Baseline Night Research Articles

The Spatiotemporal Pattern of the Human Electroencephalogram at Sleep Onset After a Period of Prolonged Wakefulness.

During the sleep onset (SO) process, the human electroencephalogram (EEG) is characterized by an orchestrated pattern of spatiotemporal changes. Sleep deprivation (SD) strongly affects both wake and sleep EEG, but a description of the topographical EEG power spectra and oscillatory activity during the wake-sleep transition after a period of prolonged wakefulness is still missing. The increased homeostatic sleep pressure should induce an earlier onset of sleep-related EEG oscillations. The aim of the present study was to assess the spatiotemporal EEG pattern at SO following SD. A dataset of a previous study was analyzed. We assessed the spatiotemporal EEG changes (19 cortical derivations) during the SO (5 min before vs. 5 min after the first epoch of Stage 2) of a recovery night after 40 h of SD in 39 healthy subjects, analyzing the EEG power spectra (fast Fourier transform) and the oscillatory activity [better oscillation (BOSC) detection method]. The spatiotemporal pattern of the EEG power spectra mostly confirmed the changes previously observed during the wake-sleep transition at baseline. The comparison between baseline and recovery showed a wide increase of the post- vs. pre-SO ratio during the recovery night in the frequency bins ≤10 Hz. We found a predominant alpha oscillatory rhythm in the pre-SO period, while after SO the theta oscillatory activity was prevalent. The oscillatory peaks showed a generalized increase in all frequency bands from delta to sigma with different predominance, while beta activity increased only in the fronto-central midline derivations. Overall, the analysis of the EEG power replicated the topographical pattern observed during a baseline night of sleep but with a stronger intensity of the SO-induced changes in the frequencies ≤10 Hz, and the detection of the rhythmic activity showed the rise of several oscillations at SO after SD that was not observed during the wake-sleep transition at baseline (e.g., alpha and frontal theta in correspondence of their frequency peaks). Beyond confirming the local nature of the EEG pattern at SO, our results show that SD has an impact on the spatiotemporal modulation of cortical activity during the falling-asleep process, inducing the earlier emergence of sleep-related EEG oscillations.

Changes in Subjective-Objective Sleep Discrepancy Following Inpatient Cognitive Behavior Therapy for Insomnia

Discrepancy between objective and subjective sleep parameters is a frequent symptom in persons suffering from insomnia. Since it has an impairing effect on daytime well-being and neglects possible positive objective improvements, it would be useful if it was treated. Apart from hypnotics, cognitive behavior therapy (CBT-I) is the therapy of choice for chronic forms of insomnia. However, there is limited information about whether CBT-I can also improve subjective-objective sleep discrepancy. We investigated a large sample of patients showing chronic forms of insomnia regarding their subjective-objective sleep discrepancy pre and post CBT-I. Objective sleep data were obtained from 3 nights (2 baseline nights and 1 night after therapy) using polysomnography in our sleep laboratory. All 92 patients participated in a 14-day inpatient program with CBT-I including psychoeducation about subjective-objective sleep discrepancy. Repeated measures analyses showed an improvement in subjective-objective sleep discrepancy parameters after CBT-I. Those parameters were also correlated with perceived quality of sleep. We conclude that CBT-I is a useful tool to improve subjective-objective sleep discrepancy in patients showing chronic forms of insomnia.

Two nights of recovery sleep restores the dynamic lipemic response, but not the reduction of insulin sensitivity, induced by five nights of sleep restriction.

Chronic inadequate sleep is associated with increased risk of cardiometabolic diseases. The mechanisms involved are poorly understood but involve changes in insulin sensitivity, including within adipose tissue. The aim of this study was to assess the effects of sleep restriction on nonesterified fatty acid (NEFA) suppression profiles in response to an intravenous glucose tolerance test (IVGTT) and to assess whether 2 nights of recovery sleep (a "weekend") is sufficient to restore metabolic health. We hypothesized that sleep restriction impairs both glucose and lipid metabolism, specifically adipocyte insulin sensitivity, and the dynamic lipemic response of adipocyte NEFA release during an IVGTT. Fifteen healthy men completed an inpatient study of 3 baseline nights (10 h of time in bed/night), followed by 5 nights of 5 h of time in bed/night and 2 recovery nights (10 h of time in bed/night). IVGTTs were performed on the final day of each condition. Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity P = 0.002; acute insulin response to glucose P = 0.23). The disposition index was suppressed by sleep restriction and did not recover after recovery sleep (P < 0.0001 and P = 0.01, respectively). Fasting NEFAs were not different from baseline in either the restriction or recovery conditions. NEFA rebound was significantly suppressed by sleep restriction (P = 0.01) but returned to baseline values after recovery sleep. Our study indicates that sleep restriction impacts NEFA metabolism and demonstrates that 2 nights of recovery sleep may not be adequate to restore glycemic health.

