Examining the Effects of Sleep Deprivation on Workplace Deviance: A Self-Regulatory Perspective

The causes of workplace deviance are of increasing interest to organizations. We integrate psychological and neurocognitive perspectives to examine the effects of sleep deprivation on workplace deviance. Utilizing self-regulatory resource theories, we argue that sleep deprivation decreases individuals’ self-control while increasing hostility, resulting in increased workplace deviance. We test our hypotheses using two samples: one comprised of nurses from a large medical center and another comprised of undergraduate students participating in a lab study. Results from both samples largely converge in supporting our hypotheses.

This research paper examines the effect of sleep deprivation on workplace deviance through selfregulatory mechanism.The self-regulatory mechanism includes state hostility and self-control.Sleep deprivation decreases individual's self-control while increasing state hostility leads to increased workplace deviance.The sample has been taken from medical residents from 6 hospitals in Karachi, Pakistan.Findings suggest that self-control does not mediate the relation between sleep deprivation and workplace deviance but state hostility fully mediates the relationship between sleep deprivation and workplace deviance.

To examine whether monetary incentives attenuate the negative effects of sleep deprivation on cognitive performance in a flanker task that requires higher-level cognitive-control processes, including error monitoring. Twenty-four healthy adults aged 18 to 23 years were randomly divided into 2 subject groups: one received and the other did not receive monetary incentives for performance accuracy. Both subject groups performed a flanker task and underwent electroencephalographic recordings for event-related brain potentials after normal sleep and after 1 night of total sleep deprivation in a within-subject, counterbalanced, repeated-measures study design. Monetary incentives significantly enhanced the response accuracy and reaction time variability under both normal sleep and sleep-deprived conditions, and they reduced the effects of sleep deprivation on the subjective effort level, the amplitude of the error-related negativity (an error-related event-related potential component), and the latency of the P300 (an event-related potential variable related to attention processes). However, monetary incentives could not attenuate the effects of sleep deprivation on any measures of behavior performance, such as the response accuracy, reaction time variability, or posterror accuracy adjustments; nor could they reduce the effects of sleep deprivation on the amplitude of the Pe, another error-related event-related potential component. This study shows that motivation incentives selectively reduce the effects of total sleep deprivation on some brain activities, but they cannot attenuate the effects of sleep deprivation on performance decrements in tasks that require high-level cognitive-control processes. Thus, monetary incentives and sleep deprivation may act through both common and different mechanisms to affect cognitive performance.

The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30–36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.

Introduction This study was conducted to determine how sleep deprivation affects headache perception and brain structure in an animal model of headache. Methods The effect of sleep deprivation on mechanical pain threshold was assessed in two groups of animals: (i) NSD-C group and (ii) SD group. The VFMF thresholds were assessed every day during 96 hours of sleep deprivation. After 96 hours sleep deprivation, the brain of each groups were analyzed with immunohistochemistry staining. The effect of sleep deprivation in supradural capsicin infusion were assessed in two groups. The VFMF threshold was performed during sleep deprivation and 4 weeks of recovery phase. Results 1) The effect of sleep deprivation on mechanical pain threshold. In comparison between SD and NSD-C group, the significant difference appeared after 1 day of sleep deprivation and lasted 4 days. 2) The effect of sleep deprivation on FOS reactivity. In hyptothalamus, the number of Fos-positive cells in PoHT increased significantly in SD group compared NSD-C group. In PAG, the number of Fos-positive cells in VLPAG increased significantly in SD group compared NSD-C group. The number of Fos-positive cells of supf C in TCC increased significantly in SD group compared NSD-C group. 3) The effect of sleep deprivation on mechanical pain threshold in supradural capsicin infusion. SD-Capsicin showed the tendency of lower VFMF threshold compared to NSD-Capsicin, which reach to statistical significant 3rd days of capsicin infusion period. During the recovery phase, the reduced VFMF threshold of NSD-Capsicin group was persisted 1 week after sleep deprivation and returned to baseline thereafter. In SD-Capsicin group, the reduced VFMF threshold was persisted 3 week after sleep deprivation. Conclusion In this study, pain lasted for 1 week after 4 days of continuous infusion of capsicin without sleep deprivation, but lasted for more than 3 weeks when combined with sleep deprivation, confirming the possibility that sleep deprivation contributes to the chronicity of headache. The chronicity and persistence of headache is associated with the centralization of pain. The findings of this study that sleep deprivation results in changes in TNC activity, which plays an important role in centralization, support this possibility. Support (if any)

