Left Ventricular Ejection Time Measured by Echocardiography Differentiates Neurobehavioral Resilience and Vulnerability to Sleep Loss and Stress

There are substantial individual differences (resilience and vulnerability) in performance resulting from sleep loss and psychosocial stress, but predictive potential biomarkers remain elusive. Similarly, marked changes in the cardiovascular system from sleep loss and stress include an increased risk for cardiovascular disease. It remains unknown whether key hemodynamic markers, including left ventricular ejection time (LVET), stroke volume (SV), heart rate (HR), cardiac index (CI), blood pressure (BP), and systemic vascular resistance index (SVRI), differ in resilient vs. vulnerable individuals and predict differential performance resilience with sleep loss and stress. We investigated for the first time whether the combination of total sleep deprivation (TSD) and psychological stress affected a comprehensive set of hemodynamic measures in healthy adults, and whether these measures differentiated neurobehavioral performance in resilient and vulnerable individuals. Thirty-two healthy adults (ages 27–53; 14 females) participated in a 5-day experiment in the Human Exploration Research Analog (HERA), a high-fidelity National Aeronautics and Space Administration (NASA) space analog isolation facility, consisting of two baseline nights, 39 h TSD, and two recovery nights. A modified Trier Social Stress Test induced psychological stress during TSD. Cardiovascular measure collection [SV, HR, CI, LVET, BP, and SVRI] and neurobehavioral performance testing (including a behavioral attention task and a rating of subjective sleepiness) occurred at six and 11 timepoints, respectively. Individuals with longer pre-study LVET (determined by a median split on pre-study LVET) tended to have poorer performance during TSD and stress. Resilient and vulnerable groups (determined by a median split on average TSD performance) showed significantly different profiles of SV, HR, CI, and LVET. Importantly, LVET at pre-study, but not other hemodynamic measures, reliably differentiated neurobehavioral performance during TSD and stress, and therefore may be a biomarker. Future studies should investigate whether the non-invasive marker, LVET, determines risk for adverse health outcomes.

The cyclic interaction between daytime behavior and the sleep behavior of laboratory dogs

Sleep deprivation has been found to negatively affect an individual´s physical and psychological health. Sleep loss affects activity patterns, increases anxiety-like behaviors, decreases cognitive performance and is associated with depressive states. The activity/rest cycle of dogs has been investigated before, but little is known about the effects of sleep loss on the behavior of the species. Dogs are polyphasic sleepers, meaning the behavior is most observed at night, but bouts are also present during the day. However, sleep can vary with ecological and biological factors, such as age, sex, fitness, and even human presence. In this study, kennelled laboratory adult dogs’ sleep and diurnal behavior were recorded during 24-h, five-day assessment periods to investigate sleep quality and its effect on daily behavior. In total, 1560 h of data were analyzed, and sleep metrics and diurnal behavior were quantified. The relationship between sleeping patterns and behavior and the effect of age and sex were evaluated using non-parametric statistical tests and GLMM modelling. Dogs in our study slept substantially less than previously reported and presented a modified sleep architecture with fewer awakenings during the night and almost no sleep during the day. Sleep loss increased inactivity, decreased play and alert behaviors, while increased time spent eating during the day. Males appeared to be more affected by sleep fragmentation than females. Different age groups also experienced different effects of sleep loss. Overall, dogs appear to compensate for the lack of sleep during the night by remaining inactive during the day. With further investigations, the relationship between sleep loss and behavior has the potential to be used as a measure of animal welfare.

The Effect of Sleep Deprivation and Subsequent Recovery Period on the Synaptic Proteome of Rat Cerebral Cortex