Differential effects of split and continuous sleep on neurobehavioral function and glucose tolerance in sleep-restricted adolescents.

Study ObjectivesMany adolescents are exposed to sleep restriction on school nights. We assessed how different apportionment of restricted sleep (continuous vs. split sleep) influences neurobehavioral function and glucose levels.MethodsAdolescents, aged 15–19 years, were evaluated in a dormitory setting using a parallel-group design. Following two baseline nights of 9-hour time-in-bed (TIB), participants underwent either 5 nights of continuous 6.5-h TIB (n = 29) or 5-hour nocturnal TIB with a 1.5-hour afternoon nap (n = 29). After two recovery nights of 9-hour TIB, participants were sleep restricted for another three nights. Sleep was assessed using polysomnography (PSG). Cognitive performance and mood were evaluated three times per day. Oral glucose tolerance tests (OGTT) were conducted on mornings after baseline sleep, recovery sleep, and the third day of each sleep restriction cycle.ResultsThe split sleep group had fewer vigilance lapses, better working memory and executive function, faster processing speed, lower level of subjective sleepiness, and more positive mood, even though PSG-verified total sleep time was less than the continuous sleep group. However, vigilance in both sleep-restricted groups was inferior to adolescents in a prior sample given 9-hour nocturnal TIB. During both cycles of sleep restriction, blood glucose during the OGTT increased by a greater amount in the split sleep schedule compared with persons receiving 6.5-hour continuous sleep.ConclusionsIn adolescents, modest multinight sleep restriction had divergent negative effects on cognitive performance and glucose levels depending on how the restricted sleep was apportioned. They are best advised to obtain the recommended amount of nocturnal sleep.Trial registration https://clinicaltrials.gov/ct2/show/NCT03333512

Insomnia treatment response as a function of objectively measured sleep duration

ObjectivesTo examine the potential moderating effect of objectively measured sleep duration at baseline on the response to cognitive behavioral therapy for insomnia (CBT-I), administered singly or combined with medication (CBT-I + Med). MethodsBased on the average PSG-derived sleep duration across two baseline nights and the type of treatment received, 159 adults with insomnia (50.3 ± 10.1 years; 61.0% women) were classified into one of four groups: participants with short sleep duration (ie, ≤ 6 h) treated with CBT-I (n = 26) or CBT-I+Med (n = 25), and participants with normal sleep duration (ie, > 6 h) treated with CBT-I (n = 54) or CBT-I+Med (n = 54). Primary outcome measures were sleep/wake parameters derived from a sleep diary and insomnia severity and secondary outcomes were beliefs about sleep, fatigue, depression and anxiety. ResultsPatients with both short and normal sleep durations at baseline improved significantly on most sleep continuity parameters with CBT-I administered singly or combined with medication. Irrespective of treatment received, participants with short sleep duration also showed significantly greater improvements in subjective sleep (ie, reduced wake after sleep onset, increased sleep efficiency) relative to those with normal sleep duration. Conversely, participants with normal sleep duration showed greater improvements on some measures of daytime functioning and sleep satisfaction. ConclusionsThere was no moderating effect of baseline sleep duration on treatment response to cognitive behavioral therapy. Despite some marginal differential treatment response on selected daytime functioning outcomes, the benefits from CBT-I were not significantly different as a function of short or normal sleep duration at baseline. Further prospective investigation of insomnia phenotypes taking into account other variables than sleep duration is warranted in order to develop more targeted insomnia therapies. Trial registrationwww.clinicaltrials.gov (#NCT 00042146).