Sleep Deprivation and Emotion Recognition

The treatment of geriatric depression is complicated by a variable and delayed response to antidepressant treatment. The present study was undertaken to test the hypothesis that combined total sleep deprivation and paroxetine treatment would produce a persistent reduction in glucose metabolism in the anterior cingulate cortex similar to that reported after long-term antidepressant treatment. Six elderly depressed patients who met the DSM-IV criteria for major depressive disorder and six age-matched comparison subjects underwent serial positron emission tomography (PET) studies at baseline, after total sleep deprivation, after recovery sleep (after the initial paroxetine dose), and after 2 weeks of paroxetine treatment (patients only). The PET data were analyzed by using statistical parametric mapping methods. The patients' scores on a 13-item version of the Hamilton Depression Rating Scale were decreased after total sleep deprivation, after recovery sleep, and after 2 weeks of treatment. The Hamilton depression scores of the comparison subjects were not significantly altered. In the patients, the greatest reductions in normalized, relative glucose metabolism after sleep deprivation were observed in the anterior cingulate cortex (Brodmann area 24), and they persisted after recovery sleep and antidepressant treatment. The comparison subjects demonstrated increased metabolism in these areas. Improvement in the patients' depressive symptoms was accompanied by reduced glucose metabolism in the right anterior cingulate cortex and right medial frontal cortex. These preliminary data indicate that in elderly depressed patients, total sleep deprivation may accelerate the clinical and glucose metabolic response to antidepressant treatment.

Background: Extensive research has been done to demystify the effects of sleep deprivation on cognitive functions, memory, and reasoning ability. However, there is a lacuna in regard to the effects on autonomic function and perceived stress as well as its modulation through yogic relaxation. Healthcare professionals often work at night, and the effect of acute overnight sleep deprivation on their performance is crucial. Aims and Objectives: The present study was undertaken to study the effects of overnight sleep deprivation on autonomic function and perceived stress in health-care professionals and to determine its modulation through yogic relaxation (Shavasana). Materials and Methods: A total of 35 healthcare professionals, aged between 20 and 25 years, were recruited from emergency services wing (casualty) of MGMC and RI, Puducherry, and taught yogic relaxation. Heart rate (HR), blood pressure (BP), and HR variability (HRV) were recorded and Cohen’s perceived stress scale (PSS) administered before the commencement of day duty. Parameters were again recorded after overnight sleep deprivation due to night shift work and then after they practiced yogic relaxation (Shavasana). As data passed normality testing, Student’s paired t-test was used to compare the changes after sleep deprivation and then after yogic relaxation. Results: Overnight sleep deprivation resulted in statistically significant (P < 0.05) increases in systolic BP (SBP), low frequency (LF), LF/high frequency (HF), diastolic BP (DBP), PSS, and mean HR. This was coupled with significant decreases in mean RR, SDNN, pNN50, HF, and RMSSD. Following yogic relaxation, these changes were reversed, and significant decreases were witnessed in LF, LF/ HF, SBP, mean HR, DBP, and PSS with significant increases in mean RR, pNN50, HF, RMSSD, and SDNN. Conclusion: The findings of our study reiterate the negative effects of sleep deprivation on cardiac autonomic status. Such deleterious effects may be partially reversed by practicing yogic relaxation (Shavasana). Such conscious relaxation may be able to help correct imbalance of autonomic nervous system by enhancing parasympathetic tone and reducing sympathetic overactivity.

