Effects of moderate alcohol consumption and hypobaric hypoxia: implications for passengers' sleep, oxygen saturation and heart rate on long-haul flights.

BACKGROUND: Passengers on long-haul flights frequently consume alcohol. Inflight sleep exacerbates the fall in blood oxygen saturation (SpO2) caused by the decreased oxygen partial pressure in the cabin. We investigated the combined influence of alcohol and hypobaric hypoxia on sleep, SpO2 and heart rate. METHODS: Two groups of healthy individuals spent either two nights with a 4-hour sleep opportunity (00:00-04:00 hours) in the sleep laboratory (n=23; 53 m above sea level) or in the altitude chamber (n=17; 753 hPa corresponding to 2438 m above sea level, hypobaric condition). Participants consumed alcohol before one of the nights (mean±SE blood alcohol concentration 0.043±0.003%). The order of the nights was counterbalanced. Two 8-hour recovery nights (23:00-07:00 hours) were scheduled between conditions. Polysomnography, SpO2 and heart rate were recorded. RESULTS: The combined exposure to alcohol and hypobaric condition decreased SpO2 to a median (25th/75th percentile) of 85.32% (82.86/85.93) and increased heart rate to a median (25th/75th percentile) of 87.73 bpm (85.89/93.86) during sleep compared with 88.07% (86.50/88.49) and 72.90 bpm (70.90/78.17), respectively, in the non-alcohol hypobaric condition, 94.97% (94.59/95.33) and 76.97 bpm (65.17/79.52), respectively, in the alcohol condition and 95.88% (95.72/96.36) and 63.74 bpm (55.55/70.98), respectively, in the non-alcohol condition of the sleep laboratory group (all p<0.0001). Under the combined exposure SpO2 was 201.18 min (188.08/214.42) below the clinical hypoxia threshold of 90% SpO2 compared with 173.28 min (133.25/199.03) in the hypobaric condition and 0 min (0/0) in both sleep laboratory conditions. Deep sleep (N3) was reduced to 46.50 min (39.00/57.00) under the combined exposure compared with both sleep laboratory conditions (alcohol: 84.00 min (62.25/92.75); non-alcohol: 67.50 min (58.50/87.75); both p<0.003). CONCLUSIONS: The combination of alcohol and inflight hypobaric hypoxia reduced sleep quality, challenged the cardiovascular system and led to extended duration of hypoxaemia (SpO2 <90%).

Repeated caffeine intake suppresses cerebral grey matter responses to chronic sleep restriction in an A1 adenosine receptor-dependent manner: a double-blind randomized controlled study with PET-MRI.

Evidence has shown that both sleep loss and daily caffeine intake can induce changes in grey matter (GM). Caffeine is frequently used to combat sleepiness and impaired performance caused by insufficient sleep. It is unclear (1) whether daily use of caffeine could prevent or exacerbate the GM alterations induced by 5-day sleep restriction (i.e. chronic sleep restriction, CSR), and (2) whether the potential impact on GM plasticity depends on individual differences in the availability of adenosine receptors, which are involved in mediating effects of caffeine on sleep and waking function. Thirty-six healthy adults participated in this double-blind, randomized, controlled study (age = 28.9 ± 5.2 y/; F:M = 15:21; habitual level of caffeine intake < 450 mg; 29 homozygous C/C allele carriers of rs5751876 of ADORA2A, an A2A adenosine receptor gene variant). Each participant underwent a 9-day laboratory visit consisting of one adaptation day, 2 baseline days (BL), 5-day sleep restriction (5 h time-in-bed), and a recovery day (REC) after an 8-h sleep opportunity. Nineteen participants received 300 mg caffeine in coffee through the 5 days of CSR (CAFF group), while 17 matched participants received decaffeinated coffee (DECAF group). We examined GM changes on the 2nd BL Day, 5th CSR Day, and REC Day using magnetic resonance imaging and voxel-based morphometry. Moreover, we used positron emission tomography with [18F]-CPFPX to quantify the baseline availability of A1 adenosine receptors (A1R) and its relation to the GM plasticity. The results from the voxel-wise multimodal whole-brain analysis on the Jacobian-modulated T1-weighted images controlled for variances of cerebral blood flow indicated a significant interaction effect between caffeine and CSR in four brain regions: (a) right temporal-occipital region, (b) right dorsomedial prefrontal cortex (DmPFC), (c) left dorsolateral prefrontal cortex (DLPFC), and (d) right thalamus. The post-hoc analyses on the signal intensity of these GM clusters indicated that, compared to BL, GM on the CSR day was increased in the DECAF group in all clusters  but decreased in the thalamus, DmPFC, and DLPFC in the CAFF group. Furthermore, lower baseline subcortical A1R availability predicted a larger GM reduction in the CAFF group after CSR of all brain regions except for the thalamus. In conclusion, our data suggest an adaptive GM upregulation after 5-day CSR, while concomitant use of caffeine instead leads to a GM reduction. The lack of consistent association with individual A1R availability may suggest that CSR and caffeine affect thalamic GM plasticity predominantly by a different mechanism. Future studies on the role of adenosine A2A receptors in CSR-induced GM plasticity are warranted.