Brain dynamics during the sleep onset transition: An EEG source localization study

EEG source localization is an essential tool to reveal the cortical sources underlying brain oscillatory activity. We applied LORETA, a technique of EEG source localization, to identify the principal brain areas involved in the process of falling asleep (sleep onset, SO). We localized the contributing brain areas of activity in the classical frequency bands and tracked their temporal evolution (in 2-min intervals from 2 min prior to SO up to 10 min after SO) during a baseline night and subsequent recovery sleep after total sleep deprivation of 40 h.Delta activity (0.5–5 Hz) gradually increased both in baseline and recovery sleep, starting in frontal areas and finally involving the entire cortex. This increase was steeper in the recovery condition. The evolution of sigma activity (12–16 Hz) resembled an inverted U-shape in both conditions and the activity was most salient in the parietal cortex. In recovery, sigma activity reached its maximum faster than in baseline, but attained lower levels. Theta activity (5–8 Hz) increased with time in large parts of the occipital lobe (baseline and recovery) and in recovery involved additionally frontal areas. Changes in alpha activity (8–12 Hz) at sleep onset involved large areas of the cortex, whereas activity in the beta range (16–24 Hz) was restricted to small cortical areas. The dynamics in recovery could be considered as a “fast-forward version” of the one in baseline.Our results confirm that the process of falling asleep is neither spatially nor temporally a uniform process and that different brain areas might be falling asleep at a different speed potentially reflecting use dependent aspects of sleep regulation.

Cognitive behavioral treatment for insomnia is equally effective in insomnia patients with objective short and normal sleep duration

BackgroundIt has been suggested that insomnia patients with short sleep duration and insomnia patients with normal sleep duration may respond differently to cognitive behavioral treatment for insomnia (CBT-I). To evaluate this hypothesis, we retrospectively examined a large sample of patients with chronic insomnia regarding their outcome post-treatment and six months after participating in a two-week standardized inpatient CBT-I program. ObjectivesSeventy-two women and 20 men with chronic insomnia received standardized inpatient CBT-I and were examined with three nights of polysomnography (two baseline nights and one post-treatment night directly following the two-week treatment). Follow-up measurements of subjective insomnia symptoms were conducted after six months. The CBT-I outcome was compared between insomnia patients with polysomnographically determined short (< 6 h) and normal (≥ 6 h) sleep duration. ResultsConcerning subjective outcomes, CBT-I was equally effective in insomnia patients with objective short and normal sleep duration. Secondary analyses of polysomnographic data collected at post-treatment revealed that insomnia patients with short sleep duration showed a better treatment response in comparison to those with normal sleep duration. ConclusionsThese results suggest that the distinction in insomnia between objective short and normal sleep duration may be of limited value for treatment decisions regarding CBT-I. However, as the overall picture of the literature on this issue is not conclusive, we conclude that further prospective research is necessary to investigate the clinical validity of phenotyping insomnia patients by objective sleep data.

Heart rate variability rebound following exposure to persistent and repetitive sleep restriction.

While it is well established that slow-wave sleep electroencephalography (EEG) rebounds following sleep deprivation, very little research has investigated autonomic nervous system recovery. We examined heart rate variability (HRV) and cardiovagal baroreflex sensitivity (BRS) during four blocks of repetitive sleep restriction and sequential nights of recovery sleep. Twenty-one healthy participants completed the 22-day in-hospital protocol. Following three nights of 8-hr sleep, they were assigned to a repetitive sleep restriction condition. Participants had two additional 8-hr recovery sleep periods at the end of the protocol. Sleep EEG, HRV, and BRS were compared for the baseline, the four blocks of sleep restriction, and the second (R2) and third (R3) nocturnal recovery sleep periods following the last sleep restriction block. Within the first hour of each sleep period, vagal activation, as indexed by increase in high frequency (HF; HRV spectrum analysis), showed a rapid increase, reaching its 24-hr peak. HF was more pronounced (rebound) in R2 than during baseline (p < 0.001). The BRS increased within the first hour of sleep and was higher across all sleep restriction blocks and recovery nights (p = 0.039). Rebound rapid eye movement sleep was observed during both R2 and R3 (p = 0.004), whereas slow-wave sleep did not differ between baseline and recovery nights (p > 0.05). Our results indicate that the restoration of autonomic homeostasis requires a time course that includes at least three nights, following an exposure to multiple nights of sleep curtailed to about half the normal nightly amount.

