The cortisol awakening response after sleep deprivation: Is the cortisol awakening response a “response” to awakening or a circadian process?

2017 ◽  
Vol 25 (7) ◽  
pp. 900-912 ◽  
Author(s):  
Ivan Vargas ◽  
Nestor Lopez-Duran
Keyword(s):  
Sleep Deprivation ◽  
Salivary Cortisol ◽  
Deprivation Condition ◽  
Cortisol Awakening Response ◽  
Total Sleep Deprivation ◽  
Morning Cortisol ◽  
Sleep Condition

This study tested whether the cortisol awakening response is dependent on the transition from sleep to awakening, or alternatively, a circadian-driven process that is independent of awakening. A total of 40 participants were randomly assigned to either a total sleep deprivation or a sleep condition. Salivary cortisol was also assessed. Participants in the sleep condition demonstrated a traditional cortisol awakening response, whereas participants in the total sleep deprivation condition showed no increases in morning cortisol. These results are consistent with the notion that if circadian-driven processes are related to the cortisol awakening response, they may only be activated when awakening occurs or is anticipated.

scholarly journals Sleep Deprivation and Sleep-Onset Insomnia are Associated with Blunted Physiological Reactivity to Stressors

2021 ◽  
Vol 186 (Supplement_1) ◽  
pp. 246-252
Author(s):  
Devon A Hansen ◽  
Brieann C Satterfield ◽  
Matthew E Layton ◽  
Hans P A Van Dongen
Keyword(s):  
Sleep Deprivation ◽  
Laboratory Study ◽  
Salivary Cortisol ◽  
Sleep Onset ◽  
Deprivation Condition ◽  
Increased Risk ◽  
Significant Difference ◽  
Sleep Deficiency ◽  
The Impact ◽  
Chronic Sleep

ABSTRACT Introduction Military operations often involve intense exposure to stressors combined with acute sleep deprivation, while military personnel also experience high prevalence of chronic sleep deficiency from insomnia and other sleep disorders. However, the impact of acute and chronic sleep deficiency on physiologic stressor responses is poorly understood. In a controlled laboratory study with normal sleepers and individuals with chronic sleep-onset insomnia, we measured responses to an acute stressor administered in a sleep deprivation condition or a control condition. Methods Twenty-two adults (aged 22-40 years; 16 females)—11 healthy normal sleepers and 11 individuals with sleep-onset insomnia—completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day, subjects were assigned to a 38-hour total sleep deprivation (TSD) condition or a control condition; the study ended with a recovery day. At 8:00 PM after 36 hours awake in the sleep deprivation condition or 12 hours awake in the control condition, subjects underwent a Maastricht Acute Stress Test (MAST). Salivary cortisol was measured immediately before the MAST at 8:00 PM, every 15 minutes after the MAST from 8:15 PM until 9:15 PM, and 30 minutes later at 9:45 PM. Baseline salivary cortisol was collected in the evening of the baseline day. Additionally, before and immediately upon completion of the MAST, self-report ratings of affect and pain were collected. Results The MAST elicited a stressor response in both normal sleepers and individuals with sleep-onset insomnia, regardless of the condition, as evidenced by increases in negative affect and pain ratings. Relative to baseline, cortisol levels increased immediately following the MAST, peaked 30 minutes later, and then gradually returned to pre-MAST levels. At the cortisol peak, there was a significant difference across groups and conditions, reflecting a pronounced blunting of the cortisol response in the normal sleepers in the TSD condition and the sleep-onset insomnia group in both the TSD and control conditions. Conclusions Blunted stressor reactivity as a result of sleep deficiency, whether acute or chronic, may reflect reduced resiliency attributable to allostatic load and may put warfighters at increased risk in high-stakes, rapid response scenarios.

Sleep deprivation reduces vagal tone during an inspiratory endurance task in humans

SLEEP ◽  
2021 ◽  
Author(s):  
Willy-Paul Westphal ◽  
Christophe Rault ◽  
René Robert ◽  
Stéphanie Ragot ◽  
Jean-Philippe Neau ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sleep Deprivation ◽  
Vagal Tone ◽  
Deprivation Condition ◽  
Sleep Condition ◽  
Inspiratory Motor ◽  
Normal Sleep ◽  
Exercise Endurance ◽  
Normalized Units ◽  
Inspiratory Load

Abstract Study Objectives Sleep deprivation alters inspiratory endurance by reducing inspiratory motor output. Vagal tone is involved in exercise endurance. This study aimed to investigate the effect of sleep deprivation on vagal tone adaptation in healthy subjects performing an inspiratory effort. Methods Vagal tone was assessed using Heart Rate Variability normalized units of frequency domain component HF (high frequency) before, at the start, and the end of an inspiratory loading trial performed until exhaustion by 16 volunteers after one night of sleep deprivation and one night of normal sleep, where sleep deprivation reduced the inspiratory endurance by half compared to the normal sleep condition (30min vs 60 min). Results At rest, heart rate was similar in sleep deprivation and normal sleep conditions. In normal sleep condition, heart rate increased during inspiratory loading task; this increase was greater in sleep deprivation condition. In normal sleep condition, vagal tone increased at the beginning of the trial. This vagal tone increase was absent in sleep deprivation condition. Conclusions Sleep deprivation abolished vagal tone response to inspiratory load, possibly contributing to a higher heart rate during the trial and to a reduced inspiratory endurance.