Drawing on the self-regulation perspective, we propose and test a two-stage moderated mediation model that explains the mechanism as well as individual and contextual boundaries of the relationship...

Sleep is a necessary staple in our everyday lives but with advancements in society and an increase in day to day commitments it feels as though there is not enough time in the day. One of the first things to be forsaken in the hopes of maintaining a work schedule or routine is sleep. While the lack of sleep is disproportionate in most demographics, in university students in particular, a lack of sleep is a common, consistent, and necessary plague. Students can be under the impression that the effects of sleep deprivation have mostly long-term repercussions; however, prior literature has indicated that sleep deprivation impacts not just long-term consolidation but also significantly affects memory in the short-term, specifically the working memory (Xie et al. 2019; Chee et al., 2006). In this investigation, we seek to understand the effects that acute sleep deprivation has on the working memory capacity of individuals using a 2-back spatial test. A sample of convenience of upper-class undergraduate students was chosen and the participants were asked to take a specific 2-back spatial test - twice on a day that they subjectively felt as having a regular sleep schedule and twice on a day that they subjectively felt as having sleep deprivation. The team predicted that working memory 2-back task scores will be adversely affected by sleep deprivation. While there was a statistically significant difference in the working memory scores on the full sample level, this was not reflected on the individual level. This indicates that the effects of sleep deprivation are not generalizable to a full population and that they must be reviewed on a case-by-case basis. Furthermore, since greater variation was observed in the sleep deprived scores in all individuals, it implies that sleep deprivation may indirectly affect the consistency of working memory by affecting attention span and concentration.

Sleep deprivation has been cited as a major factor that plays an important role in many incidents in the transportation sector. Sleep-deprived train drivers is a fairly common phenomenon in Indonesia, with local reports indicating a good percentage of train drivers who are sleep deprived prior to work. The present study was aimed at quantifying the effects of sleep deprivation on alertness and performance during prolonged simulated train driving. A total of 12 subjects participated in this study and were asked to sleep for approximately 2 h (sleep deprived) and 8 h (normal sleep) the night before the experimental day. The experiment consisted of driving a train simulator for 4 h on a monotonous route. Fatigue and sleepiness were assessed using Psychomotor Vigilance Task (PVT) and Sustained Attention Test (SAT), conducted before and after the driving simulation. Subjective levels of fatigue and sleepiness were determined using questionnaires, while driving performance was measured based on the number of speed-limit violations. Results of this study showed that two hours of sleep was characterized with an initial subjective fatigue and sleepiness measures that were up to two to three times greater than the normal sleep condition. This condition also resulted in poorer driving performance (75% increase in the number of speeding error). While the effects of sleep deprivations on the performance of train driving is probably obvious, the quantitative effects have not been addressed extensively in the literature. It is concluded in this study that the effects of excessive sleep deprivation on fatigue and sleepiness varies, depending on the measures used.

To quantitatively describe the effects of sleep loss, we used meta-analysis, a technique relatively new to the sleep research field, to mathematically summarize data from 19 original research studies. Results of our analysis of 143 study coefficients and a total sample size of 1.932 suggest that overall sleep deprivation strongly impairs human functioning. Moreover, we found that mood is more affected by sleep deprivation than either cognitive or motor performance and that partial sleep deprivation has a more profound effect on functioning than either long-term or short-term sleep deprivation. In general, these results indicate that the effects of sleep deprivation may be underestimated in some narrative reviews, particularly those concerning the effects of partial sleep deprivation.

