). We utilized exposure to cage switch stress (CSS), a model of acute behavioral stress that subjects mice to a cage previously inhabited by other male mice. MSEW involves maternal separation 4h/day from postnatal days (PD) 2–5 and 8h/day from PD 6–16 then weaned at PD 17. Normally reared litters weaned at PD 21 were used as controls (CON). In normally reared CON and MSEW C57/BL6 male mice, telemetry transmitters were surgically placed with catheters in the carotid artery at 9 weeks of age. After recovery from surgery for 7–10 days, baseline measurements were recorded for 72 hours. Continuous 24 hour systolic and diastolic blood pressures (SBP and DBP) were similar between CON and MSEW mice (SBP: 125 ± 1 vs 121 ± 5 mmHg, p = 0.64; DBP: 89 ± 1 vs 91 ± 1 mmHg, p = 0.24). Additionally, exposure to MSEW did not significantly affect baseline day and night heart rate. We then subjected to CSS for 4 hours. In response to CSS, the peak change in SBP was significantly greater in MSEW mice compared to CON (39 ± 2 vs 27 ± 4 mmHg, respectively, p = 0.02). However, the total pressor response determined by area under the curve for SBP and DBP during the 30 minutes following onset of CSS and 30 minutes following the end of the 4 hour CSS exposure were similar between MSEW and CON mice. Heart rate significantly increased in both MSEW and CON mice compared to baseline (MSEW: 777 ± 10 vs 562 ± 20 bpm, p < 0.0001; CON: 776 ± 4 vs 575 ± 25 bpm, p < 0.0001) and thus the peak change in heart rate was not significantly different between groups (215 ± 18 vs 201 ± 23 bpm, p = 0.64). However, area under the curve analysis indicated MSEW exhibited a blunted heart rate recovery 30 minutes following the end of the 4 hours of exposure to CSS compared to CON (17998 ± 159 vs 18751 ± 287, respectively, p = 0.05). Given the changes in SBP and heart rate following CSS, these data indicate that MSEW mice have an exaggerated pressor response during exposure to acute stress. In conclusion, ELS may predispose exaggerated cardiovascular responses to stress later in life.Support or Funding InformationFunded by NIH grants HL136267 and HL69999 to D.M.P. and J.S.P. and AHA grant 17SFRN33670697 to J.S.P.

Transportation noise impairs cardiovascular function without altering sleep: The importance of autonomic arousals

AimsChronic exposure to nocturnal transportation noise has been linked to cardiovascular disorders with sleep impairment as the main mediator. Here we examined whether nocturnal transportation noise affects the main stress pathways, and whether it relates to changes in the macro and micro structure of sleep. Methods and resultsTwenty-six young healthy participants (12 women, 24.6 ± 0.7 years, mean ± SE) spent five consecutive 24-h days and one last morning in the laboratory. The first (baseline) and last (recovery) nights comprised a quiet ambient scenario. In-between, four different noise scenarios (low/medium/high intermittent road or rail scenarios with an identical equivalent continuous sound level of 45 dB) were randomly presented during the 8-h nights. Participants felt more annoyed from the transportation noise scenarios compared to the quiet ambient scenario played back during the baseline and recovery nights (F5,117 = 10.2, p < 0.001). Nocturnal transportation noise did not significantly impact polysomnographically assessed sleep macrostructure, blood pressure, nocturnal catecholamine levels and morning cytokine levels. Evening cortisol levels increased after sleeping with highly intermittent road noise compared to baseline (p = 0.002, noise effect: F4,83 = 4.0, p = 0.005), a result related to increased cumulative duration of autonomic arousals during the noise nights (F5,106 = 3.4, p < 0.001; correlation: rpearson = 0.64, p = 0.006). ConclusionUnder controlled laboratory conditions, highly intermittent nocturnal road noise exposure at 45 dB increased the cumulative duration of autonomic arousals during sleep and next-day evening cortisol levels. Our results indicate that, without impairing sleep macrostructure, nocturnal transportation noise of 45 dB is a physiological stressor that affects the hypothalamic-pituitary-adrenal axis during the following day in healthy young good sleepers.