Analysis of Sleep Deprivation Effect to Driving Performance Using ReactionTest Simulation

2015 ◽  
Vol 72 (4) ◽  
Author(s):  
Ika Nurlaili Isnainiyah ◽  
Febriliyan Samopa ◽  
Hatma Suryotrisongko ◽  
Edwin Riksakomara
Keyword(s):  
Sleep Deprivation ◽  
Traffic Accidents ◽  
Driving Simulator ◽  
Driving Performance ◽  
Deprivation Condition ◽  
Falling Asleep ◽  
Sleep Condition ◽  
Lack Of Sleep ◽  
The Difference ◽  
Social Habits

Sleep deprivation condition might lead to falling asleep through inappropriate situations, such as driving. Driving in a state of fatigue or drowsy from lack of sleep will be far worse than driving after alcohol consumption. Hence, the authors develop a driving simulator using Java to modify the control and rules of OpenDS application in order to simulate and calculate the automatic ReactionTest for 25 respondents simulating in both normal conditions and sleepy conditions when driving. Through this study, the authors obtained that the difference of driving performance in terms of reaction rate when driving the car in sleep deprivation condition and the normal condition, is equal to 1.08 seconds. The results also shown that the risk of loss of control that can occur to the driver of the car in units of meters (m), is equal to 0.3024 x the car’s speed. This study aims to reduce the number of traffic accidents caused by sleep deprivation that occur in society by giving a recommendation to the driver that forced to drive in lack of sleep condition. In top of that, the authors propose to create an understanding for changing the social habits of driving toward a better way.  

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 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.

Muscle temperature is least altered during total sleep deprivation in rats

2021 ◽  
pp. 102910
Author(s):  
Binney Sharma ◽  
Trina Sengupta ◽  
Lal Chandra Vishwakarma ◽  
Nasreen Akhtar ◽  
Hruda Nanda Mallick
Keyword(s):  
Sleep Deprivation ◽  
Muscle Temperature ◽  
Total Sleep Deprivation

scholarly journals 0308 DRD2 C957T Genotype Influences Vigilant Attention Performance Impairment During Total Sleep Deprivation

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A116-A116
Author(s):  
R A Muck ◽  
L Skeiky ◽  
M A Schmidt ◽  
B C Satterfield ◽  
J P Wisor ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Analysis Of Covariance ◽  
Genotype Distribution ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Time In Bed ◽  
Dat1 Gene ◽  
Performance Impairment ◽  
Attention Performance ◽  
Time Awake

Abstract Introduction There are substantial, phenotypical individual differences in the adverse impact of total sleep deprivation (TSD) on vigilant attention performance. Dopaminergic genotypes have been found to contribute to these phenotypical differences. Here we investigated the association between a single nucleotide polymorphism (SNP) of the dopamine receptor D2 (DRD2) gene, C957T (rs6277), on vigilant attention performance measured with the psychomotor vigilance test (PVT) in a laboratory TSD study. Methods N=46 healthy adults (ages 26.0±5.3y; 25 females) completed a 4-day in-laboratory study with a baseline day (10h time in bed: 22:00-08:00), a 38h TSD period, and a recovery day (10h time in bed: 22:00-08:00). DNA isolated from whole blood was assayed for DRD2 C957T genotype using real-time polymerase chain reaction. PVT performance was measured during TSD at 2-4h intervals, and analyzed for genotype using mixed-effects analysis of covariance of lapses of attention (RTs>500ms). Results The genotype distribution in this sample - 28.3% C/C, 50.0% C/T, 21.7% T/T - was found to be in Hardy-Weinberg Equilibrium (X21=0.0008, p=0.98). As expected, there was a significant effect of time awake on PVT performance (F14,602=26.67, p<0.001). There was a significant main effect of DRD2 genotype (F2,602=3.24, p=0.040) and a significant interaction of time awake by DRD2 genotype (F28,602=1.96, p=0.003). Subjects homozygous for the T allele showed greater impairment during extended wakefulness than carriers of the C allele. Genotype explained 7.6% of the variance in the PVT data observed during the 38h TSD period. Conclusion Subjects homozygous for the T allele of DRD2 C957T were considerably more vulnerable to TSD-induced PVT performance impairment than carriers of the C allele. A recent study showed that DRD2 C957T influences PVT performance in interaction with a SNP of the DAT1 gene. Here, DRD2 genotype was by itself also associated with PVT performance impairment during TSD. Support CDMRP awards W81XWH-16-1-0319 and W81XWH-18-1-0100.

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