137 Recovery Dynamics in a Biomathematical Model of Fatigue

SLEEP ◽  
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

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

SLEEP ◽  
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.

scholarly journals 0151 COMPARISON OF THE EFFECTS OF ACUTE TOTAL SLEEP DEPRIVATION, CHRONIC SLEEP RESTRICTION AND RECOVERY SLEEP ON POSITIVE AFFECT

SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A56-A57
Author(s):  
E Hennecke ◽  
D Lange ◽  
J Fronczek ◽  
A Bauer ◽  
D Aeschbach ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Positive Affect ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Recovery Sleep ◽  
Chronic Sleep

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

SLEEP ◽  
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

Hugin+ neurons provide a link between sleep homeostat and circadian clock neurons

2021 ◽  
Vol 118 (47) ◽  
pp. e2111183118
Author(s):  
Jessica E. Schwarz ◽  
Anna N. King ◽  
Cynthia T. Hsu ◽  
Annika F. Barber ◽  
Amita Sehgal
Keyword(s):  
Locomotor Activity ◽  
Sleep Deprivation ◽  
Circadian Clock ◽  
Sleep Loss ◽  
Daily Cycle ◽  
Shaped Body ◽  
Recovery Sleep ◽  
Sleep Homeostat ◽  
Central Clock ◽  
Homeostatic Mechanisms

Sleep is controlled by homeostatic mechanisms, which drive sleep after wakefulness, and a circadian clock, which confers the 24-h rhythm of sleep. These processes interact with each other to control the timing of sleep in a daily cycle as well as following sleep deprivation. However, the mechanisms by which they interact are poorly understood. We show here that hugin+ neurons, previously identified as neurons that function downstream of the clock to regulate rhythms of locomotor activity, are also targets of the sleep homeostat. Sleep deprivation decreases activity of hugin+ neurons, likely to suppress circadian-driven activity during recovery sleep, and ablation of hugin+ neurons promotes sleep increases generated by activation of the homeostatic sleep locus, the dorsal fan-shaped body (dFB). Also, mutations in peptides produced by the hugin+ locus increase recovery sleep following deprivation. Transsynaptic mapping reveals that hugin+ neurons feed back onto central clock neurons, which also show decreased activity upon sleep loss, in a Hugin peptide–dependent fashion. We propose that hugin+ neurons integrate circadian and sleep signals to modulate circadian circuitry and regulate the timing of sleep.

scholarly journals 0311 The Impairments in Emotional Perception Following Total Sleep Deprivation and the Restorative Effects of Napping and Time of Day

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A117-A117
Author(s):  
T J Cunningham ◽  
R M Bottary ◽  
E A Kensinger ◽  
R Stickgold
Keyword(s):  
Sleep Deprivation ◽  
Emotion Perception ◽  
Time Of Day ◽  
Error Rates ◽  
Emotional Intensity ◽  
Total Sleep Deprivation ◽  
Emotional Perception ◽  
Recovery Sleep ◽  
Socially Relevant ◽  
The Impact

Abstract Introduction The ability to perceive emotions is a socially-relevant skill critical for healthy interpersonal functioning, while deficits in this ability are associated with psychopathology. Total sleep deprivation (TSD) has been shown to have deleterious effects on emotion perception, yet the extent to which these impairments persist across the day with continued wakefulness, or if brief periods of recovery sleep can restore emotion perception abilities, remains unexplored. Methods Participants viewed slideshows of faces ranging in emotional expression and were asked to categorize (Happy, Sad, Angry, Neutral) and rate the emotional intensity (1-9) of each face at baseline (2100; Session 1), at 0900 (Session 2) following a night of sleep or TSD, and at 1400 (Session 3) following either continued wakefulness (wake group) or a 90-minute nap opportunity (nap group). Results Emotion categorization ability marginally improved from Session 1 to Session 2 following overnight sleep, however, no changes in emotion intensity ratings or vigilance were observed. TSD led to an increase in error rates during vigilance testing [t(46)=2.9, p=0.005] and impairment in emotion categorization ability [t(46)=5.5, p<0.001] from Session 1 to Session 2, although by Session 3 performance levels on both measures returned to baseline for all TSD participants. TSD also led to a decrease in emotional intensity ratings from Session 1 to Session 2, particularly for the highest tertile of emotional faces [6-9; t(46)=6.1, p<0.001]. These ratings remained suppressed at Session 3 in both the wake [t(25)=7.8, p<0.001] and nap [t(18)=3.1, p=0.006] groups. Conclusion These results indicate that time of day effects, with or without any additional benefit of a nap, can restore the impairments in vigilance and emotional categorization caused by TSD. The ability to discriminate levels of emotional intensity, however, is not restored by time of day or napping, suggesting that this ability is more sensitive to the impact of TSD. Support  

scholarly journals Free Recall of Word Lists under Total Sleep Deprivation and after Recovery Sleep