A sleep intervention study comparing effects of sleep restriction and fragmentation on sleep and vigilance and the need for recovery

PurposeSleep deprivation is present not only in sleep disorders but also in numerous high demanding jobs and negatively affects cognition, performance and health. We developed a study design to distinguish the effects and need for recovery of two short-term disturbances – intermittent sleep fragmentation and partial sleep restriction. MethodsThe randomized within-subjects design contained two weeks each with a baseline night, an intervention night of either sleep deprivation (5 h) or sleep fragmentation (light on every hour) and two undisturbed recovery nights. Twenty healthy male participants (mean age: 39.9 ± 7.4 years, mean BMI: 25.5 ± 2.2 kg/m²) underwent polysomnography, a psychomotor vigilance task (PVT), and subjective questions on well-being and sleep efficiency. ResultsPercentage-wise, the restriction night had significant less wake times, less light sleep (stage 1), less REM sleep, but more deep sleep (stage 3) than the fragmentation night. The restriction week displayed a significant recovery effect regarding these sleep stages. The sleep fragmentation week presented a significant recovery effect regarding sleep onset times. PVT performance showed only a slight recovery effect after sleep restriction. Subjective sleep quality was reduced after both interventions with a significant recovery effect during restriction week only. ConclusionsShort-term sleep restriction presented as a stronger sleep disturbance than short-term intermittent sleep fragmentation, including a stronger need for recovery. Already a one night sleep deprivation had an effect beyond two recovery days. The PVT was not sensitive enough to reveal significant changes. Next, autonomic parameters as possible biomarkers will be investigated.

Evidence That Homeostatic Sleep Regulation Depends on Ambient Lighting Conditions during Wakefulness.

We examined whether ambient lighting conditions during extended wakefulness modulate the homeostatic response to sleep loss as indexed by. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA) in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e., sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800 K), and once under either white light (WL: 250 lux, 2800 K) or blue-enriched white light (BL: 250 lux, 9000 K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.

The Effects of Deep-Breathing Exercises on Postoperative Sleep Duration and Quality in Patients Undergoing Coronary Artery Bypass Graft (CABG): a Randomized Clinical Trial.

Introduction: Disordered sleep occurs frequently in patients who have undergone coronary bypass graft surgery, and it contributes to increased morbidity, mortality, and resource utilization. The present study aimed to determine the effects of deep-breathing exercises on postoperative sleep duration and quality in patients undergoing coronary artery bypass graft.Methods: This study was a clinical trial. The study sample included 64 patients who were coronary artery bypass graft hospitalized from January 2015 to April 2015 in Qazvin Booali-Sina hospital. The patients were selected by convenient sampling and then the participants were randomly allocated to the intervention and control groups. The baseline and postoperative (day 7) sleep duration and quality metrics were measured. The St Mary's Hospital Sleep Questionnaire was used to evaluate sleep quality in two groups.Results: Baseline night sleep duration was 5.72 (1.63) hours in the control group and 5.58 (1.07) hours in the intervention group. The initial findings showed that the mean of sleep quality score of patients in the intervention and control groups were 19.72 (2.68) and 18.22 (3.81) respectively. These measurements did not decline postoperatively in the intervention group while night sleep duration and quality declined in the control group. Deep breathing exercise program had a significant effect on sleep quality score in the intervention group compared to the control group.Conclusion: The results indicated that deep breathing exercises prevent decline in sleep quality postoperatively. It seems to be a safe method with no side effects for these patients. Furthermore, it is a simple method to implement and does not impose a high cost.

Robust stability of trait-like vulnerability or resilience to common types of sleep deprivation in a large sample of adults.

Sleep loss produces large individual differences in neurobehavioral responses, with marked vulnerability or resilience among individuals. Such differences are stable with repeated exposures to acute total sleep deprivation (TSD) or chronic sleep restriction (SR) within short (weeks) and long (years) intervals. Whether trait-like responses are observed to commonly experienced types of sleep loss and across various demographically defined groups remains unknown. Eighty-three adults completed two baseline nights (10 h-12 h time-in-bed, TIB) followed by five 4 h TIB SR nights or 36 h TSD. Participants then received four 12-h TIB recovery nights followed by five SR nights or 36 h TSD, in counterbalanced order to the first sleep loss sequence. Neurobehavioral tests were completed every 2 h during wakefulness. Participants who displayed neurobehavioral vulnerability to TSD displayed vulnerability to SR, evidenced by substantial to near perfect intraclass correlation coefficients (ICCs; 78%-91% across measures). Sex, race, age, body mass index (BMI), season, and sleep loss order did not impact ICCs significantly. Individuals exhibited significant consistency of responses within, but not between, performance and self-reported domains. Using the largest, most diverse sample to date, we demonstrate for the first time the remarkable stability of phenotypic neurobehavioral responses to commonly experienced sleep loss types, across demographic variables and different performance and self-reported measures. Since sex, race, age, BMI, and season did not affect ICCs, these variables are not useful for determining stability of responses to sleep loss, underscoring the criticality of biological predictors. Our findings inform mathematical models and are relevant for the general population and military and health professions.

