Cognitive throughput and working memory raw scores consistently differentiate resilient and vulnerable groups to sleep loss

Brieva, Tess; Casale, Courtney; Yamazaki, Erika; Antler, Caroline; Goel, Namni

doi:10.1093/sleep/zsab197

Cited by 12 publications

(16 citation statements)

References 66 publications

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“…During sleep deprivation and psychological stress, the range of the Spearman relative rank correlations between the two objective performance measures (3-min PVT and DSST) was ρ = −0.579, p = 0.001, and the range between the objective performance measures and the KSS was ρ = −0.142-0.371, p = 0.036-0.439. The profiles of change in NTB performance and self-report scores with sleep loss and psychological stress are comparable to results obtained in laboratory studies (Dennis et al, 2017;Yamazaki and Goel, 2020;Brieva et al, 2021;Casale et al, 2021b;Yamazaki et al, 2021a,b).…”

Section: Neurobehavioral Deficits Induced By Sleep Loss and Psychological Stresssupporting

confidence: 85%

“…Sleep-wake episodes were verified objectively by wrist actigraphy (Philips Respironics Healthcare, Bend, OR, United States). Actigraphic sleep data were analyzed as in our prior studies ( Dennis et al, 2017 ; Moreno-Villanueva et al, 2018 ; Yamazaki and Goel, 2020 ; Brieva et al, 2021 ; Casale et al, 2021b ; Yamazaki et al, 2021a ).…”

Section: Methodsmentioning

confidence: 99%

“…The KSS ( Åkerstedt and Gillberg, 1990 ) measures self-reported sleepiness. All tests are well-validated measures to examine sleep loss and they show stable, robust individual differences in healthy populations ( Dennis et al, 2017 ; Yamazaki and Goel, 2020 ; Brieva et al, 2021 ; Casale et al, 2021b ; Yamazaki et al, 2021a ), and were administered in the following order during all test bouts: DSST, KSS, 3-min PVT. As such, resilient and vulnerable individuals were determined by a median split on average values from the three NTB sessions during TSD ( Patanaik et al, 2015 ; Moreno-Villanueva et al, 2018 ; Caldwell et al, 2020 ) for 3-min PVT total lapses and errors, DSST performance, and KSS scores.…”

Section: Methodsmentioning

confidence: 99%

“…As such, resilient and vulnerable individuals were determined by a median split on average values from the three NTB sessions during TSD ( Patanaik et al, 2015 ; Moreno-Villanueva et al, 2018 ; Caldwell et al, 2020 ) for 3-min PVT total lapses and errors, DSST performance, and KSS scores. We dichotomized participants as such given that, for initial examination and categorization of novel biomarkers, it is more suitable and applicable to create resilient and vulnerable groups in healthy adult samples, as per convention in the field ( Chuah et al, 2009 ; Rocklage et al, 2009 ; Chee and Tan, 2010 ; Diekelmann et al, 2010 ; Patanaik et al, 2015 ; Yeo et al, 2015 ; Xu et al, 2016 ; Moreno-Villanueva et al, 2018 ; Caldwell et al, 2020 ; Salfi et al, 2020 ; Brieva et al, 2021 ; Casale et al, 2021b ; Yamazaki et al, 2021b ), especially given our sample size. Importantly, systematic examination of multiple approaches and thresholds for evaluating differential neurobehavioral vulnerability to sleep loss has demonstrated that median splits on averaged performance scores, rather than change from baseline or variance in scores, are consistent indicators of resilience and vulnerability during sleep deprived and well-rested periods ( Brieva et al, 2021 ; Casale et al, 2021b ; Yamazaki et al, 2021b ), thus further justifying our methods.…”

Section: Methodsmentioning

confidence: 99%

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Cortisol and C-Reactive Protein Vary During Sleep Loss and Recovery but Are Not Markers of Neurobehavioral Resilience

et al. 2021

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Cortisol and C-reactive protein (CRP) typically change during total sleep deprivation (TSD) and psychological stress; however, it remains unknown whether these biological markers can differentiate robust individual differences in neurobehavioral performance and self-rated sleepiness resulting from these stressors. Additionally, little is known about cortisol and CRP recovery after TSD. In our study, 32 healthy adults (ages 27–53; mean ± SD, 35.1 ± 7.1 years; 14 females) participated in a highly controlled 5-day experiment in the Human Exploration Research Analog (HERA), a high-fidelity National Aeronautics and Space Administration (NASA) space analog isolation facility, consisting of two baseline nights, 39 h TSD, and two recovery nights. Psychological stress was induced by a modified Trier Social Stress Test (TSST) on the afternoon of TSD. Salivary cortisol and plasma CRP were obtained at six time points, before (pre-study), during [baseline, the morning of TSD (TSD AM), the afternoon of TSD (TSD PM), and recovery], and after (post-study) the experiment. A neurobehavioral test battery, including measures of behavioral attention and cognitive throughput, and a self-report measure of sleepiness, was administered 11 times. Resilient and vulnerable groups were defined by a median split on the average TSD performance or sleepiness score. Low and high pre-study cortisol and CRP were defined by a median split on respective values at pre-study. Cortisol and CRP both changed significantly across the study, with cortisol, but not CRP, increasing during TSD. During recovery, cortisol levels did not return to pre-TSD levels, whereas CRP levels did not differ from baseline. When sex was added as a between-subject factor, the time × sex interaction was significant for cortisol. Resilient and vulnerable groups did not differ in cortisol and CRP, and low and high pre-study cortisol/CRP groups did not differ on performance tasks or self-reported sleepiness. Thus, both cortisol and CRP reliably changed in a normal, healthy population as a result of sleep loss; however, cortisol and CRP were not markers of neurobehavioral resilience to TSD and stress in this study.

