Impact Of Sleep Deprivation Research Articles

The impact of sleep deprivation on the endocrine system of adolescents

The impact of sleep deprivation on the endocrine system of adolescents

Acute sleep deprivation induces synaptic remodelling at the soleus muscle neuromuscular junction in rats.

Sleep is important for cognitive and physical performance. Sleep deprivation not only affects neural functions but also results in muscular fatigue. A good night's sleep reverses these functional derangements caused by sleep deprivation. The role of sleep in brain function has been extensively studied. However, its role in neuromuscular junction or skeletal muscle morphology is sparsely addressed although skeletal muscle atonia and suspended thermoregulation during rapid eye movement sleep possibly provide a conducive environment for the muscle to rest and repair; somewhat similar to slow-wave sleep for synaptic downscaling. In the present study, we have investigated the effect of 24h sleep deprivation on the neuromuscular junction morphology and neurochemistry using electron microscopy and immunohistochemistry in the rat soleus muscle. Acute sleep deprivation altered synaptic ultra-structure viz. mitochondria, synaptic vesicle, synaptic proteins, basal lamina, and junctional folds needed for neuromuscular transmission. Further acute sleep deprivation showed the depletion of the neurotransmitter acetylcholine and the overactivity of its degrading enzyme acetylcholine esterase at the neuromuscular junction. The impact of sleep deprivation on synaptic homeostasis in the brain has been extensively reported recently. The present evidence from our studies shows new information on the role of sleep on neuromuscular junction homeostasis and its functioning.

Impact of Sleep Deprivation on Major Neuroinflammatory Signal Transduction Pathways

Impact of Sleep Deprivation on Major Neuroinflammatory Signal Transduction Pathways

Impact of sleep deprivation on attentional networks: disentangling orienting components

While it is well accepted that sleep deprivation (SD) negatively affects overall vigilance and performance, research on the extent to which SD affects discrete components of attention has produced inconsistent results.The present study aims at exploring the effects of SD on attentional components and their interactions using the revised attentional network test (ANT-R) which allows to examine the three attentional networks: alerting, orienting and executive control. Additionally, it allows the evaluation of subcomponents of orienting. The ANT-R was administered following two sleep conditions: Baseline (BL) – a regular night of uninterrupted sleep, and SD − 24 h of wakefulness. Our data show that SD selectively affects the three attentional networks. We have found a significant slowing down of executive control and a slight detriment of alerting. As far as orienting is concerned, the disengagement component was affected, while validity effect remained unaffected by SD. Our findings have relevant implications for intervention research, highlighting the importance of targeting specifically disengagement and executive control processes.

Quarreling After a Sleepless Night: Preliminary Evidence of the Impact of Sleep Deprivation on Interpersonal Conflict

Although poor sleep has been found to correlate with deteriorations in romantic relationships, its causal impact on interpersonal conflict has not previously been studied. Therefore, 30 couples were randomly assigned to either a single night of total sleep deprivation or a night of normal sleep to test the effects of sleep deprivation on couples’ conflict. After the experimental night, all participants discussed a topic of recurrent conflict for 15 min. We collected pre- and post-conflict measures of cortisol, self-reports of feelings, and satisfaction with the conflictual discussion. Multilevel analyses revealed higher cortisol levels during conflict and less positive affect prior to and after the conflict for sleep-deprived couples compared to couples in the control condition. These findings provide initial evidence for a causal negative impact of sleep deprivation on couples’ conflicts.

Sleep deprivation and memory: Meta-analytic reviews of studies on sleep deprivation before and after learning.