A Novel Insight of Effects of a 3-Hz Binaural Beat on Sleep Stages During Sleep.

The dichotic presentation of two almost equivalent pure tones with slightly different frequencies leads to virtual beat perception by the brain. In this phenomenon, the so-called binaural beat has a frequency equaling the difference of the frequencies of the two pure tones. The binaural beat can entrain neural activities to synchronize with the beat frequency and induce behavioral states related to the neural activities. This study aimed to investigate the effect of a 3-Hz binaural beat on sleep stages, which is considered a behavioral state. Twenty-four participants were allocated to experimental and control groups. The experimental period was three consecutive nights consisting of an adaptation night, a baseline night, and an experimental night. Participants in both groups underwent the same procedures, but only the experimental group was exposed to the 3-Hz binaural beat on the experimental night. The stimulus was initiated when the first epoch of the N2 sleep stage was detected and stopped when the first epoch of the N3 sleep stage detected. For the control group, a silent sham stimulus was used. However, the participants were blinded to their stimulus group. The results showed that the N3 duration of the experimental group was longer than that of the control group, and the N2 duration of the experimental group was shorter than that of the control group. Moreover, the N3 latency of the experimental group was shorter.

Adverse impact of nocturnal transportation noise on glucose regulation in healthy young adults: Effect of different noise scenarios

BackgroundEpidemiological evidence indicates an association between transportation noise exposure and a higher risk of developing type 2 diabetes. Sleep disturbances are thought to be one of the mechanisms as it is well established that a few nights of short or poor sleep impair glucose tolerance and insulin sensitivity in healthy good sleepers. ObjectivesThe present study aimed to determine the extent to which exposure to nocturnal transportation noise affects glucose metabolism, and whether it is related to noise-induced sleep alterations. MethodsTwenty-one young healthy volunteers (nine women) participated in a six-day laboratory study starting with a noise-free baseline night, then four nights sleeping with randomly-presented transportation noise scenarios (three road and one railway noise scenario) with identical average sound level of 45dB but differing in eventfulness and ending with a noise-free recovery night. Sleep was measured by polysomnography. Glucose tolerance and insulin sensitivity were measured after the baseline, the last noise night and the recovery nights with an oral glucose tolerance test using Matsuda and Stumvoll insulin sensitivity indexes. Eleven participants were assigned a less eventful noise scenario during the last noise night (LE-group), while the other ten had a more eventful noise scenario (ME-group). Baseline metabolic and sleep variables between the two intervention groups were compared using a non-parametric Mann-Whitney U test while mixed models were used for repeated measure analysis. ResultsAll participants had increased glucoseAUC (mean±SE, 14±2%, p<0.0001) and insulinAUC (55±10%, p<0.0001) after the last noise night compared to the baseline night. 2h-glucose level tended to increase only in the ME-group between baseline (5.1±0.22mmol·L−1) and the last noise night (6.1±0.39mmol·L−1, condition: p=0.001, interaction: p=0.08). Insulin sensitivity assessed with Matsuda and Stumvoll indexes respectively decreased by 7±8% (p=0.001) and 9±2% (p<0.0001) after four nights with transportation noise. Only participants in the LE-group showed beneficial effects of the noise-free recovery night on glucose regulation (relative change to baseline: glucoseAUC: 1±2%, p=1.0 for LE-group and 18±4%, p<0.0001 for ME-group; Stumvoll index: 3.2±2.6%, p=1.0 for LE-group and 11±2.5%, p=0.002 for ME-group). Sleep was mildly impaired with increased sleep latency of 8±2min (<0.0001) and more cortical arousals per hour of sleep (1.8±0.6arousals/h, p=0.01) during the last noise night compared to baseline. No significant associations between sleep measures and glucose tolerance and insulin sensitivity were found. ConclusionIn line with epidemiological findings, sleeping four nights with transportation noise impaired glucose tolerance and insulin sensitivity. Based on the presented sound exposure, the eventfulness of the noise scenarios seems to play an important role for noise-induced alterations in glucose regulation. However, we could not confirm our hypothesis that transportation noise impairs glucose regulation via deterioration in sleep quality and quantity. Therefore, other factors, such as stress-related pathways, may need to be considered as potential triggers for noise-evoked glucose intolerance in future research.

Effects of slow-wave activity on mood disturbance in major depressive disorder.