A genetic variation in the adenosine A2A receptor gene contributes to variability in oscillatory alpha power in wake and sleep EEG and A1 adenosine receptor availability in the human brain.

The EEG alpha rhythm (∼ 8-13 Hz) is one of the most salient human brain activity rhythms, modulated by the level of attention and vigilance and related to cerebral energy metabolism. Spectral power in the alpha range in wakefulness and sleep strongly varies among individuals based on genetic predisposition. Knowledge about the underlying genes is scarce, yet small studies indicated that the variant rs5751876 of the gene encoding A2A adenosine receptors (ADORA2A) may contribute to the inter-individual variation. The neuromodulator adenosine is directly linked to energy metabolism as product of adenosine tri-phosphate breakdown and acts as a sleep promoting molecule by activating A1 and A2A adenosine receptors. We performed sleep and positron emission tomography studies in 59 healthy carriers of different rs5751876 alleles, and quantified EEG oscillatory alpha power in wakefulness and sleep, as well as A1 adenosine receptor availability with 18F-CPFPX. Oscillatory alpha power was higher in homozygous C-allele carriers (n = 27, 11 females) compared to heterozygous and homozygous carriers of the T-allele (n(C/T) = 23, n(T/T) = 5, 13 females) (F(18,37) = 2.35, p = 0.014, Wilk's Λ = 0.487). Furthermore, a modulatory effect of ADORA2A genotype on A1 adenosine receptor binding potential was found across all considered brain regions (F(18,40) = 2.62, p = 0.006, Wilk's Λ = 0.459), which remained significant for circumscribed occipital region of calcarine fissures after correction for multiple comparisons. In female participants, a correlation between individual differences in oscillatory alpha power and A1 receptor availability was observed. In conclusion, we confirmed that a genetic variant of ADORA2A affects individual alpha power, while a direct modulatory effect via A1 adenosine receptors in females is suggested.

Associations between resting state brain activity and A1 adenosine receptor availability in the healthy brain: Effects of acute sleep deprivation.

Introduction: Previous resting-state fMRI (Rs-fMRI) and positron emission tomography (PET) studies have shown that sleep deprivation (SD) affects both spontaneous brain activity and A1 adenosine receptor (A1AR) availability. Nevertheless, the hypothesis that the neuromodulatory adenosinergic system acts as regulator of the individual neuronal activity remains unexplored. Methods: Therefore, fourteen young men underwent Rs-fMRI, A1AR PET scans, and neuropsychological tests after 52 h of SD and after 14 h of recovery sleep. Results: Our findings suggested higher oscillations or regional homogeneity in multiple temporal and visual cortices, whereas decreased oscillations in cerebellum after sleep loss. At the same time, we found that connectivity strengths increased in sensorimotor areas and decreased in subcortical areas and cerebellum. Discussion: Moreover, negative correlations between A1AR availability and rs-fMRI metrics of BOLD activity in the left superior/middle temporal gyrus and left postcentral gyrus of the human brain provide new insights into the molecular basis of neuronal responses induced by high homeostatic sleep pressure.