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Section: Neurobehavioral Deficits Induced By Sleep Loss and Psychological Stresssupporting

confidence: 85%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Cortisol and C-Reactive Protein Vary During Sleep Loss and Recovery but Are Not Markers of Neurobehavioral Resilience

et al. 2021

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“…Chronic sleep deprivation is a significant public health issue and is associated with multiple adverse health risks such as cardiovascular disease, obesity, diabetes, cancer, and overall morbidity and mortality ( Ferrie et al, 2007 ; Gallicchio and Kalesan, 2009 ; Mullington et al, 2009 ). For many individuals, sleep loss increases self-rated sleepiness and deficits in sustained attention ( Banks and Dinges, 2007 ; Goel et al, 2009 ; Brieva et al, 2021 ; Casale et al, 2021 ; Yamazaki et al, 2021a , b ). However, large, highly replicable, phenotypic individual differences occur in response to sleep deprivation, whereby some individuals are vulnerable, and others are resilient to sleep loss ( Van Dongen et al, 2004 ; Goel, 2017 ; Yamazaki and Goel, 2020 ; Brieva et al, 2021 ; Casale et al, 2021 ; Yamazaki et al, 2021a , b ).…”

Section: Introductionmentioning

confidence: 99%

Left Ventricular Ejection Time Measured by Echocardiography Differentiates Neurobehavioral Resilience and Vulnerability to Sleep Loss and Stress

et al. 2022

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There are substantial individual differences (resilience and vulnerability) in performance resulting from sleep loss and psychosocial stress, but predictive potential biomarkers remain elusive. Similarly, marked changes in the cardiovascular system from sleep loss and stress include an increased risk for cardiovascular disease. It remains unknown whether key hemodynamic markers, including left ventricular ejection time (LVET), stroke volume (SV), heart rate (HR), cardiac index (CI), blood pressure (BP), and systemic vascular resistance index (SVRI), differ in resilient vs. vulnerable individuals and predict differential performance resilience with sleep loss and stress. We investigated for the first time whether the combination of total sleep deprivation (TSD) and psychological stress affected a comprehensive set of hemodynamic measures in healthy adults, and whether these measures differentiated neurobehavioral performance in resilient and vulnerable individuals. Thirty-two healthy adults (ages 27–53; 14 females) participated in a 5-day experiment in the Human Exploration Research Analog (HERA), a high-fidelity National Aeronautics and Space Administration (NASA) space analog isolation facility, consisting of two baseline nights, 39 h TSD, and two recovery nights. A modified Trier Social Stress Test induced psychological stress during TSD. Cardiovascular measure collection [SV, HR, CI, LVET, BP, and SVRI] and neurobehavioral performance testing (including a behavioral attention task and a rating of subjective sleepiness) occurred at six and 11 timepoints, respectively. Individuals with longer pre-study LVET (determined by a median split on pre-study LVET) tended to have poorer performance during TSD and stress. Resilient and vulnerable groups (determined by a median split on average TSD performance) showed significantly different profiles of SV, HR, CI, and LVET. Importantly, LVET at pre-study, but not other hemodynamic measures, reliably differentiated neurobehavioral performance during TSD and stress, and therefore may be a biomarker. Future studies should investigate whether the non-invasive marker, LVET, determines risk for adverse health outcomes.

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Enhanced amygdala–cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation

Chai

Gehrman

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Sleep loss robustly disrupts mood and emotion regulation in healthy individuals but can have a transient antidepressant effect in a subset of patients with depression. The neural mechanisms underlying this paradoxical effect remain unclear. Previous studies suggest that the amygdala and dorsal nexus (DN) play key roles in depressive mood regulation. Here, we used functional MRI to examine associations between amygdala- and DN-related resting-state connectivity alterations and mood changes after one night of total sleep deprivation (TSD) in both healthy adults and patients with major depressive disorder using strictly controlled in-laboratory studies. Behavioral data showed that TSD increased negative mood in healthy participants but reduced depressive symptoms in 43% of patients. Imaging data showed that TSD enhanced both amygdala- and DN-related connectivity in healthy participants. Moreover, enhanced amygdala connectivity to the anterior cingulate cortex (ACC) after TSD associated with better mood in healthy participants and antidepressant effects in depressed patients. These findings support the key role of the amygdala–cingulate circuit in mood regulation in both healthy and depressed populations and suggest that rapid antidepressant treatment may target the enhancement of amygdala–ACC connectivity.

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Cognitive throughput and working memory raw scores consistently differentiate resilient and vulnerable groups to sleep loss

Cited by 12 publications

References 66 publications

Cortisol and C-Reactive Protein Vary During Sleep Loss and Recovery but Are Not Markers of Neurobehavioral Resilience

Cortisol and C-Reactive Protein Vary During Sleep Loss and Recovery but Are Not Markers of Neurobehavioral Resilience

Left Ventricular Ejection Time Measured by Echocardiography Differentiates Neurobehavioral Resilience and Vulnerability to Sleep Loss and Stress

Enhanced amygdala–cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation

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