Nocturnal cognitive arousal is associated with objective sleep disturbance and indicators of physiologic hyperarousal in good sleepers and individuals with insomnia disorder

BackgroundCognitive arousal is central to models of sleep disturbance and insomnia, but findings remain mixed regarding whether cognitive arousal is associated with objective sleep disturbance and physiologic hyperarousal. This study explored associations of objective nocturnal wakefulness and indicators of physiologic hyperarousal with cognitive arousal in healthy sleepers and individuals with insomnia. MethodsIn sum, 52 adults (51.9% women; 18 with insomnia disorder, 34 healthy sleepers) underwent two overnight polysomnography (PSG) studies (adaptation + baseline nights) and a multiple sleep latency test (MSLT). Baseline depression was assessed and presleep cognitive arousal and somatic arousal were recorded for each night. Multivariate regression was used to evaluate associations of PSG sleep parameters with insomnia, cognitive arousal, and somatic arousal. ResultsAnalyses showed that high levels of nocturnal cognitive arousal were associated with prolonged sleep latency, lower sleep efficiency, and shorter total sleep time by PSG on both nights. An association between nocturnal cognitive arousal and wake after sleep onset was observed on night one only. Moreover, greater nocturnal cognitive arousal was associated with greater likelihood of obtaining short sleep and with longer MSLT sleep latencies. Insomnia diagnosis, depression, and somatic arousal were not associated with PSG sleep parameters or MSLT latency. ConclusionsHeightened cognitive arousal at night is linked to objective sleep disturbances and indicators of physiologic hyperarousal at night and during the day. For patients with insomnia, cognitive arousal may contribute to the 24-hr physiologic hyperarousal. Cognitive arousal may be a critical therapeutic target for severe or treatment-resistant sleep disturbance.

Distributed slow-wave dynamics during sleep predict memory consolidation and its impairment in schizophrenia

The slow waves (SW) of non-rapid eye movement (NREM) sleep reflect neocortical components of network activity during sleep-dependent information processing; their disruption may therefore impair memory consolidation. Here, we quantify sleep-dependent consolidation of motor sequence memory, alongside sleep EEG-derived SW properties and synchronisation, and SW–spindle coupling in 21 patients suffering from schizophrenia and 19 healthy volunteers. Impaired memory consolidation in patients culminated in an overnight improvement in motor sequence task performance of only 1.6%, compared with 15% in controls. During sleep after learning, SW amplitudes and densities were comparable in healthy controls and patients. However, healthy controls showed a significant 45% increase in frontal-to-occipital SW coherence during sleep after motor learning in comparison with a baseline night (baseline: 0.22 ± 0.05, learning: 0.32 ± 0.05); patient EEG failed to show this increase (baseline: 0.22 ± 0.04, learning: 0.19 ± 0.04). The experience-dependent nesting of spindles in SW was similarly disrupted in patients: frontal-to-occipital SW–spindle phase-amplitude coupling (PAC) significantly increased after learning in healthy controls (modulation index baseline: 0.17 ± 0.02, learning: 0.22 ± 0.02) but not in patients (baseline: 0.13 ± 0.02, learning: 0.14 ± 0.02). Partial least-squares regression modelling of coherence and PAC data from all electrode pairs confirmed distributed SW coherence and SW–spindle coordination as superior predictors of overnight memory consolidation in healthy controls but not in patients. Quantifying the full repertoire of NREM EEG oscillations and their long-range covariance therefore presents learning-dependent changes in distributed SW and spindle coordination as fingerprints of impaired cognition in schizophrenia.

A Novel Approach to Assess Sleep-Related Rhythmic Movement Disorder in Children Using Automatic 3D Analysis.