Total Sleep Deprivation Increases Brain Age Prediction Reversibly in Multisite Samples of Young Healthy Adults.

Sleep loss pervasively affects the human brain at multiple levels. Age-related changes in several sleep characteristics indicate that reduced sleep quality is a frequent characteristic of aging. Conversely, sleep disruption may accelerate the aging process, yet it is not known what will happen to the age status of the brain if we can manipulate sleep conditions. To tackle this question, we used an approach of brain age to investigate whether sleep loss would cause age-related changes in the brain. We included MRI data of 134 healthy volunteers (mean chronological age of 25.3 between the age of 19 and 39 years, 42 females/92 males) from five datasets with different sleep conditions. Across three datasets with the condition of total sleep deprivation (>24 h of prolonged wakefulness), we consistently observed that total sleep deprivation increased brain age by 1-2 years regarding the group mean difference with the baseline. Interestingly, after one night of recovery sleep, brain age was not different from baseline. We also demonstrated the associations between the change in brain age after total sleep deprivation and the sleep variables measured during the recovery night. By contrast, brain age was not significantly changed by either acute (3 h time-in-bed for one night) or chronic partial sleep restriction (5 h time-in-bed for five continuous nights). Together, the convergent findings indicate that acute total sleep loss changes brain morphology in an aging-like direction in young participants and that these changes are reversible by recovery sleep.SIGNIFICANCE STATEMENT Sleep is fundamental for humans to maintain normal physical and psychological functions. Experimental sleep deprivation is a variable-controlling approach to engaging the brain among different sleep conditions for investigating the responses of the brain to sleep loss. Here, we quantified the response of the brain to sleep deprivation by using the change of brain age predictable with brain morphologic features. In three independent datasets, we consistently found increased brain age after total sleep deprivation, which was associated with the change in sleep variables. Moreover, no significant change in brain age was found after partial sleep deprivation in another two datasets. Our study provides new evidence to explain the brainwide effect of sleep loss in an aging-like direction.

Sleep-Induced Hypoxia under Flight Conditions: Implications and Countermeasures for Long-Haul Flight Crews and Passengers.

PURPOSE: Recuperation during sleep on board of commercial long-haul flights is a safety issue of utmost importance for flight crews working extended duty periods. We intended to explore how sleep and blood oxygenation (in wake versus sleep) are affected by the conditions in an airliner at cruising altitude. METHODS: Healthy participants' sleep was compared between 4-h sleep opportunities in the sleep laboratory (n = 23; sleep lab, ie, 53 m above sea level) and in an altitude chamber (n = 20; flight level, ie, 753 hPa, corresponding to 2438 m above sea level). A subgroup of 12 participants underwent three additional conditions in the altitude chamber: 1) 4-h sleep at ground level, 2) 4-h sleep at flight level with oxygen partial pressure equivalent to ground level, 3) 4-h monitored wakefulness at flight level. Sleep structure and blood oxygenation were analysed with mixed ANOVAs. RESULTS: Total sleep time at flight level compared to in the sleep laboratory was shorter (Δ mean ± standard error -11.1 ± 4.2 min) and included less N3 sleep (Δ -17.6 ± 5.4 min), while blood oxygenation was decreased. Participants spent 69.7% (± 8.3%) of the sleep period time but only 13.2% (± 3.0%) of monitored wakefulness in a hypoxic state (<90% oxygen saturation). Oxygen enrichment of the chamber prevented oxygen desaturation. CONCLUSION: Sleep - but not wakefulness - under flight conditions induces hypobaric hypoxia which may contribute to impaired sleep. The results caution against the assumption of equivalent crew recovery in-flight and on the ground but hold promise for oxygen enrichment as a countermeasure. The present results have implications for flight safety and possible long-term consequences for health in crews.

Road traffic noise impacts sleep continuity in suburban residents: Exposure-response quantification of noise-induced awakenings from vehicle pass-bys at night.