Research suggests that sleep deprivation both before and after encoding has a detrimental effect on memory for newly learned material. However, there is as yet no quantitative analyses of the size of these effects. We conducted two meta-analyses of studies published between 1970 and 2020 that investigated effects of total, acute sleep deprivation on memory (i.e., at least one full night of sleep deprivation): one for deprivation occurring before learning and one for deprivation occurring after learning. The impact of sleep deprivation after learning on memory was associated with Hedges’ g = 0.277, 95% CI [0.177, 0.377]. Whether testing took place immediately after deprivation or after recovery sleep moderated the effect, with significantly larger effects observed in immediate tests. Procedural memory tasks also showed significantly larger effects than declarative memory tasks. The impact of sleep deprivation before learning was associated with Hedges’ g = 0.621, 95% CI [0.473, 0.769]. Egger’s tests for funnel plot asymmetry suggested significant publication bias in both meta-analyses. Statistical power was very low in most of the analyzed studies. Highly powered, preregistered replications are needed to estimate the underlying effect sizes more precisely.

Cerebrospinal fluid egress to human parasagittal dura and the impact of sleep deprivation

Emerging evidence suggests that the glymphatic system and meningeal lymphatic vessels are instrumental for clearance of toxic metabolites from the brain. Animal and human studies suggest that glymphatic circulation is up-regulated during sleep. Meningeal lymphatic clearance may be more efficient in the wake state, as shown in rodents. We have previously shown clearance of cerebrospinal fluid directly from the subarachnoid space to the parasagittal dura, which harbors meningeal lymphatic vessels. Hence, assessing molecular clearance from parasagittal dura provides an opportunity to decipher the role of sleep/sleep deprivation in human lymphatic clearance function. In this study, we applied magnetic resonance imaging to explore whether sleep deprivation modifies molecular clearance from human parasagittal dura, utilizing an intrathecal magnetic resonance imaging contrast agent as tracer. We hypothesized that tracer enhancement in parasagittal dura would differ after sleep deprivation. One group of individuals (n = 7) underwent one night’s total sleep deprivation while a control group (n = 9) was allowed unrestricted sleep. There were no sleep restrictions after the 24-hour time point. After one night of sleep deprivation (at 24 h), we found neither evidence for altered tracer enrichment in the parasagittal dura, nor after a day of unrestricted sleep (at 48 h). The hypothesis of altered molecular egress to parasagittal dura after sleep deprivation was not supported by our data. Further studies are required to determine the role of sleep for molecular clearance from cerebrospinal fluid to meningeal lymphatic vessels in humans.

The Impact of Sleep Deprivation on Work Performance towards Night-shift Healthcare Workers: An Evidence-based Case Report

Background. Poor sleep and excessive fatigue among workers can reduce well-being and physical fitness. However, not many studies have mentioned how sleeping deprivation among night-shift healthcare workers impacted their work performance in multiple aspects.
 Method. We conducted an evidence-based case report (EBCR) of a night shift nurse who was worried about the impact of her sleep deprivation on her work performance in the future due to prior history of needle-stick injuries. We aimed to determine whether sleeping deprivation caused by regular night shifts leads to decreased work performance among night-shift healthcare workers by formulating a clinical question. Evidence was searched systematically using five major journal databases (Proquest, EBSCO-Host, PubMed, ScienceDirect, and Cochrane) and was assessed thoroughly using inclusion and exclusion criteria.
 Results. Eleven eligible studies were obtained with a medium level of evidence (III-IV), three systematic reviews with meta-analyses (SR-MA), three SR without MA, and five observational studies. All of them were analyzed and critically appraised using Oxford Evidence-Based Medicine and Joanna Briggs Institute tools. We found that reduced quantity and quality of sleep impacted all dimensions of work performance among healthcare professionals, be it in task performance (e.g., skill proficiency), contextual performance (e.g., communication skill and mental health issues), and patient and health worker safety (accident and medication error). It could also encourage counterproductive work behavior, such as absenteeism. Furthermore, sleep deprivation changes circadian rhythms, causing decreased information processing and affective recognition functions in some vital brain areas, ultimately affecting several work dimensions.
 Conclusion. In conclusion, stakeholders need to adjust proper shift scheduling for health care workers, practice sleep hygiene, maintain physical fitness, and consume nutritional food, positively correlated to health and productivity.

Sleep deprivation reduces the density of individual spine subtypes in a branch-specific fashion in CA1 neurons.

