Impact of Sleep Deprivation and Subsequent Recovery Sleep on Cortisol in Unmedicated Depressed Patients

Abstract Background Sleep is critical for maintaining homeostasis in bodily and neurobehavioral functions. This homeostasis can be disturbed by sleep interruption and restored to normal by subsequent recovery sleep. Most research regarding recovery sleep (RS) effects has been conducted in specialized sleep laboratories, whereas small, less-well equipped research units may lack the possibilities to run studies in this area. Hence, the aims of the present study were to develop and validate an experimental protocol, which allows a thorough assessment of at-home recovery sleep after sleep deprivation. Methods The experimental protocol, comprising one night of baseline sleep (BL) at home, one night of monitored total sleep deprivation and a subsequent recovery night at home, was tested in a sample of 30 healthy participants. Subjects’ fatigue and alertness were assessed prior to and after each night. Sleep at home (BL, RS) was objectively assessed using portable polysomnography. To check whether our at-home sleep assessments yielded results that are comparable to those conducted in sleep laboratories, we compared the sleep data assessed in our study with sleep data assessed in laboratory studies. Results Sleep parameters assessed during RS exhibited changes as expected (prolonged total sleep time, better sleep efficiency, slow wave sleep rebound). Sleep parameters of BL and RS were in line with parameters assessed in previous studies examining sleep in a laboratory setting. Fatigue normalized after one night of RS; alertness partly recovered. Conclusions Our results suggest a successful implementation of our new experimental protocol, emphasizing it as a useful tool for future studies on RS outside of well-equipped sleep laboratories.

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Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽

10.1093/sleep/zsaa224 ◽

2020 ◽

Author(s):

Erika M Yamazaki ◽

Caroline A Antler ◽

Charlotte R Lasek ◽

Namni Goel

Keyword(s):

Sleep Deprivation ◽

Response Speed ◽

Sleep Loss ◽

Sleep Restriction ◽

Total Sleep Deprivation ◽

Psychomotor Vigilance Test ◽

Recovery Sleep ◽

Time In Bed ◽

Neurobehavioral Deficits ◽

Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

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Effects of transcranial direct current stimulation on performance and recovery sleep during acute sleep deprivation: a pilot study

Sleep Medicine ◽

10.1016/j.sleep.2021.01.014 ◽

2021 ◽

Vol 79 ◽

pp. 124-133

Author(s):

Jin-xiang Cheng ◽

Xianchao Zhao ◽

Jian Qiu ◽

Yingcong Jiang ◽

Jiafeng Ren ◽

...

Keyword(s):

Pilot Study ◽

Sleep Deprivation ◽

Direct Current ◽

Transcranial Direct Current Stimulation ◽

Direct Current Stimulation ◽

Recovery Sleep ◽

Acute Sleep Deprivation

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137 Recovery Dynamics in a Biomathematical Model of Fatigue

SLEEP ◽

10.1093/sleep/zsab072.136 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A56-A56

Author(s):

Mark McCauley ◽

Peter McCauley ◽

Hans Van Dongen

Keyword(s):