Nocturnal traffic noise has been associated with adverse health outcomes in exposed residents. Precise quantification of traffic noise effects on sleep is thus of great importance. Here we establish an exposure-response relationship for the awakening probability due to intermittent road traffic noise in suburban residents. We conducted a field study in residential areas where road traffic was the dominant noise source, and noise events were attributable to separate vehicle pass-bys. Forty healthy participants underwent polysomnography for five consecutive nights at their homes. A total of 11,003 road traffic noises derived from simultaneous acoustic measurements at the sleepers' ears were included in an event-related analysis of awakenings. Logistic regression analysis revealed that the awakening probability due to road traffic noise increased with the maximum sound pressure level (SPL) and the maximum slope of the increasing SPL of a vehicle pass-by, as well as the age of the exposed individual. Compared to sleep stage 2, the awakening probability was higher in rapid eye movement sleep (REMS) and lower in slow wave sleep (SWS). The protective effect of both stage 2 and SWS against awakenings decreased with age, whereas no age-dependent change was observed for REMS. When adjusting for other contributing factors, the probability of a noise-induced awakening ranged from 0% at a maximum SPL of 27.1 dB(A) to 2.0% at 70 dB(A). Road traffic noise at night - even in suburban areas with moderate traffic density - negatively impacts residents' sleep continuity. Exposure-response quantification for traffic noise-induced awakenings may serve as a basis for noise protection efforts by regulators and policy makers.

Traffic noise-induced changes in wake-propensity measured with the Odds-Ratio Product (ORP).

Nocturnal traffic noise can disrupt sleep and impair physical and mental restoration, but classical sleep scoring techniques may not fully capture subtle yet clinically relevant alterations of sleep induced by noise. We used a validated continuous measure of sleep depth and quality based on automatic analysis of physiologic sleep data, termed Wake Propensity (WP), to investigate temporal changes of sleep in response to nocturnal noise events in 3-s epochs. Seventy-two healthy participants (mean age 40.3 years, range 18-71 years, 40 females, 32 males) slept for 11 nights in a laboratory, during which we measured sleep with polysomnography. In 8 nights, participants were exposed to 40, 80 or 120 road, rail and/or aircraft noise events with maximum noise levels of 45-65 dB LAS,max during 8-h sleep opportunities. We analyzed sleep macrostructure and event-related change of WP during noise exposure with linear mixed models. Nocturnal traffic noise led to event-related shifts towards wakefulness and less deep, more unstable sleep (increase in WP relative to pre-noise baseline ranging from +29.5% at 45 dB to +38.3% at 65 dB; type III effect p < 0.0001). Sleep depth decreased dynamically with increasing noise level, peaking when LAS,max was highest. This change in WP was stronger and occurred more quickly for events where the noise onset was more rapid (road and rail) compared to more gradually time-varying noise (aircraft). Sleep depth did not immediately recover to pre-noise WP, leading to decreased sleep stability across the night compared to quiet nights, which was greater with an increasing number of noise events (standardized ß = 0.053, p = 0.003). Further, WP was more sensitive to noise than classical arousals. Results demonstrate the usefulness of WP as a measure of the effects of external stimuli on sleep, and show WP is a more sensitive measure of noise-induced sleep disruption than traditional methods of sleep analysis.

Cerebral A1 adenosine receptor availability in female and male participants and its relationship to sleep.

The neuromodulator adenosine and its receptors are mediators of sleep-wake regulation which is known to differ between sexes. We, therefore, investigated sex differences in A1 adenosine receptor (A1AR) availability in healthy human subjects under well-rested conditions using [18F]CPFPX and positron emission tomography (PET). [18F]CPFPX PET scans were acquired in 50 healthy human participants (20 females; mean age ± SD 28.0 ± 5.3 years). Mean binding potential (BPND; Logan's reference tissue model with cerebellum as reference region) and volume of distribution (VT) values were calculated in 12 and 15 grey matter brain regions, respectively. [18F]CPFPX BPND was higher in females compared to males in all investigated brain regions (p < 0.025). The largest differences were found in the pallidum and anterior cingulate cortex, where mean BPND values were higher by 29% in females than in males. In females, sleep efficiency correlated positively and sleep latency negatively with BPND in most brain regions. VT values did not differ between sexes. Sleep efficiency correlated positively with VT in most brain regions in female participants. In conclusion, our analysis gives a first indication for potential sex differences in A1AR availability even under well-rested conditions. A1AR availability as measured by [18F]CPFPX BPND is higher in females compared to males. Considering the involvement of adenosine in sleep-wake control, this finding might partially explain the known sex differences in sleep efficiency and sleep latency.