SLEEP ◽  
2012 ◽  
Vol 35 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Gislaine de Almeida Valverde Zanini ◽  
Sérgio Tufik ◽  
Monica Levy Andersen ◽  
Raquel Cristina Martins da Silva ◽  
Orlando Francisco Amodeo Bueno ◽  
...  
Keyword(s):  
Free Recall ◽  
Sleep Deprivation ◽  
Total Sleep Deprivation ◽  
Recovery Sleep ◽  
Word Lists

Amphetamine effects on recovery sleep following total sleep deprivation

1991 ◽  
Vol 6 (4) ◽  
pp. 319-323 ◽  
Author(s):  
D. M. Penetar ◽  
H. C. Sing ◽  
D. R. Thorne ◽  
M. L. Thomas ◽  
J. B. Fertig ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Total Sleep Deprivation ◽  
Recovery Sleep

scholarly journals 0265 Cortisol and C-Reactive Protein Fail to Predict Individual Differences in Neurobehavioral Performance Responses to Total Sleep Deprivation and Psychological Stress

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A101-A101
Author(s):  
N Goel ◽  
E M Yamazaki ◽  
L E MacMullen ◽  
A J Ecker
Keyword(s):  
Individual Differences ◽  
Sleep Deprivation ◽  
Psychological Stress ◽  
Salivary Cortisol ◽  
Time Of Day ◽  
C Reactive Protein ◽  
Total Sleep Deprivation ◽  
Time Points ◽  
Reactive Protein ◽  
Recovery Sleep

Abstract Introduction Individuals show marked differential vulnerability in neurobehavioral deficits from psychosocial stress and sleep deprivation. Although changes in salivary cortisol and C-reactive protein (CRP) typically occur across total sleep deprivation (TSD) and recovery sleep, whether these biological markers during fully rested conditions predict individual differences in cognitive performance during TSD and stress remains unknown. Methods Thirty-one healthy adults (ages 27–53; mean ± SD, 35.4 ± 7.1y; 14 females) participated in a five-day experiment consisting of two 8h time-in-bed (TIB) baseline nights, followed by 39h TSD, and two 8h-10h TIB recovery nights. A modified Trier Social Stress Test (TSST) was conducted on the day of TSD to induce psychological stress. Salivary cortisol and CRP from blood were obtained at six time points during the study (pre-study, baseline, during TSD, during TSD after the TSST, after recovery, and post-study). A median split of TSD performance [total lapses (>500 ms response time) and errors] on the 10-minute Psychomotor Vigilance Test (PVT) defined cognitively resilient (n=15) and cognitively vulnerable (n=16) groups. Repeated measures ANOVA and post-hoc comparisons corrected for multiple testing, examined cortisol and CRP across time points between groups. Results In both cognitively resilient and vulnerable individuals, cortisol increased with TSD compared to baseline in the morning and decreased with TSD + psychological stress in the afternoon compared to TSD alone. By contrast, there were no significant changes in CRP levels throughout the experiment. In addition, there were no significant time*group interactions in cortisol or CRP levels. Conclusion Salivary cortisol increased with TSD compared to baseline and showed a time-of-day effect with stress during TSD. Notably, cortisol and CRP did not differ between cognitively resilient and vulnerable individuals across TSD, psychological stress or recovery sleep and thus are not reliable biomarkers for predicting performance under these conditions. Support NASA NNX14AN49G.

scholarly journals Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
George H. Trksak ◽  
Bethany K. Bracken ◽  
J. Eric Jensen ◽  
David T. Plante ◽  
David M. Penetar ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Cognitive Performance ◽  
Sleep Loss ◽  
Continuous Performance ◽  
Digit Symbol ◽  
Continuous Performance Task ◽  
Performance Task ◽  
Recovery Sleep ◽  
Symbol Substitution ◽  
Healthy Control

In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent[31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep,[31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brainβ-NTP (direct measure of adenosine triphosphate),α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse.

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