Impact Of Sleep Restriction And Recovery On Motivation During Repeated Cognitive Performance Testing

Introduction: Both motivation and sleep deprivation affect cognitive performance. Especially during long-lasting studies with repeated cognitive performance tasks there is concern that subjects will lose motivation over time. Results may be confounded due to changes in motivation. Methods: In an ongoing study, 29 healthy volunteers performed 55 cognitive performance tasks at three-hourly intervals in a 12-day inpatient study. After two baseline nights with 8 h time in bed (TIB) the intervention group (N=20; mean age 26 ± 4 years, 9 females) underwent chronic sleep restriction for 5 nights (5 h TIB) with a following recovery night of 8 h TIB. The control group (N=9; mean age 25 ± 5 years, 3 females) had the opportunity to sleep 8 hours every night. Participants completed the Karolinska Sleepiness Scale (KSS) and a questionnaire about their motivation (from 1=very little/not motivated to 5=very motivated) at 6 p.m. on all days. Results: Wilcoxon signed-rank tests showed a significant decrease in motivation (p=.0439) and a significant increase in subjective sleepiness (p=.0184) from baseline (motivation: 2.8 ± 0.6 (SD), sleepiness: 3.2 ± 1.2) to the last day of chronic sleep restriction (motivation: 2.2 ± 0.5, sleepiness: 5.1 ± 1.8) for the experimental group. Motivation remained low after recovery sleep (2.2 ± 0.8; p=.0198). Sleepiness and motivation scores showed a significant Spearman correlation (r=-0.43, p<0.001). Discussion: Chronic sleep restriction for five days leads to an increase in sleepiness and a decrease in motivation. One night of recovery is insufficient to reverse the motivation loss, contrasting with the beneficial effect on sleepiness. During chronic sleep restriction conditions subjective motivation seems to decrease as a function of subjective sleepiness

Residents’ negative attitude towards air traffic is associated with impaired objective sleep quality

Objectives: Nocturnal aircraft noise induces sleep disturbances and is associated with impaired quality of life. The magnitude of physiological and psychological responses to noise varies among individuals. Stable individual vulnerabilities have been reported for aircraft noise induced awakenings. To date it is unknown, whether the subjective attitude towards air traffic and residents' sleep quality impact on each other. Methods: Seventy-four out of 81 investigated residents around Frankfurt Airport (Germany) rated their attitude towards air traffic (from 1 = negative to 5 = positive; negative attitude: score ≤ 2, N=28, mean age 44 ± 16 years; moderate to positive attitude: score > 3, N=46, mean age 44 ± 15 years) and evaluated its necessity (from 1 = not necessary to 5 = highly necessary; no to moderate necessity: score ≤ 3, N=22, mean age 45 ± 10 years; high necessity: score > 3, N=52, mean age 43 ± 17 years). In addition, polysomnographical recordings were obtained in residents' home environment. These investigations were part of the NORAH sleep study in 2012. Results: Significant impairments in sleep quality (prolonged sleep onset latency, increased wake after sleep onset, reduced sleep efficiency, and less deep sleep) were found for participants with a negative attitude towards air traffic. The judgement of no or moderate necessity of air traffic was associated with a significantly reduced deep sleep duration. Conclusions: Residents' subjective attitude towards air traffic and their objective sleep quality are related. Cause and effect in this relationship remain to be identified

Interindividual variabilities in cognitive performance degradation after alcohol consuption and sleep loss are related