Reliability and validity of a 3-min psychomotor vigilance task in assessing sensitivity to sleep loss and alcohol: fitness for duty in aviation and transportation.

STUDY OBJECTIVES: The psychomotor vigilance task (PVT) is a widely used objective method to measure sustained attention, but the standard 10-min version is often impractical in operational settings. We investigated the reliability and validity of a 3-min PVT administered on a portable handheld device assessing sensitivity to sleep loss and alcohol in relation to a 10-min PVT and to applied tasks. METHODS: A total of 47 healthy volunteers underwent a 12 consecutive days sleep lab protocol. A cross-over design was adopted including total sleep deprivation (38 h awake), sleep restriction (SR, 4 h sleep opportunity), acute alcohol consumption, and SR after alcohol intake (SR/Alc 4 h sleep opportunity). Participants performed a 10-min and 3-min PVT and operationally relevant tasks related to demands in aviation and transportation. RESULTS: Sleep loss resulted in significant performance impairments compared with baseline measurements detected by both PVT versions-particularly for mean speed (both p < 0.001)-and the operationally relevant tasks. Similar effects were observed due to alcohol intake (speed: both p < 0.001). The 3-min and 10-min PVT results were highly correlated (speed: between r = 0.72 and r = 0.89). Three of four aviation-related tasks showed robust correlations with the 3-min PVT. Correlations with the parameters of the task related to transportation were lower, but mainly significant. CONCLUSION: The 3-min PVT showed a high reliability and validity in assessing sleep loss and alcohol-induced impairments in cognitive performance. Thus, our results underline its usefulness as potential fitness for duty self-monitoring tool in applied settings.

Short-Term Annoyance Due to Night-Time Road, Railway, and Air Traffic Noise: Role of the Noise Source, the Acoustical Metric, and Non-Acoustical Factors.

Field studies on traffic noise-induced annoyance have predominantly used estimated outside noise levels. We intended to complement existing knowledge with exposure-response relationships that are based on precise indoor noise measurements. Acoustic recordings inside the bedrooms of nightly road traffic and annoyance ratings in the following morning were obtained from 40 suburban residents (mean age 29.1 years ± 11.7; 26 females). We derived exposure-response functions for the probability to be "annoyed at least a little" (%LA). Further analyses compared data from the current study with those from two earlier studies on railway and aircraft noise. Annoyance increased with the number of traffic events and the equivalent sound pressure level. The inclusion of non-acoustical factors (such as assessment of road transport) improved the prediction considerably. When comparing the different traffic noise sources, %LA was higher for road than for air traffic at a given LAeq,night, but higher for road and railway than for air traffic at a given number of noise events. Acoustical as well as non-acoustical factors impact short-term annoyance induced by road, railway, and air traffic. Annoyance varies across noise sources, which may be due to differences in acoustical characteristics or in the temporal noise distribution throughout the night.

Coffee effectively attenuates impaired attention in ADORA2A C/C-allele carriers during chronic sleep restriction.

Many people consume coffee to attenuate increased sleepiness and impaired vigilance and attention due to insufficient sleep. We investigated in genetically caffeine sensitive men and women whether 'real world' coffee consumption during a simulated busy work week counteracts disabling consequences of chronically restricted sleep. We subjected homozygous C-allele carriers of ADORA2A (gene encoding adenosine A2A receptors) to five nights of only 5 h time-in-bed. We administered regular coffee (n = 12; 200 mg caffeine at breakfast and 100 mg caffeine after lunch) and decaffeinated coffee (n = 14) in double-blind fashion on all days following sleep restriction. At regular intervals four times each day, participants rated their sleepiness and performed the psychomotor vigilance test, the visual search task, and the visuo-spatial and letter n-back tasks. At bedtime, we quantified caffeine and the major caffeine metabolites paraxanthine, theobromine and theophylline in saliva. The two groups did not differ in age, body-mass-index, sex-ratio, chronotype and mood states. Subjective sleepiness increased in both groups across consecutive sleep restriction days and did not differ. By contrast, regular coffee counteracted the impact of repeated sleep loss on sustained and selective attention, as well as executive control when compared to decaffeinated coffee. The coffee also induced initial or transient benefits on different aspects of baseline performance during insufficient sleep. All differences between the groups disappeared after the recovery night and the cessation of coffee administration. The data suggest that 'real world' coffee consumption can efficiently attenuate sleep restriction-induced impairments in vigilance and attention in genetically caffeine sensitive individuals. German Clinical Trial Registry: # DRSK00014379.