SummarySleep deprivation has a negative impact on hippocampus‐dependent memory, which is thought to depend on cellular plasticity. We previously found that 5 h of sleep deprivation robustly decreases dendritic spine density in the CA1 area of the hippocampus in adult male mice. However, recent work by others suggests that sleep deprivation increases the density of certain spine types on specific dendritic branches. Based on these recent findings and our previous work, we conducted a more in‐depth analysis of different spine types on branches 1, 2 and 5 of both apical and basal dendrites to assess whether 5 h of sleep deprivation may have previously unrecognized spine‐type and branch‐specific effects. This analysis shows no spine‐type specific changes on branch 1 and 2 of apical dendrites after sleep deprivation. In contrast, sleep deprivation decreases the number of mushroom and branched spines on branch 5. Likewise, sleep deprivation reduces thin, mushroom and filopodia spine density on branch 5 of the basal dendrites, without affecting spines on branch 1 and 2. Our findings indicate that sleep deprivation leads to local branch‐specific reduction in the density of individual spine types, and that local effects might not reflect the overall impact of sleep deprivation on CA1 structural plasticity. Moreover, our analysis underscores that focusing on a subset of dendritic branches may lead to potential misinterpretation of the overall impact of, in this case, sleep deprivation on structural plasticity.

Impact of Sleep Deprivation on Emotional Regulation and the Immune System of Healthcare Workers as a Risk Factor for COVID 19: Practical Recommendations From a Task Force of the Latin American Association of Sleep Psychology.

Healthcare workers who are on the front line of coronavirus disease 2019 (COVID-19) and are also undergoing shift schedules face long work hours with few pauses, experience desynchronization of their circadian rhythm, and an imbalance between work hours effort and reward in saving lives, resulting in an impact on work capacity, aggravated by the lack of personal protective equipment (PPE), few resources and precarious infrastructure, and fear of contracting the virus and contaminating family members. Some consequences are sleep deprivation, chronic insomnia, stress-related sleep disorders, and post-traumatic stress disorder. These sleep alterations critically affect mental health, precipitating or perpetuating anxiety, stress, and depression, resulting in the inability to regulate positive and negative emotions. Pre-existing sleep disorders are an important risk factor for the development and maintenance of PSTD when individuals are exposed to an important stressor such as a COVID-19 pandemic. At the same time, how an individual regulates the emotion associated with worries during daytime functioning impacts nighttime sleep, precipitating and perpetuating difficulties in sleeping. All of these changes in sleep and emotional regulation also alter the immune system. Sleep deprivation is commonly associated with chronic inflammatory diseases, due to the desynchronizations in circadian rhythms, causing possible psychophysiological disorders and impaired neuroimmune-endocrine homeostasis. From this perspective, we clarify in this article how sleep disorders affect the immune system and emotional regulation, explaining their phenomenological and neurobiological mechanisms, and discussing elements of cognitive and behavioral coping for health professionals to adopt and manage a healthier sleep pattern in the COVID-19 outbreak.

Re: Impact of Sleep Deprivation on the Hypothalamic-Pituitary-Gonadal Axis and Erectile Tissue.

No AccessJournal of UrologyUrological Survey1 Nov 2020Re: Impact of Sleep Deprivation on the Hypothalamic-Pituitary-Gonadal Axis and Erectile Tissue Sean P. ElliottMD Sean P. ElliottSean P. Elliott More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000001257.01AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Re: Impact of Sleep Deprivation on the Hypothalamic-Pituitary-Gonadal Axis and Erectile Tissue." The Journal of Urology, 204(5), pp. 1088–1089 © 2020 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 204Issue 5November 2020Page: 1088-1089 Advertisement Copyright & Permissions© 2020 by American Urological Association Education and Research, Inc.MetricsAuthor Information Sean P. Elliott More articles by this author Expand All Advertisement PDF DownloadLoading ...