Introduction The sleep inducing effects of alcohol as well as the increase in sleep propensity and sleepiness after sleep loss have been linked to the adenosinergic system in the brain. While the performance impairing effects of ethanol have partly been related to the inhibitory effects of cerebral adenosine, sleep loss has been found to increase adenosine receptor density. The interindividual variability of cognitive performance impairments after alcohol intake as well as after sleep loss is extensive. Thus, we examined in humans whether performance degradations resulting from sleep loss and alcohol consumption are related. Methods Performance in a 10-min Psychomotor Vigilance Task (PVT) was tested in 47 healthy volunteers (mean age 27 ± 5 (SD) years, 21 females) at 6 pm 1) after an 8 hour control night, 2) after alcohol consumption (aiming at a blood alcohol concentration (BAC) of 0.08%), and 3) after 35 hours of total sleep deprivation. After alcohol intake, 35 of the participants reached a BAC of more than 0.06% prior to the performance testing (mean BAC 0.074%, SD 0.009%, min. 0.063%, max. 0.095%) and were included in the analyses. Two recovery nights were scheduled between conditions. Results Performance impairments due to acute alcohol intake and due to 35 hours of sustained wakefulness were calculated as differences from performance under control conditions. The degree in performance degradation correlated highly between both conditions (i.e. 10% slowest reaction times: Pearson’s r=0.73, p<0.0001; standard deviation of reaction times: r=0.75, p<0.0001; mean reaction time: r=0.59, p=0.0002). Conclusions Participants whose PVT performance proved to be vulnerable to the effects of alcohol consumption were also vulnerable to sleep loss, whereas individuals who were resilient against the effects of alcohol were also less susceptible to the impact of sleep deprivation. These results suggest that the effects of alcohol and sleep deprivation on performance are mediated – at least in part – by a common pathway that may involve the adenosinergic system in the brain

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 individuals 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 5 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 4 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 2 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 induced benefits on different aspects of performance lasted for 4-5 days of 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

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 A 2A 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 [ 18 F]‑CPFPX to quantify the baseline availability of A 1 adenosine receptors (A 1 R) 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 A 1 R 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 A 1 R availability may suggest that CSR and caffeine affect thalamic GM plasticity predominantly by a different mechanism. Future studies on the role of adenosine A 2A receptors in CSR‑induced GM plasticity are warranted

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

Mesolimbic fMRI activations during reward anticipation correlate with reward-related ventral striatal dopamine release

The dopaminergic mechanisms that control reward-motivated behavior are the subject of intense study, but it is yet unclear how, in humans, neural activity in mesolimbic reward-circuitry and its functional neuroimaging correlates are related to dopamine release. To address this question, we obtained functional magnetic resonance imaging (fMRI) measures of reward-related neural activity and [11C] raclopride positron emission tomography (PET) measures of dopamine release in the same human participants, while they performed a delayed monetary incentive task. Across the cohort, a positive correlation emerged between neural activity of the substantia nigra / ventral tegmental area (SN/VTA), the main origin of dopaminergic neurotransmission, during reward anticipation and reward-related [11C] raclopride displacement as an index of dopamine release in the ventral striatum, major target of SN/VTA dopamine neurons. Neural activity in the ventral striatum / nucleus accumbens itself also correlated with ventral striatal dopamine release.Additionally, high reward-related dopamine release was associated with increased activation of limbic structures, such as the amygdala and the hippocampus. The observed correlations of reward-related mesolimbic fMRI activation and dopamine release provide evidence that dopaminergic neurotransmission plays a quantitative role in human mesolimbic reward processing. Moreover, the combined neurochemical and hemodynamic imaging approach used here opens up new perspectives for the investigation of molecular mechanisms underlying human cognition

Effects of 30days bed rest and exercise countermeasures on PBMC bioenergetics

Abstract Aim: Altered mitochondrial function across various tissues is a key determinant of spaceflight-induced physical deconditioning. In comparison to tissue biopsies, blood cell bioenergetics holds promise as a systemic and more readily accessible biomarker, which was evaluated during head-down tilt bed rest (HDTBR), an established ground-based analog for spaceflight-induced physiological changes in humans. More specifically, this study explored the effects of HDTBR and an exercise countermeasure on mitochondrial respiration in peripheral blood mononuclear cells (PBMCs). Methods: We subjected 24 healthy participants to a strict 30-day HDTBR protocol. The control group (n=12) underwent HDTBR only, while the countermeasure group (n=12) engaged in regular supine cycling exercise followed by veno-occlusive thigh cuffs post-exercise for 6h. We assessed routine blood parameters 14 days before bed rest, the respiratory capacity of PBMCs via highresolution respirometry, and citrate synthase activity 2days before and at day 30 of bed rest. We confirmed PBMC composition by flow cytometry. Results: The change of the PBMC maximal oxidative phosphorylation capacity (OXPHOS) amounted to an 11% increase in the countermeasure group, while it decreased by 10% in the control group (p=0.04). The limitation of OXPHOS increased in control only while other respiratory states were not affected by either intervention. Correlation analysis revealed positive associations between white blood cells, lymphocytes, and basophils with PBMC bioenergetics in both groups. Conclusion: This study reveals that a regular exercise countermeasure has a positive impact on PBMC mitochondrial function, confirming the potential application of blood cell bioenergetics for human spaceflight