Sleep deprivation (SD) is commonplace in the modern way of life and has a substantial social, medical, and human cost. Sleep deprivation induces cognitive impairment such as loss of executive attention, working memory decline, poor emotion regulation, increased reaction times, and higher cognitive functions are particularly vulnerable to sleep loss. Furthermore, SD is associated with obesity, diabetes, cardiovascular diseases, cancer, and a vast majority of psychiatric and neurodegenerative disorders are accompanied by sleep disturbances. Despite the widespread scientific interest in the effect of sleep loss on synaptic function, there is a lack of investigation focusing on synaptic transmission on the proteome level. In the present study, we report the effects of SD and recovery period (RP) on the cortical synaptic proteome in rats. Synaptosomes were isolated after 8 h of SD performed by gentle handling and after 16 h of RP. The purity of synaptosome fraction was validated with western blot and electron microscopy, and the protein abundance alterations were analyzed by mass spectrometry. We observed that SD and RP have a wide impact on neurotransmitter-related proteins at both the presynaptic and postsynaptic membranes. The abundance of synaptic proteins has changed to a greater extent in consequence of SD than during RP: we identified 78 proteins with altered abundance after SD and 39 proteins after the course of RP. Levels of most of the altered proteins were upregulated during SD, while RP showed the opposite tendency, and three proteins (Gabbr1, Anks1b, and Decr1) showed abundance changes with opposite direction after SD and RP. The functional cluster analysis revealed that a majority of the altered proteins is related to signal transduction and regulation, synaptic transmission and synaptic assembly, protein and ion transport, and lipid and fatty acid metabolism, while the interaction network analysis revealed several connections between the significantly altered proteins and the molecular processes of synaptic plasticity or sleep. Our proteomic data implies suppression of SNARE-mediated synaptic vesicle exocytosis and impaired endocytic processes after sleep deprivation. Both SD and RP altered GABA neurotransmission and affected protein synthesis, several regulatory processes and signaling pathways, energy homeostatic processes, and metabolic pathways.

Prospective longitudinal study of ‘Sleepless in Lockdown’: unpacking differences in sleep loss during the coronavirus pandemic in the UK

ObjectivesCOVID-19 is having a disproportionate impact on Black, Asian and minority ethnic (BAME) groups and women. Concern over direct and indirect effects may also impact on sleep. We explore the levels and social determinants of self-reported sleep loss among the UK population during the pandemic, focusing on ethnic and gender disparities.SettingThis prospective longitudinal study analysed data from seven waves of the Understanding Society: COVID-19 Study collected from April 2020 to January 2021 linked to prepandemic data from the 2019 mainstage interviews, providing baseline information about the respondents prior to the pandemic.ParticipantsThe analytical sample included 8163 respondents aged 16 and above who took part in all seven waves with full information on sleep loss, defined as experiencing ‘rather more’ or ‘much more’ than usual sleep loss due to worry, providing 57 141 observations.Primary outcome measuresSelf-reported sleep loss. Mixed-effects regression models were fitted to consider within-individual and between-individual differences.ResultsWomen were more likely to report sleep loss than men (OR 2.1, 95% CI 1.9 to 2.4) over the 10-month period. Being female, having young children, perceived financial difficulties and COVID-19 symptoms were all predictive of sleep loss. Once these covariates were controlled for, the bivariate relationship between ethnicity and sleep loss (1.4, 95% CI 1.6 to 2.4) was reversed (0.7, 95% CI 0.5 to 0.8). Moreover, the strength of the association between gender and ethnicity and the risk of sleep loss varied over time, being weaker among women in July (0.6, 95% CI 0.5 to 0.7), September (0.7, 95% CI 0.6 to 0.8), November (0.8, 95% CI 0.7 to 1.0) and January 2021 (0.8, 95% CI 0.7 to 0.9) compared with April 2020, but positively stronger among BAME individuals in May (1.4, 95% CI 1.0 to 2.1), weaker only in September (0.7, 95% CI 0.5 to 1.0).ConclusionsThe pandemic has widened sleep deprivation disparities, with women with young children, COVID-19 infection and BAME individuals experiencing sleep loss, which may adversely affect their mental and physical health.

Can People Sleep Too Much? Effects of Extended Sleep Opportunity on Sleep Duration and Timing