The impact of sleep deprivation on sexual behaviors and FAAH expression in the prefrontal cortex of male rats

Sleep deprivation (SD) causes alterations in the function of the endocannabinoid (EC) system and also results in alteration in many behaviors such as increased anxiety, deteriorated alertness, memory deficits, as well as sexual behaviors. Controversial data about the effects of SD on sexual response are provided. Fatty acid amide hydrolase (FAAH), the enzymes involved in the degradation of the EC system play an important role in the function of the EC system. This study aimed to investigate the effect of REM SD (RSD) and total SD (TSD) on the sexual behaviors and FAAH expression in the prefrontal cortex (PFC) of male rats. RSD was carried out through the flower pot technique for 24 h and 48 h, and TSD also was induced by keeping awake the rats by gentle handling for 6 h. Immediately after RSD and TSD, sexual behaviors were recorded for 45 min. Sexual behaviors were reduced by both types of RSD and TSD. The deleterious effects of 24 h RSD were more severe compared with 6 h of TSD. Serum testosterone concentration was significantly higher after TSD but not RSD compared to the normal sleep (NS) group. FAAH expression in the PFC was significantly reduced after both RSD and TSD compared to the NS group. Given that the function of the EC system has been previously shown to change different behaviors such as sexual activity, our results could suggest that behavioral effects of both types of SD on sexual behavior may partially result from activation of this signaling pathway by the reduction of FAAH in the PFC.

The impact of sleep deprivation and alcohol on driving: a comparative study

BackgroundThere is concern about the detrimental effects of shift-workers’ increasing working hours particularly when driving sleep deprived. The approach to measuring the magnitude of driving impairment caused by sleep deprivation was by comparing it to alcohol. The study compared driving performance after 24-h of wakefulness to performance with a BrAC of just over 22 μg/100mls of breath which is equal to 50 mg of alcohol per 100mls of blood (Scottish drink-drive limit). The effectiveness of coffee as a countermeasure for driver fatigue and the association between subjective impairment and actual performance was also investigated.MethodsA study of 30 participants (11 male and 19 female; mean age 21) was conducted. Subjects were tested under three conditions: fully rested, sleep deprived, and alcohol intoxicated – BrAC mean [SD] 25.95 μg [2.78]. Under each condition, subjects were tested before and after coffee ingestion. This involved driving simulation (Lane Change Task and Reaction Test) and subjective Likert scales (Karolinska Sleepiness Scale and driver impairment scale). Outcome measures included lane tracking adaptive mean deviation, reaction time, and subjective sleepiness and impairment ratings.ResultsCompared to alcohol, sleep deprived mean reaction times were slower (2.86 s vs. 2.34 s) and lateral control of the vehicle was reduced (lane tracking adaptive mean deviation: 0.5 vs. 0.3). Coffee did not produce an improvement when sleep deprived, and instead, performance deteriorated. Females were less impaired following sleep deprivation than males. Following prolonged wakefulness, the correlation between subjective impairment and actual performance was significant.ConclusionsIt was concluded that sleep deprivation has a greater impact on driving performance than a BrAC of 22 μg/100mls of breath, as measured by driving simulation. Coffee is not an effective countermeasure for sleep deprived driving and drivers’ ability to judge this impairment is suggested to be limited.

Effects of acute sleep deprivation on H reflex and V wave.

The impact of sleep deprivation on muscular strength and power remains poorly understood. We aimed to determine the acute effects of 24hr of sleep deprivation on H-reflex and V-wave excitability. Fourteen healthy young adults (eight men, six women) were included. Participants visited the laboratory on two different occasions, without and with 24hr of sleep deprivation. In each session, participants were tested for maximal voluntary contraction (MVC) of the plantar flexors and dorsiflexors, soleus H- and M-recruitment curves, and evoked V wave, as well as tibialis anterior/soleus electromyographic co-activation. Twenty-four hours of sleep deprivation did not affect either plantarflexion MVC or soleus electromyographic normalized amplitude (p>.05). Moreover, H-reflex and V-wave peak-to-peak normalized amplitude did not change with sleep deprivation (p>.05). Conversely, we obtained a significant increase in antagonist/agonist level of co-activation during MVC post-sleep deprivation (6.2±5.2%, p<.01). In conclusion, we found that H-reflex and V-wave responses are well preserved after 24hr of sleep deprivation, revealing that descending neural drive and/or modulation in Ia afferent input remains largely unaffected under these circumstances. Yet, sleep deprivation affects motor control by exacerbating the magnitude of antagonist/agonist co-activation during forceful muscle contractions and this is novel.