Sleep Deprivation ◽

Goodness Of Fit ◽

Sleep Loss ◽

Sleep Restriction ◽

Commercial Aviation ◽

Circadian Misalignment ◽

Total Sleep Deprivation ◽

Homeostatic Process ◽

Recovery Sleep

Abstract Introduction In commercial aviation and other operational settings where biomathematical models of fatigue are used for fatigue risk management, accurate prediction of recovery during rest periods following duty periods with sleep loss and/or circadian misalignment is critical. The recuperative potential of recovery sleep is influenced by a variety of factors, including long-term, allostatic effects of prior sleep/wake history. For example, recovery tends to be slower after sustained sleep restriction versus acute total sleep deprivation. Capturing such dynamics has proven to be challenging. Methods Here we focus on the dynamic biomathematical model of McCauley et al. (2013). In addition to a circadian process, this model features differential equations for sleep/wake regulation including a short-term sleep homeostatic process capturing change in the order of hours/days and a long-term allostatic process capturing change in the order of days/weeks. The allostatic process modulates the dynamics of the homeostatic process by shifting its equilibrium setpoint, which addresses recently observed phenomena such as reduced vulnerability to sleep loss after banking sleep. It also differentiates the build-up and recovery rates of fatigue under conditions of chronic sleep restriction versus acute total sleep deprivation; nonetheless, it does not accurately predict the disproportionately rapid recovery seen after total sleep deprivation. To improve the model, we hypothesized that the homeostatic process may also modulate the allostatic process, with the magnitude of this effect scaling as a function of time awake. Results To test our hypothesis, we added a parameter to the model to capture modulation by the homeostatic process of the allostatic process build-up during wakefulness and dissipation during sleep. Parameter estimation using previously published laboratory datasets of fatigue showed this parameter as significantly different from zero (p<0.05) and yielding a 10%–20% improvement in goodness-of-fit for recovery without adversely affecting goodness-of-fit for pre-recovery days. Conclusion Inclusion of a modulation effect of the allostatic process by the homeostatic process improved prediction accuracy in a variety of sleep loss and circadian misalignment scenarios. In addition to operational relevance for duty/rest scheduling, this finding has implications for understanding mechanisms underlying the homeostatic and allostatic processes of sleep/wake regulation. Support (if any) Federal Express Corporation

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108 Attentional Control Deficits during Total Sleep Deprivation: Independence from Reduced Vigilant Attention

SLEEP ◽

10.1093/sleep/zsab072.107 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A44-A45

Author(s):

Darian Lawrence-Sidebottom ◽

John Hinson ◽

Paul Whitney ◽

Kimberly Honn ◽

Hans Van Dongen

Keyword(s):

Sleep Deprivation ◽

Attentional Control ◽

Phase 1 ◽

Principal Component ◽

Relative Accuracy ◽

Target Pair ◽

Continuous Performance Task ◽

Total Sleep Deprivation ◽

Recovery Sleep ◽

Variance Explained

Abstract Introduction Total sleep deprivation (TSD) has been shown to impair performance on a two-phase attentional control task, the AX-type continuous performance task with switch (AX-CPTs). Here we investigate whether the observed AX-CPTs impairments are a downstream consequence of TSD-induced non-specific effects (e.g., reduced vigilant attention) or reflect a distinct impact on attentional control. Methods N=55 healthy adults (aged 26.0±0.7y; 32 women) participated in a 4-day laboratory study with 10h baseline sleep (22:00-08:00) followed by 38h TSD and then 10h recovery sleep. At baseline (09:00 day 2) and after 25h and 30h TSD (09:00 and 14:00 day 3), subjects were tested on a 10min psychomotor vigilance test (PVT), an assay of vigilant attention, and on the AX-CPTs. The AX-CPTs required subjects to differentiate designated target from non-target cue-probe pairs. In phase 1, target trials occurred frequently, which promoted prepotent anticipatory responses; in phase 2, the target pair was switched. Accuracy of responses to various different AX-CPTs trial types was expressed relative to accuracy on phase 1 neutral (non-target cue and probe) trials, which should capture non-specific impairments on the task. For all three test sessions, these relative accuracy measures, along with accuracy on phase 1 neutral trials and lapses (RT>500ms) on the PVT, were subjected to principal component analysis (PCA). Results The PCA revealed three statistically independent factors. Following varimax rotation, factor 1 (36.3% variance explained) and factor 3 (14.8% variance explained) each had high loadings for relative accuracy on multiple AX-CPTs trial types from phases 1 and 2; whereas factor 2 (17.9% variance explained) had high loadings for accuracy on phase 1 neutral trials, relative accuracy on phase 1 target trials, and PVT lapses. Conclusion These results indicate a statistical separation between AX-CPTs phase 1 neutral trials and phase 1 target trials, in conjunction with PVT lapses, versus the various other AX-CPTs trial types. This suggests a dissociation between TSD-induced, non-specific impairments on the task—potentially related to reduced vigilant attention—and TSD-induced specific impairments related to attentional control. Thus, TSD-induced deficits in attentional control are unlikely to be a downstream consequence of non-specific impairments. Support (if any) CDMRP grant W81XWH-16-1-0319