Many people are concerned about whether they are getting “enough” sleep, and if they can “sleep too much.” These concerns can be approached scientifically using experiments probing long-term (i.e., multi-night) sleep homeostatic processes, since homeostatic processes move the system toward its physiological setpoint (i.e., between “not enough” and “too much”). We analyzed sleep data from two human studies with sleep opportunities much longer than people usually stay in bed (i.e., conditions in which sleep homeostatic responses could be documented): sleep opportunities were 14–16 h per day for 3–28 days. Across the nights of the extended sleep opportunities, total sleep duration, Rapid Eye Movement (REM) sleep duration and non-REM sleep durations decreased and sleep latency increased. Multiple nights were required to reach approximately steady-state values. These results suggest a multi-day homeostatic sleep process responding to self-selected insufficient sleep duration prior to the study. Once steady state-values were reached, there were large night-to-night variations in total sleep time and other sleep metrics. Our results therefore answer these concerns about sleep amount and are important for understanding the basic physiology of sleep and for two sleep-related topics: (i) the inter-individual and intra-individual variability are relevant to understanding “normal” sleep patterns and for people with insomnia and (ii) the multiple nights of sleep required for recovery from insufficient sleep from self-selected sleep loss is important for public health and other efforts for reducing the adverse effects of sleep loss on multiple areas of physiology.

Sleep markers in psychiatry: do insomnia and disturbed sleep play as markers of disrupted neuroplasticity in mood disorders? A proposed model

Introduction: Since insomnia and disturbed sleep may affect neuroplasticity, we aimed at reviewing their potential role as markers of disrupted neuroplasticity involved in mood disorders. Method: We performed a systematic review, according to PRIMA, on PubMed, PsycINFO and Embase electronic databases for literature regarding mood disorders, insomnia, sleep loss/deprivation in relation to different pathways involved in the impairment of neuroplasticity in mood disorders such as 1] alterations in neurodevelopment 2] activation of the stress system 3] neuroinflammation 4] neurodegeneration/neuroprogression, 4] deficit in neuroprotection. Results: Sixty-five articles were analyzed and a narrative/ theoretical review was conducted. Studies showed that insomnia, sleep loss and sleep deprivation might impair brain plasticity of those areas involved in mood regulation throughout different pathways. Insomnia and disrupted sleep may act as neurobiological stressors that by over-activating the stress and inflammatory systems may affect neural plasticity causing neuronal damage. In addition, disturbed sleep may favor a deficit in neuroprotection hence contributing to impaired neuroplasticity. Conclusions: Insomnia and disturbed sleep may play a role as markers of alteration in brain plasticity in mood disorders. Assessing and targeting insomnia in the clinical practice may potentially play a neuroprotective role, contributing to “repairing” alterations in neuroplasticity or to the functional recovery of those areas involved in mood and emotion regulation.

Cortisol and C-Reactive Protein Vary During Sleep Loss and Recovery but Are Not Markers of Neurobehavioral Resilience

Cortisol and C-reactive protein (CRP) typically change during total sleep deprivation (TSD) and psychological stress; however, it remains unknown whether these biological markers can differentiate robust individual differences in neurobehavioral performance and self-rated sleepiness resulting from these stressors. Additionally, little is known about cortisol and CRP recovery after TSD. In our study, 32 healthy adults (ages 27–53; mean ± SD, 35.1 ± 7.1 years; 14 females) participated in a highly controlled 5-day experiment in the Human Exploration Research Analog (HERA), a high-fidelity National Aeronautics and Space Administration (NASA) space analog isolation facility, consisting of two baseline nights, 39 h TSD, and two recovery nights. Psychological stress was induced by a modified Trier Social Stress Test (TSST) on the afternoon of TSD. Salivary cortisol and plasma CRP were obtained at six time points, before (pre-study), during [baseline, the morning of TSD (TSD AM), the afternoon of TSD (TSD PM), and recovery], and after (post-study) the experiment. A neurobehavioral test battery, including measures of behavioral attention and cognitive throughput, and a self-report measure of sleepiness, was administered 11 times. Resilient and vulnerable groups were defined by a median split on the average TSD performance or sleepiness score. Low and high pre-study cortisol and CRP were defined by a median split on respective values at pre-study. Cortisol and CRP both changed significantly across the study, with cortisol, but not CRP, increasing during TSD. During recovery, cortisol levels did not return to pre-TSD levels, whereas CRP levels did not differ from baseline. When sex was added as a between-subject factor, the time × sex interaction was significant for cortisol. Resilient and vulnerable groups did not differ in cortisol and CRP, and low and high pre-study cortisol/CRP groups did not differ on performance tasks or self-reported sleepiness. Thus, both cortisol and CRP reliably changed in a normal, healthy population as a result of sleep loss; however, cortisol and CRP were not markers of neurobehavioral resilience to TSD and stress in this study.

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

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