Differential Impact of Sleep Deprivation and Circadian Timing on Reflexive Versus Inhibitory Control of Attention

In a visually stimulating environment with competing stimuli, we continually choose where to allocate attention, and what to ignore. Wake and circadian-dependent modulation of attentional control and resolution of conflict is poorly understood. Twenty-two participants (17males; 25.6 ± 5.6 years) completed ocular motor tasks throughout 40 hours of sleep deprivation under constant routine conditions. A prosaccade task required a reflexive saccade toward a stimulus (no conflict), while an antisaccade task required inhibiting a reflexive saccade to the peripheral stimulus, and looking in the mirror opposite instead (conflict resolution). Antisaccade inhibitory errors showed circadian modulation, being highest in the morning, progressively decreasing until melatonin onset, before returning to the prior morning’s peak throughout the biological night. This diurnal rhythm was blunted by sleep loss (>24 hours), with inhibitory control remaining impaired across the second biological day. For prosaccade, responses slowed down during the biological night. Taken together, we provide evidence for a circadian modulation of attentional bias: the morning being biased toward reflexive responding, and the evening toward higher inhibitory control. Our data show that sleep loss and circadian timing differentially impact attention, depending on whether a response conflict is present (antisaccade) or absent (prosaccade).

Impact of Sleep Deprivation on Respiratory Motor Output and Endurance. A Physiological Study.

Rationale: Sleep deprivation can alter endurance of skeletal muscles, but its impact on respiratory command is unknown.Objectives: We aimed to assess the effect of sleep deprivation on respiratory motor output and inspiratory endurance.Methods: Inspiratory endurance was investigated twice in random order, following a normal sleep night and a sleepless night. Healthy participants were asked to breathe as long as possible until task failure against a moderate inspiratory threshold constraint. Transdiaphragmatic pressure and diaphragm electrical activity were measured throughout the trial to assess pressure output of the diaphragm and overall respiratory motor output. Cortical contribution to respiratory motor output was assessed by measurement of preinspiratory motor potential amplitude and by cervical magnetic simulation.Measurements and Main Results: Twenty healthy male participants were studied. Time to task failure was significantly shorter after sleep deprivation than after normal sleep: (30 min [interquartile range [IQR], 17-41] vs. 60 min [IQR, 45-60], P = 0.002). At the beginning of the trial, preinspiratory motor potential amplitude was significantly lower in the sleep-deprivation condition (4.5 μV [IQR, 2.5-6.4] vs. 7.3 μV [IQR, 4.3-10.4], P = 0.02) and correlated significantly with the duration of the endurance trial. In the sleep-deprivation condition, preinspiratory motor potential amplitude, electrical activity of the diaphragm, pressure output of the diaphragm, and Vt decreased and the respiratory rate increased significantly from the beginning to the end of the trial. Such decreases did not occur in the normal-sleep condition.Conclusions: One night of sleep deprivation reduces respiratory motor output by altering its cortical component with subsequent reduction of inspiratory endurance by half. These results suggest that altered sleep triggers severe brain dysfunctions that could precipitate respiratory failure.

Impact of Sleep Deprivation and Caffeine in Medical Professionals

Impact of Sleep Deprivation and Caffeine in Medical Professionals

Impact of sleep deprivation and high-fat feeding on insulin sensitivity and beta cell function in dogs.