Electroencephalographic methods were used to study the effects of total sleep deprivation on thermoregulatory measures of the fever response in pigeons (Columba livia): brain temperature, peripheral vasomotor reactions, thoracic muscle contractile activity, and the recovery of somatic functions and the time characteristics of waking and sleep in lipopolysaccharide (LPS)-induced endotoxemia. Sleep deprivation during the period in which the quantity of slow-wave sleep increased on administration of LPS induced decreases in the latent period of fever onset and in the duration of fever, along with more significant increases in brain temperature and the level of muscle contractile activity as compared with the effects of LPS alone. The period after sleep deprivation was characterized by more prolonged recovery of muscle contractile activity and the time characteristics of sleep and waking states, along with more prolonged compensatory "rebound" of slow-wave sleep as compared with the effects of sleep deprivation alone. Thus, sleep deprivation in endotoxemia led to decreases in the latent period of fever onset, exacerbation of fever, and increases in the latent period of recovery of physiological functions.

We studied the effects of sleep deprivation on executive functions using a task battery which included a modified Sternberg task, a probed recall task, and a phonemic verbal fluency task. These tasks were selected because they allow dissociation of some important executive processes from non-executive components of cognition. Subjects were randomized to a total sleep deprivation condition or a control condition. Performance on the executive functions task battery was assessed at baseline, after 51 h of total sleep deprivation (or no sleep deprivation in the control group), and following 2 nights of recovery sleep, at fixed time of day (11:00). Performance was also measured repeatedly throughout the experiment on a control task battery, for which the effects of total sleep deprivation had been documented in previously published studies. Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Twenty-three healthy adults (age range 22-38 y; 11 women). Twelve subjects were randomized to the sleep deprivation condition; the others were controls. Performance on the control task battery was considerably degraded during sleep deprivation. Overall performance on the modified Sternberg task also showed impairment during sleep deprivation, as compared to baseline and recovery and compared to controls. However, two dissociated components of executive functioning on this task--working memory scanning efficiency and resistance to proactive interference--were maintained at levels equivalent to baseline. On the probed recall task, resistance to proactive interference was also preserved. Executive aspects of performance on the phonemic verbal fluency task showed improvement during sleep deprivation, as did overall performance on this task. Sleep deprivation affected distinct components of cognitive processing differentially. Dissociated non-executive components of cognition in executive functions tasks were degraded by sleep deprivation, as was control task performance. However, the executive functions of working memory scanning efficiency and resistance to proactive interference were not significantly affected by sleep deprivation, nor were dissociated executive processes of phonemic verbal fluency performance. These results challenge the prevailing view that executive functions are especially vulnerable to sleep loss. Our findings also question the idea that impairment due to sleep deprivation is generic to cognitive processes subserved by attention.

Sleep restriction and circadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance, and diabetes. The metabolic pathways involved in human sleep, however, have yet to be investigated with the use of a metabolomics approach. Here we have used untargeted and targeted liquid chromatography (LC)/MS metabolomics to examine the effect of acute sleep deprivation on plasma metabolite rhythms. Twelve healthy young male subjects remained in controlled laboratory conditions with respect to environmental light, sleep, meals, and posture during a 24-h wake/sleep cycle, followed by 24 h of wakefulness. Two-hourly plasma samples collected over the 48 h period were analyzed by LC/MS. Principal component analysis revealed a clear time of day variation with a significant cosine fit during the wake/sleep cycle and during 24 h of wakefulness in untargeted and targeted analysis. Of 171 metabolites quantified, daily rhythms were observed in the majority (n = 109), with 78 of these maintaining their rhythmicity during 24 h of wakefulness, most with reduced amplitude (n = 66). During sleep deprivation, 27 metabolites (tryptophan, serotonin, taurine, 8 acylcarnitines, 13 glycerophospholipids, and 3 sphingolipids) exhibited significantly increased levels compared with during sleep. The increased levels of serotonin, tryptophan, and taurine may explain the antidepressive effect of acute sleep deprivation and deserve further study. This report, to our knowledge the first of metabolic profiling during sleep and sleep deprivation and characterization of 24 h rhythms under these conditions, offers a novel view of human sleep/wake regulation.