Studies have demonstrated that decreases in slow-wave activity (SWA) predict decreases in depressive symptoms in those with major depressive disorder (MDD), suggesting that there may be a link between SWA and mood. The aim of the present study was to determine if the consequent change in SWA regulation following a mild homeostatic sleep challenge would predict mood disturbance. Thirty-seven depressed and fifty-nine healthy adults spent three consecutive nights in the sleep laboratory. On the third night, bedtime was delayed by 3 h, as this procedure has been shown to provoke SWA. The Profile of Mood States questionnaire was administered on the morning following the baseline and sleep delay nights to measure mood disturbance. Results revealed that following sleep delay, a lower delta sleep ratio, indicative of inadequate dissipation of SWA from the first to the second non-rapid eye movement period, predicted increased mood disturbance in only those with MDD. These data demonstrate that in the first half of the night, individuals with MDD who have less SWA dissipation as a consequence of impaired SWA regulation have greater mood disturbance, and may suggest that appropriate homeostatic regulation of sleep is an important factor in the disorder.

Exploring gene expression biomarker candidates for neurobehavioral impairment from total sleep deprivation

BackgroundAlthough sleep deprivation is associated with neurobehavioral impairment that may underlie significant risks to performance and safety, there is no reliable biomarker test to detect dangerous levels of impairment from sleep loss in humans. This study employs microarrays and bioinformatics analyses to explore candidate gene expression biomarkers associated with total sleep deprivation (TSD), and more specifically, the phenotype of neurobehavioral impairment from TSD. Healthy adult volunteers were recruited to a sleep laboratory for seven consecutive days (six nights). After two Baseline nights of 10 h time in bed, 11 subjects underwent an Experimental phase of 62 h of continuous wakefulness, followed by two Recovery nights of 10 h time in bed. Another six subjects underwent a well-rested Control condition of 10 h time in bed for all six nights. Blood was drawn for measuring gene expression on days two, four, and six at 4 h intervals from 08:00 to 20:00 h, corresponding to 12 timepoints across one Baseline, one Experimental, and one Recovery day.ResultsAltogether 212 genes changed expression in response to the TSD Treatment, with most genes exhibiting down-regulation during TSD. Also, 28 genes were associated with neurobehavioral impairment as measured by the Psychomotor Vigilance Test. The results support previous findings associating TSD with the immune response and ion signaling, and reveal novel candidate biomarkers such as the Speedy/RINGO family of cell cycle regulators.ConclusionsThis study serves as an important step toward understanding gene expression changes during sleep deprivation. In addition to exploring potential biomarkers for TSD, this report presents novel candidate biomarkers associated with lapses of attention during TSD. Although further work is required for biomarker validation, analysis of these genes may aid fundamental understanding of the impact of TSD on neurobehavioral performance.

Leg Movement Activity During Sleep in Adults With Attention-Deficit/Hyperactivity Disorder.

Objectives: To conduct a first detailed analysis of the pattern of leg movement (LM) activity during sleep in adult subjects with Attention-Deficit/Hyperactivity Disorder (ADHD) compared to healthy controls.Methods: Fifteen ADHD patients and 18 control subjects underwent an in-lab polysomnographic sleep study. The periodic character of LMs was evaluated with established markers of “periodicity,” i.e., the periodicity index, intermovement intervals, and time distribution of LM during sleep, in addition to standard parameters such as the periodic leg movement during sleep index (PLMSI) and the periodic leg movement during sleep arousal index (PLMSAI). Subjective sleep and psychiatric symptoms were assessed using several, self-administered, screening questionnaires.Results: Objective sleep parameters from the baseline night did not significantly differ between ADHD and control subjects, except for a longer sleep latency (SL), a longer duration of the periodic leg movements during sleep (PLMS) in REM sleep and a higher PLMSI also in REM sleep. Data from the sleep questionnaires showed perception of poor sleep quality in ADHD patients.Conclusions: Leg movements during sleep in ADHD adults are not significantly more frequent than in healthy controls and the nocturnal motor events do not show an increased periodicity in these patients. The non-periodic character of LMs in ADHD has already been shown in children and seems to differentiate ADHD from other pathophysiological related conditions like restless legs syndrome (RLS) or periodic limb movement disorder (PLMD). The reduced subjective sleep quality reported by ADHD adults contrasted with the normal objective polysomnographic parameters, which could suggest a sleep-state misperception in these individuals or more subtle sleep abnormalities not picked up by the traditional sleep staging.