Insufficient sleep is increasingly recognised as a major risk factor for the development of obesity and diabetes, and short-term sleep loss in clinical studies leads to a reduction in insulin sensitivity. Sleep loss-induced metabolic impairments are clinically relevant, since reductions in insulin sensitivity after sleep loss are comparable to insulin sensitivity differences between healthy individuals and those with impaired glucose tolerance. However, the relative effects of sleep loss vs high-fat feeding in the same individual have not been assessed. In addition, to our knowledge no diurnal (active during the daytime) non-human mammalian model of sleep loss-induced metabolic impairment exists, which limits our ability to study links between sleep and metabolism. This study examined the effects of one night of total sleep deprivation on insulin sensitivity and beta cell function, as assessed by an IVGTT, before and after 9months of high-fat feeding in a canine model. One night of total sleep deprivation in lean dogs impaired insulin sensitivity to a similar degree as a chronic high-fat diet (HFD)(normal sleep: 4.95 ± 0.45mU-1l-1min-1; sleep deprivation: 3.14 ± 0.21mU-1l-1min-1; HFD: 3.74 ± 0.48mU-1l-1min-1; mean ± SEM). Hyperinsulinaemic compensation was induced by the chronic HFD, suggesting adequate beta cell response to high-fat feeding. In contrast, there was no beta cell compensation after one night of sleep deprivation, suggesting that there was metabolic dysregulation with acute sleep loss that, if sustained during chronic sleep loss, could contribute to the risk of type 2 diabetes. After chronic high-fat feeding, acute total sleep deprivation did not cause further impairments in insulin sensitivity (sleep deprivation + chronic HFD: 3.28mU-1l-1min-1). Our findings provide further evidence that sleep is important for metabolic health and establish a diurnal animal model of metabolic disruption during insufficient sleep.

The Impact of Sleep Deprivation on Patients’ Pain Level, Mood, and Overall Hospital Satisfaction

Objective: To identify the correlation between sleep deprivation and patient pain, mood, and satisfaction of stay.Design: Quasi-experimental, DescriptiveSetting: Hays Medical Center Acute Care UnitParticipants: Acute Care patients of Western Rural KansasMethods: During their hospital treatment, patients will be subcategorized into two groups. One group will have nighttime disturbances limited to three events per night. The other group will have no changes to their nighttime treatment. Patients will then receive surveys to collect data on pain level, mood, and satisfaction of hospital stay. They will receive these surveys on day one, day three, and the day of discharge.Results/Conclusion: Pending results and data collection.

Sleep deprivation of rats increases postsurgical expression and activity of L-type calcium channel in the dorsal root ganglion and slows recovery from postsurgical pain

Perioperative sleep disturbance is a risk factor for persistent pain after surgery. Clinical studies have shown that patients with insufficient sleep before and after surgery experience more intense and long-lasting postoperative pain. We hypothesize that sleep deprivation alters L-type calcium channels in the dorsal root ganglia (DRG), thus delaying the recovery from post-surgical pain. To verify this hypothesis, and to identify new predictors and therapeutic targets for persistent postoperative pain, we first established a model of postsurgical pain with perioperative sleep deprivation (SD) by administering hind paw plantar incision to sleep deprivation rats. Then we conducted behavioral tests, including tests with von Frey filaments and a laser heat test, to verify sensory pain, measured the expression of L-type calcium channels using western blotting and immunofluorescence of dorsal root ganglia (an important neural target for peripheral nociception), and examined the activity of L-type calcium channels and neuron excitability using electrophysiological measurements. We validated the findings by performing intraperitoneal injections of calcium channel blockers and microinjections of dorsal root ganglion cells with adeno-associated virus. We found that short-term sleep deprivation before and after surgery increased expression and activity of L-type calcium channels in the lumbar dorsal root ganglia, and delayed recovery from postsurgical pain. Blocking these channels reduced impact of sleep deprivation. We conclude that the increased expression and activity of L-type calcium channels is associated with the sleep deprivation-mediated prolongation of postoperative pain. L-type calcium channels are thus a potential target for management of postoperative pain.