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Sleep after arousal from hibernation is not homeostatically regulated

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.2.r522 ◽

1999 ◽

Vol 276 (2) ◽

pp. R522-R529 ◽

Cited By ~ 10

Author(s):

Jennie E. Larkin ◽

H. Craig Heller

Keyword(s):

Sleep Deprivation ◽

Brain Function ◽

Extended Period ◽

Nrem Sleep ◽

Wave Activity ◽

Ground Squirrels ◽

Recovery Sleep ◽

Sleep Homeostasis ◽

Homeostatic Response ◽

Periodic Arousals

Electroencephalographic slow-wave activity (SWA) in non-rapid eye movement (NREM) sleep is directly related to prior sleep/wake history, with high levels of SWA following extended periods of wake. Therefore, SWA has been thought to reflect the level of accumulated sleep need. The discovery that euthermic intervals between hibernation bouts are spent primarily in sleep and that this sleep is characterized by high and monotonically declining SWA has led to speculation that sleep homeostasis may play a fundamental role in the regulation of the timing of bouts of hibernation and periodic arousals to euthermia. It was proposed that because the SWA profile seen after arousal from hibernation is strikingly similar to what is seen in nonhibernating mammals after extended periods of wakefulness, that hibernating mammals may arouse from hibernation with significant accumulated sleep need. This sleep need may accumulate during hibernation because the low brain temperatures during hibernation may not be compatible with sleep restorative processes. In the present study, golden-mantled ground squirrels were sleep deprived during the first 4 h of interbout euthermia by injection of caffeine (20 mg/kg ip). We predicted that if the SWA peaks after bouts of hibernation reflected a homeostatic response to an accumulated sleep need, sleep deprivation should simply have displaced and possibly augmented the SWA to subsequent recovery sleep. Instead we found that after caffeine-induced sleep deprivation of animals just aroused from hibernation, the anticipated high SWA typical of recovery sleep did not occur. Similar results were found in a study that induced sleep deprivation by gentle handling (19). These findings indicate that the SWA peak immediately after hibernation does not represent homeostatic regulation of NREM sleep, as it normally does after prolonged wakefulness during euthermia, but instead may reflect some other neurological process in the recovery of brain function from an extended period at low temperature.

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The Link Between Sleep, Stress and BDNF

European Psychiatry ◽

10.1016/j.eurpsy.2017.02.132 ◽

2017 ◽

Vol 41 (S1) ◽

pp. S282-S282 ◽

Cited By ~ 1

Author(s):

A. Eckert ◽

S. Karen ◽

J. Beck ◽

S. Brand ◽

U. Hemmeter ◽

...

Keyword(s):

Sleep Deprivation ◽

Serum Levels ◽

Bdnf Expression ◽

Depressed Patients ◽

Level Increase ◽

Stress Experience ◽

Partial Sleep Deprivation ◽

Competing Interest ◽

Fast Increase ◽

Serum Bdnf

The protein brain derived neurotrophic factor (BDNF) is a major contributor to neuronal plasticity. There is numerous evidence that BDNF expression is decreased by experiencing psychological stress and that accordingly a lack of neurotrophic support causes depression. The use of serum BDNF concentration as a potential indicator of brain alteration is justified through extensive evidence. Recently, we reported, for the first time, a relationship between BDNF and insomnia, since we could show that reduced levels of serum BDNF are correlated with sleep impairment in control subjects, while partial sleep deprivation was able to induce a fast increase in serum BDNF levels in depressed patients. Using a bi-directional stress model as an explanation approach, we propose the hypothesis that chronic stress might induce a deregulation of the HPA system leading in the long term to sleep disturbance and decreased BDNF levels, whereas acute sleep deprivation, can be used as therapeutical intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial sleep deprivation (PSD) induced a very fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Moreover, we revealed that stress experience and subjective sleep perception interact with each other and affect serum BDNF levels. We identified sleep as a mediator of the association between stress experience and serum BDNF levels.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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