Adverse interaction effects of chronic and acute sleep deficits on spatial working memory but not on verbal working memory or declarative memory.

The accumulation of chronic sleep deficits combined with acute sleep loss is common in shift workers and increases the risk of errors and accidents. We investigated single and combined effects of chronic and acute sleep loss and recovery sleep on working memory performance (N-back task) and on overnight declarative memory recall (paired-associate lists) in 36 healthy participants. After baseline measurements, the chronic sleep restriction group (n = 21; mean [SD] age 26 [4] years) underwent 5 nights of sleep restriction (5-hr time in bed [TIB]), whereas the control group (n = 15; mean [SD] age 28 [6] years) had 8-hr TIB during those nights. Afterwards, both groups spent 1 night with 8-hr TIB prior to acute sleep deprivation for 38 hr, and a final recovery night (10-hr TIB). Chronic sleep restriction decreased spatial N-back performance compared to baseline (omissions: p = .001; sensitivity: p = .012), but not letter N-back performance or word-pair recall. Acute sleep deprivation impaired spatial N-back performance more in the chronic sleep restriction group than in the control group (interaction between group and time awake: p ≤ .02). No group differences during acute sleep loss appeared in letter N-back performance or word recall. It is concluded that chronic sleep loss, even when followed by a night of recovery sleep, increases the vulnerability to impairments in spatial working memory during subsequent acute sleep loss. Verbal working memory and declarative memory were not affected by restricted sleep.

ADORA2A variation and adenosine A1 receptor availability in the human brain with a focus on anxiety-related brain regions: modulation by ADORA1 variation.

Adenosine, its interacting A1 and A2A receptors, and particularly the variant rs5751876 in the A2A gene ADORA2A have been shown to modulate anxiety, arousal, and sleep. In a pilot positron emission tomography (PET) study in healthy male subjects, we suggested an effect of rs5751876 on in vivo brain A1 receptor (A1AR) availability. As female sex and adenosinergic/dopaminergic interaction partners might have an impact on this rs5751876 effect on A1AR availability, we aimed to (1) further investigate the pilot male-based findings in an independent, newly recruited cohort including women and (2) analyze potential modulation of this rs5751876 effect by additional adenosinergic/dopaminergic gene variation. Healthy volunteers (32/11 males/females) underwent phenotypic characterization including self-reported sleep and A1AR-specific quantitative PET. Rs5751876 and 31 gene variants of adenosine A1, A2A, A2B, and A3 receptors, adenosine deaminase, and dopamine D2 receptor were genotyped. Multivariate analysis revealed an rs5751876 effect on A1AR availability (P = 0.047), post hoc confirmed in 30 of 31 brain regions (false discovery rate (FDR) corrected P values < 0.05), but statistically stronger in anxiety-related regions (e.g., amygdala, hippocampus). Additional effects of ADORA1 rs1874142 were identified; under its influence rs5751876 and rs5751876 × sleep had strengthened effects on A1AR availability (Pboth < 0.02; post hoc FDR-corrected Ps < 0.05 for 29/30 regions, respectively). Our results support the relationship between rs5751876 and A1AR availability. Additional impact of rs1874142, together with rs5751876 and sleep, might be involved in regulating arousal and thus the development of mental disorders like anxiety disorders. The interplay of further detected suggestive ADORA2A × DRD2 interaction, however, necessitates larger future samples more comparable to magnetic resonance imaging (MRI)-based samples.

Sleeping with Elevated Upper Body Does Not Attenuate Acute Mountain Sickness: Pragmatic Randomized Clinical Trial.