Sleep spindle characteristics and arousability from nighttime transportation noise exposure in healthy young and older individuals.

Nighttime transportation noise elicits awakenings, sleep-stage changes, and electroencephalographic (EEG) arousals. Here, we investigated the potential sleep-protective role of sleep spindles on noise-induced sleep alterations. Twenty-six young (19-33 years, 12 women) and 18 older (52-70 years, 9 women) healthy volunteers underwent a repeated measures polysomnographic 6-day laboratory study. Participants spent one noise-free baseline night, followed by four transportation noise-exposure nights (road traffic or railway noise; continuous or intermittent: average sound levels of 45 dB, maximum sound levels of 50-62 dB), and one noise-free recovery night. Sleep stages were scored manually and fast sleep spindle characteristics were quantified automatically using an individual band-pass filtering approach. Nighttime exposure to transportation noise significantly increased sleep EEG arousal indices. Sleep structure and continuity were not differentially affected by noise exposure in individuals with a low versus a high spindle rate. Spindle rates showed an age-related decline along with more noise-induced sleep alterations. All-night spindle rates did not predict EEG arousal or awakening probability from single railway noise events. Spindle characteristics were affected in noise-exposure nights compared to noise-free nights: we observed a reduction of the spindle amplitude in both age groups and of the spindle rate in the older group. We have evidence that spindle rate is more likely to represent a trait phenomenon, which does not seem to play a sleep-protective role in nighttime transportation noise-induced sleep disruptions. However, the marked reduction in spindle amplitude is most likely a sensitive index for noise-induced sleep alterations.

Glucose Metabolism after Sleep Restriction, Total Sleep Deprivation, and Recovery

ObjectiveSleep deficiency which is prevalent in shift work has been associated with an increased metabolic disease risk. Experimentally induced sleep restriction has been shown to impair glucose metabolism and has been linked to reduced slow wave sleep (SWS) as a possible causal factor. This study examined (i) whether total sleep deprivation exhibits similar effects on glucose tolerance and insulin sensitivity as sleep restriction, (ii) whether one recovery night after sleep restriction is sufficient to restore impaired glucose metabolism, and (iii) whether the combination of total sleep deprivation with prior sleep restriction shows cumulative effects.MethodsThirty‐six healthy volunteers participated in a 12‐day study. After one adaptation night and two baseline nights with 8 h of scheduled sleep each, sleep opportunities were restricted for 5 nights either to 5 h (21 participants, 9 females, mean ± SD, age 26 ± 4 yrs, BMI 23.1 ± 1.9) or maintained at 8 h (control, 15 participants, 5 females, age 28 ± 6 yrs, BMI 23.6 ± 2.9). Then, both groups underwent a single 8‐h night of recovery sleep, a 38‐h period of wakefulness, and a final recovery night. Oral glucose tolerance tests (OGTT) were conducted in the morning following lights on (&gt;10 h fasting) after the second baseline night, after 5 nights of sleep restriction, after the first recovery night, and after 24 h of sleep deprivation. Blood was sampled immediately prior to the OGTT and then at 30‐min intervals for 2 h. Polysomnograms were recorded. SWS per night and areas under the curve (AUC) for glucose, insulin, and HOMA were analyzed in each of the two groups with mixed ANOVAs with ‘sleep condition’ (4x) and ‘sex’ (2x) as factors (post‐hoc Bonferroni‐Holm adjustment).ResultsGlucose tolerance and insulin sensitivity decreased after sleep restriction (mean ± SEM, glucose Δ 32.5 ± 7.0 mg*h/dl, p&lt;0.0001; insulin Δ 44.9 ± 9.2 mU*h/dl, p&lt;0.0001; HOMA Δ 20.7 ± 3.9, p&lt;0.0001) and remained low after recovery sleep (glucose Δ 17.3 ± 6.8 mg*h/dl, p=0.0139; insulin Δ 24.7 ± 9.2 mU*h/dl, p=0.0102; HOMA Δ 11.3 ± 3.8, p=0.0053) compared to baseline. After 24 h awake, these parameters were not different from baseline in both groups. The amount of SWS in the final sleep restriction night (Δ 0.6 ± 4.7 min, p=0.8949) and the recovery night (Δ 9.2 ± 4.7 min, p=0.0534) did not significantly differ from baseline.ConclusionSleep restriction for 5 nights negatively impacts glucose metabolism. This impairment appears to occur independently of SWS, and to outlast a single night of recovery sleep. In contrast, prolonged wakefulness does neither acutely affect glucose metabolism nor exhibit cumulative effects with prior sleep restriction. Chronic sleep loss and acutely extended wake duration appear to activate different regulatory responses in glucose metabolism.Support or Funding InformationFunded by the German Aerospace Center and the Research Center JuelichThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The degree of radiation-induced DNA strand breaks is altered by acute sleep deprivation and psychological stress and is associated with cognitive performance in humans.