Background: Unlike other episodic sleep disorders in childhood, there are no agreed severity indices for rhythmic movement disorder. While movements can be characterized in detail by polysomnography, in our experience most children inhibit rhythmic movement during polysomnography. Actigraphy and home video allow assessment in the child’s own environment, but both have limitations. Standard actigraphy analysis algorithms fail to differentiate rhythmic movements from other movements. Manual annotation of 2D video is time consuming. We aimed to develop a sensitive, reliable method to detect and quantify rhythmic movements using marker free and automatic 3D video analysis. Method: Patients with rhythmic movement disorder (n = 6, 4 male) between age 5 and 14 years (M: 9.0 years, SD: 4.2 years) spent three nights in the sleep laboratory as part of a feasibility study (https://clinicaltrials.gov/ct2/show/NCT03528096). 2D and 3D video data recorded during the adaptation and baseline nights were analyzed. One ceiling-mounted camera captured 3D depth images, while another recorded 2D video. We developed algorithms to analyze the characteristics of rhythmic movements and built a classifier to distinguish between rhythmic and non-rhythmic movements based on 3D video data alone. Data from 3D automated analysis were compared to manual 2D video annotations to assess algorithm performance. Novel indices were developed, specifically the rhythmic movement index, frequency index, and duration index, to better characterize severity of rhythmic movement disorder in children. Result: Automatic 3D video analysis demonstrated high levels of agreement with the manual approach indicated by a Cohen’s kappa >0.9 and F1-score >0.9. We also demonstrated how rhythmic movement assessment can be improved using newly introduced indices illustrated with plots for ease of visualization. Conclusion: 3D video technology is widely available and can be readily integrated into sleep laboratory settings. Our automatic 3D video analysis algorithm yields reliable quantitative information about rhythmic movements, reducing the burden of manual scoring. Furthermore, we propose novel rhythmic movement disorder severity indices that offer a means to standardize measurement of this disorder in both clinical and research practice. The significance of the results is limited due to the nature of a feasibility study and its small number of samples. A larger follow up study is needed to confirm presented results.

Assessments of demand response potential in small commercial buildings across the United States

Buildings are responsible for more than 73% of the total electricity usage in the United States and have a significant contribution to peak electrical demand of the power grid. Thus, proper building demand management could improve the robustness and efficiency of grid operation and could also result in economic benefits for building owners. Almost half of the building electricity usage occurs in the commercial building sector where 60% of the installed cooling capacity is attributed to small commercial buildings employing packaged air-conditioning systems (e.g., rooftop units). Thus, understanding the demand response potential and economic benefits for the small commercial sector is of great importance. In particular, the effect of climate, building type, and utility structure on demand response potential is valuable information for building managers in identifying the most beneficial demand response strategies and for utilities in developing better utility structure rate incentives to achieve demand reduction. This article presents a simulation-based assessment approach and highlights the key assessment results for three demand response strategies—thermostat, shade, and lighting controls—across a range of building types, vintages, locations, and utility rate structures. The control performance is evaluated in terms of utility cost savings, peak demand reductions, and indoor comfort impacts in comparison to a baseline night setup strategy. The tradeoff between cost savings and comfort is also explicitly investigated. The assessment results show that the demand response controls lead to slightly worse indoor comfort compared to the baseline control, with an increase in the median percentage of people dissatisfied from 5.7% to 8.1%. However, significant demand reductions and cost savings could be achieved across all tested cases with the magnitudes dependent on the weather condition and building type. Annual electricity cost savings of 5 to 25 cents/ft2 (54 to 269 cents/m2) were demonstrated for time-of-use energy rates with demand charges, whereas the savings were relatively small, below 5 cents/ft2 (54 cents/m2) for most cases, when buildings subscribed to flat rates without demand charges.

0213 Acute Total Sleep Deprivation Impairs the Ability to Manage Response Conflict

The attention network test (ANT) measures the ability to use an alerting cue to detect a stimulus (alerting effect), use a spatial cue to shift the location of visual attention (orienting effect), and manage response conflict (conflict effect). Total sleep deprivation (TSD) has been shown to negatively affect cognitive functions, including distinct aspects of attention. As part of a laboratory study, we measured performance on the ANT to examine the impact of TSD on attentional functioning. 14 healthy adults (ages 21-39; 7 females/7 males) completed a 4-day (3-night) in-laboratory study. After a baseline night of sleep (9h sleep opportunity; 22:00-07:00), subjects underwent 38h TSD, followed by one night of recovery sleep (9h sleep opportunity; 22:00-07:00). A version of the ANT with variable inter-stimulus interval was administered at 09:00 during baseline, after 26h TSD, and after recovery sleep. Mixed-effects analysis of variance (ANOVA) showed marked impairment in the conflict effect during TSD (F2,26=4.74, P=0.018). The alerting (F2,26=0.02, P=0.98) and orienting (F226=0.25, P=0.78) effects were not significantly affected by TSD. Consistent with earlier findings, TSD did not significantly degrade the alerting effect on the ANT. In this study, TSD also did not significantly reduce the orienting effect. Thus, subjects maintained the ability to detect a stimulus and shift visual attention in response to cues, despite sleep deprivation. However, TSD had significant impact on the conflict effect, indicating that subjects experienced considerable difficulty managing response conflict while sleep-deprived. This finding is consistent with recent evidence that, independent of its effect on vigilant attention, sleep deprivation causes profound deficits in attentional flexibility. Jazz Pharmaceuticals