Are you vulnerable to sleep loss? Association between a priori self-assessed sensitivity to sleep deprivation and waking EEG dynamics

1. Objectives: Sleep deprivation leads to EEG power increases especially in lower frequency bands. Inter-individual differences exist in neurocognitive consequences of sleep loss. We aimed at developing a questionnaire that identifies individuals who are vulnerable to sleep loss. Here we investigated whether a priori self-assessed sensitivity to sleep loss is related to the changes in waking EEG power between a sleep deprived and a well-rested state. 2. Methods: 17 healthy men (M = 27 years) were sleep deprived for 58 h. In the beginning of the study, participants rated their sensitivity to sleep deprivation. Every 6 h during wakefulness participants performed a test battery (waking EEG, Karolinska Sleepiness Scale (KSS) and cognitive tests). EEG power density after 50 h was expressed as a percentage of power after 2 h of wakefulness following 14 h of recovery sleep, and correlated with the results from the sensitivity questionnaire and the KSS (2-50 h). 3. Results: Self-assessed sensitivity to sleep deprivation correlated with the change in theta power (rs (15) = -.52, p = .046) and delta power (rs (15) = -.57, p = .026). The KSS did not correlate with theta or delta power. 4. Conclusions: Individuals with lower sensitivity to sleep deprivation showed a greater decline in waking EEG theta and delta power between sleep deprivation and recovery, suggesting that they recover faster than individuals with high sensitivity. Individuals might be able to predict their vulnerability to sleep loss based on their recovery experience

A priori self-assessed sensitivity to sleep deprivation correlates with individual cognitive Performance Impairment during prolonged Wakefulness

Research question: Differences exist in the individual susceptibility to performance impairments induced by sleep deprivation. Identifying people who are at high risk for such impairments prior to exposure to prolonged wakefulness would offer the possibility to increase safety. This study investigated the relationship between cognitive performance impairment during 58 h of sustained wakefulness and self-assessed sensitivity to sleep deprivation based on prior experience. In addition, cognitive performance impairment was compared with subjective fatigue and sleepiness during the sleep deprivation. Methods: 17 healthy, male volunteers (mean age 27 ± 5 SD, age-span 19-36 years) participated in the study. At the beginning of the study, participants answered a self-assessment questionnaire about their sensitivity to sleep deprivation. During sleep deprivation, fatigue and sleepiness were assessed in 6-h-intervals by the Fatigue Checklist and Karolinska Sleepiness Scale, respectively; cognitive performance was measured by the sum of correct responses in the N-Back Task. The differences in the aforementioned measures between 2 and 50 h of wakefulness and the self-assessed sensitivity to sleep deprivation were used for correlation analysis. Results: The decrease of correct responses in the N-Back Task showed a significant correlation with the sensitivity to sleep deprivation (Spearman’s rs (17) = .59, p = .01) which was based on prior experience. There was no significant correlation between cognitive performance impairment and either fatigue (rs (17) = .19, p = .46) or sleepiness (rs (17) = -.00, p = .99). Conclusion: Participants who rated themselves as sensitive to sleep deprivation performed worse in the cognitive test than those who rated themselves as less sensitive. Whereas acute performance impairments during prolonged wakefulness were not paralleled by changes in subjective fatigue and sleepiness, individuals appear to be capable of predicting such impairments based on prior experience with exposure to sleep deprivation. Possibly, performance under sleep deprivation can be predicted on the basis of a few questions on sensitivity to sleep deprivation