Sleep deprivation is associated with impaired immune responses, cancer, and morbidity and mortality, and can degrade cognitive performance, although individual differences exist in such responses. Sleep deprivation induces DNA strand breaks and DNA base oxidation in animals, and psychological stress is associated with increased DNA damage in humans. It remains unknown whether sleep deprivation or psychological stress in humans affects DNA damage response from environmental stressors, and whether these responses predict cognitive performance during sleep deprivation. Sixteen healthy adults (ages 29-52 years; mean age ± SD, 36.4 ± 7.1 years; seven women) participated in a 5-day experiment involving two 8 hr time-in-bed (TIB) baseline nights, followed by 39 hr total sleep deprivation (TSD), and two 8-10 hr TIB recovery nights. A modified Trier Social Stress Test was conducted on the day after TSD. The Psychomotor Vigilance Test measured behavioral attention. DNA damage was assessed in blood cells collected at 5 time points, and blood cells were irradiated ex vivo. TSD, alone or in combination with psychological stress, did not induce significant increases in DNA damage. By contrast, radiation-induced DNA damage decreased significantly in response to TSD, but increased back to baseline when combined with psychological stress. Cognitively vulnerable individuals had more radiation-induced DNA strand breaks before TSD, indicating their greater sensitivity to DNA damage from environmental stressors. Our results provide novel insights into the molecular consequences of sleep deprivation, psychological stress, and performance vulnerability. They are important for fields involving sleep loss, radiation exposure, and cognitive deficits, including cancer therapy, environmental toxicology, and space medicine.

Sleep quantity and quality during consecutive day heat training with the inclusion of cold-water immersion recovery

Exercise in the heat is a common occurrence among athletes and often is intentional in order to gain heat acclimation benefits, however, little is known about how such training may affect sleep. Therefore, this study investigated five days of training in the heat of varying intensity and duration and inclusion of cold-water immersion (CWI) recovery on sleep quantity and quality. Thirty recreationally-trained male participants completed five days of heat training (HT) and were randomised into three interventions including (i) 90 min cycling at 40% power at maximal aerobic capacity (Pmax) with 15 min passive recovery (90HT); (ii) 90 min cycling at 40% Pmax with 15 min CWI recovery (90CWI); or (iii) 30 min cycling alternating between 40% and 70% Pmax, with 15 min passive recovery (30HT). Sleep quality and quantity were assessed using Actigraphy and sleep diaries during five baseline nights (BASE) and five nights of HT which included subjective sleep quality and objective assessments of sleep quantity and quality. Total time asleep and perceived sleep quality were reduced, while awake duration and wake after sleep onset (WASO) were increased (p = 0.001–0.01) during HT compared to BASE. Latency was shorter for 30HT compared to 90HT during HT (p = 0.02), however, no differences between interventions for all other sleep variables (p > 0.05). The reduction in total sleep time due to increases in average wake duration during HT may be due to the unaccustomed increased in training frequency. Of note, reducing training in the heat duration per day improved sleep latency and sleep quality with no effect on total sleep time, while the addition of CWI has minimal effect on sleep quality or quantity.

Estimating adolescent sleep need using dose-response modeling.