PURPOSE: Acute mountain sickness commonly occurs following ascent to high altitude and is aggravated following sleep. Cephalad fluid shifts have been implicated. We hypothesized that sleeping with the upper body elevated by 30º reduces the risk of acute mountain sickness. METHODS: In a pragmatic, randomized, observer-blinded field study at 4554 meters altitude, we investigated 134 adults aged 18-70 years with a Lake Louise score between 3 and 12 points on the evening of their arrival at the altitude. The individuals were exposed to sleeping on an inflatable cushion elevating the upper body by 30º or on a sham pillow in a horizontal position. The primary endpoint was the change in the Acute Mountain Sickness-Cerebral (AMS-C) score in the morning after sleeping at an altitude of 4554 meters compared with the evening before. Sleep efficiency was the secondary endpoint. RESULTS: Among 219 eligible mountaineers, 134 fulfilled the inclusion criteria and were randomized. The AMS-C score increased by 0.250 ± 0.575 in the control group and by 0.121 ± 0.679 in the intervention group (difference 0.105; 95% confidence interval, -0.098-0.308; P = .308). Oxygen saturation in the morning was 79% ± 6% in the intervention group and 78% ± 6% in the control group (P = .863). Sleep efficiency did not differ between groups (P = .115). CONCLUSIONS: Sleeping with the upper body elevated by 30° does not lead to relevant reductions in acute mountain sickness symptoms or hypoxemia at high altitude.

Impact of acute sleep deprivation on dynamic functional connectivity states.

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

Comparing the Effects of Road, Railway, and Aircraft Noise on Sleep: Exposure⁻Response Relationships from Pooled Data of Three Laboratory Studies.

OBJECTIVES: Air, road, and railway traffic, the three major sources of traffic noise, have been reported to differently impact on annoyance. However, these findings may not be transferable to physiological reactions during sleep which are considered to decrease nighttime recovery and might mediate long-term negative health effects. Studies on awakenings from sleep indicate that railway noise, while having the least impact on annoyance, may have the most disturbing properties on sleep compared to aircraft noise. This study presents a comparison between the three major traffic modes and their probability to cause awakenings. In combining acoustical and polysomnographical data from three laboratory studies sample size and generalizability of the findings were increased. METHODS: Data from three laboratory studies were pooled, conducted at two sites in Germany (German Aerospace Center, Cologne, and Leibniz Research Centre for Working Environment and Human Factors, Dortmund). In total, the impact of 109,836 noise events on polysomnographically assessed awakenings was analyzed in 237 subjects using a random intercept logistic regression model. RESULTS: The best model fit according to the Akaike Information Criterion (AIC) included different acoustical and sleep parameters. After adjusting for these moderators results showed that the probability to wake up from equal maximum A-weighted sound pressure levels (SPL) increased in the order aircraft < road < railway noise, the awakening probability from road and railway noise being not significantly different (p = 0.988). At 70 dB SPL, it was more than 7% less probable to wake up due to aircraft noise than due to railway noise. CONCLUSIONS: The three major traffic noise sources differ in their impact on sleep. The order with which their impact increased was inversed compared to the order that was found in annoyance surveys. It is thus important to choose the correct concept for noise legislation, i.e., physiological sleep metrics in addition to noise annoyance for nighttime noise protection.

Reestablishment of individual sleep structure during a single 14-h recovery sleep episode after 58 h of wakefulness.

Sleep structure is highly stable within individuals but different between individuals. The present study investigated robustness of the individual sleep structure to extended total sleep deprivation. Seventeen healthy men spent a baseline night (23:00-07:00 hours), 58 h of sleep deprivation and a 14-h recovery night (17:00-07:00 hours) in the laboratory. Intraclass correlation coefficients showed that the agreement between baseline and recovery with respect to the proportion of the different sleep stages increased as a function of recovery sleep duration. High values were reached for most of the sleep stages at the end of 14 h of recovery sleep (intraclass correlation coefficients between 0.38 and 0.76). If sleep duration of the recovery night is extended to 14 h, sleep stage distribution resembles that of a baseline night underlining the robustness of the individual sleep structure.

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

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