This study will (1) estimate the nightly sleep need of human adolescents, (2) determine the time course and severity of sleep-related deficits when sleep is reduced below this optimal quantity, and (3) determine whether sleep restriction perturbs the circadian system as well as the sleep homeostat. Thirty-four adolescents aged 15 to 17 years spent 10 days and nine nights in the sleep laboratory. Between two baseline nights and two recovery nights with 10 hours' time in bed (TIB) per night, participants experienced either severe sleep restriction (5-hour TIB), moderate sleep restriction (7.5-hour TIB), or no sleep restriction (10-hour TIB) for five nights. A 10-minute psychomotor vigilance task (PVT; lapse = response after 500 ms) and the Karolinska Sleepiness Scale were administered every 3 hours during wake. Salivary dim-light melatonin onset was calculated at baseline and after four nights of each sleep dose to estimate circadian phase. Dose-dependent deficits to sleep duration, circadian phase timing, lapses of attention, and subjective sleepiness occurred. Less TIB resulted in less sleep, more lapses of attention, greater subjective sleepiness, and larger circadian phase delays. Sleep need estimated from 10-hour TIB sleep opportunities was approximately 9 hours, while modeling PVT lapse data suggested that 9.35 hours of sleep is needed to maintain optimal sustained attention performance. Sleep restriction perturbs homeostatic and circadian systems, leading to dose-dependent deficits to sustained attention and sleepiness. Adolescents require more sleep for optimal functioning than typically obtained.

Caffeine reversal of sleep deprivation effects on alertness, mood and repeated sprint performances in physical education students

ABSTRACTThe aim of this study was to evaluate the effects of caffeine ingestion and partial sleep deprivation on mood and cognitive and physical performances. In randomised order, 12 healthy male physical education students completed four test sessions at 18:00 h after placebo or 5 mg/kg of caffeine ingestion during a baseline night (RN) (bed time: from 22:00 to 07:00 h), or during a night of partial (four hrs) sleep deprivation (PSD). During each test session, participants performed a reaction time test, a vigilance test, the 10 s Wingate cycling test during (measuring peak power (PP) and anaerobic capacity), and the 5 m multiple shuttle test (measuring peak distance (PD), total distance (TD), and fatigue index (FI)). Compared to RN, simple reaction time, vigilance, PP, PD, TD, and FI were altered by PSD the following day after placebo ingestion with increased reaction time and FI and reduced PP, PD, TD, and vigilance (p < 0.001). Moreover, during PSD condition, PP, PD, and TD were significantly higher after caffeine ingestion in comparison with placebo ingestion (p < 0.05). However, both simple reaction times and vigilance were significantly lower after caffeine ingestion in comparison with placebo during PSD (p < 0.05). Caffeine is an effective strategy to maintain physical and cognitive performances the day after PSD.

Sleep and hypothalamic pituitary adrenal axis responses to metyrapone in posttraumatic stress disorder

Disturbed sleep is a core feature of posttraumatic stress disorder (PTSD), characterized in part by decreased delta power sleep that may result from stress-related alterations in corticotropin releasing factor (CRF), hypothalamic pituitary adrenal axis (HPA) regulation and glucocorticoid signaling. Overnight HPA axis response mediating sleep disturbances in men and women with PTSD was examined using a metyrapone challenge. Metyrapone blocks cortisol synthesis, removing negative feedback, and increases the release of hypothalamic CRF and pituitary adrenocorticotropic hormone (ACTH). Laboratory-based polysomnography was used to monitor the sleep of 66 medically healthy, medication-free men and pre-menopausal follicular phase women including 33 with chronic PTSD (16 women and 17 men) and 33 age- and sex-matched controls (14 women and 19 men) over 3 consecutive nights. Participants completed an overnight metyrapone challenge after an adaptation and baseline night of sleep and ACTH was obtained by repeated blood sampling. Metyrapone resulted in a greater increase in ACTH and greater decreases in cortisol and delta spectral power sleep in PTSD subjects compared to controls, and a greater increase in ACTH in women compared to men. There was no sex difference in metyrapone effects on delta power sleep, and no significant metyrapone by PTSD by sex interactions with either ACTH or delta power sleep. Regression analyses indicated that a greater increase in ACTH response was associated with a greater decrease in delta power sleep response in PTSD subjects, but no such relationship was found in controls. The PTSD group difference was similar in men and women. These results suggest that stress-related alterations of the HPA axis in PTSD may contribute to sleep difficulties. Therapeutics that target the HPA axis may offer promise as a potential future treatment for PTSD and related sleep difficulties.