scholarly journals 0041 Heart Rate Variability Differs in Resilient vs. Vulnerable Adults from Total Sleep Deprivation and Psychological Stress and Predicts Cognitive Performance

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A16-A17
Author(s):  
E M Yamazaki ◽  
K M Rosendahl-Garcia ◽  
L E MacMullen ◽  
A J Ecker ◽  
J N Kirkpatrick ◽  
...  

Abstract Introduction There are substantial individual differences (resilience and vulnerability) in neurobehavioral performance from psychosocial stress and sleep loss. However, the time course of heart rate variability (HRV) across baseline, total sleep deprivation (TSD), the combination of TSD + psychological stress, and recovery has not been investigated; in addition, it remains unknown whether HRV and blood pressure (BP) differ in resilient vs. vulnerable individuals and predict individual differences in cognitive performance. 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, 39h TSD, and two 8h-10h TIB recovery nights. A modified Trier Social Stress Test (TSST) induced psychological stress on the TSD day. Systolic and diastolic BP and HRV (derived from echocardiographic R-R interval) were obtained at six time points (pre-study, baseline, during TSD, during TSD after the TSST, after recovery, and post-study). Cognitively resilient (n=15) and vulnerable (n=16) groups were defined by a median split on 10-minute Psychomotor Vigilance Test (PVT) TSD performance [total lapses (>500ms response time) and errors]. Repeated measures ANOVA and post-hoc comparisons corrected for multiple testing, examined BP and HRV across time points between groups. Results HRV showed a significant time*group interaction: while resilient individuals had significantly lower HRV at pre-study compared to vulnerable individuals, their HRV increased above that of vulnerable individuals with TSD and with TSD + psychological stress. By contrast, systolic and diastolic BP did not show significant time*group interactions and did not predict cognitive vulnerability during TSD. Conclusion HRV differed between resilient and vulnerable individuals across TSD, psychological stress and recovery sleep and predicted individual differences in cognitive performance, whereby lower HRV during full-rested conditions predicted resilience to TSD and TSD + psychological stress. HRV, but not BP, is a reliable biomarker of sleep deprivation, psychological stress, and neurobehavioral vulnerability. Support NASA NNX14AN49G.

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A101-A101
Author(s):  
N Goel ◽  
E M Yamazaki ◽  
L E MacMullen ◽  
A J Ecker

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.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A17-A17
Author(s):  
E M Yamazaki ◽  
K M Rosendahl-Garcia ◽  
L E MacMullen ◽  
A J Ecker ◽  
J N Kirkpatrick ◽  
...  

Abstract Introduction Individuals show robust resilience and vulnerability in neurobehavioral performance to sleep loss and stress. For the first time, we investigated the time course of two cardiovascular measurements, stroke volume (SV) and cardiac index (CI), both derived from echocardiography, across baseline, total sleep deprivation (TSD), the combination of TSD+psychological stress, and recovery. We also determined whether these variables differ in resilient vs. vulnerable individuals and whether they predict differential vulnerability in cognitive performance. 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, 39h TSD, and two 8h-10h TIB recovery nights. A modified Trier Social Stress Test (TSST) was conducted on the TSD day to induce psychological stress. Echocardiographic measures of SV and CI were obtained at six time points (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 vulnerable (n=16) groups. Repeated measures ANOVA and post-hoc comparisons corrected for multiple testing, examined SV and CI across time points between groups. Results There was a significant time*group interaction for SV: cognitively resilient individuals had greater SV during the five-day experiment. In addition, in both resilient and vulnerable individuals, SV increased with TSD and with TSD+psychological stress compared with baseline. Like SV, there was a significant time*group interaction for CI: resilient individuals had greater CI at all points of the experiment. Conclusion SV and CI differed between resilient and vulnerable individuals across TSD, psychological stress and recovery sleep. Greater SV and greater CI at baseline predicted resilience to TSD and TSD+psychological stress. CI and SV are novel physiological biomarkers of sleep loss, stress, and individual differences in cognitive performance. Support NASA NNX14AN49G.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A4-A4
Author(s):  
Brieann Satterfield ◽  
Darian Lawrence-Sidebottom ◽  
Michelle Schmidt ◽  
Jonathan Wisor ◽  
Hans Van Dongen

Abstract Introduction The activity-regulated cytoskeleton associated protein (ARC) gene is an immediate early gene that is involved in synaptic plasticity. Recent evidence from a rodent model suggests that Arc may also be involved in sleep homeostasis. However, little is known about the molecular mechanisms regulating the sleep homeostat. In humans, sleep homeostasis is manifested by a marked increase in slow wave sleep (SWS) following acute total sleep deprivation (TSD). There are large, trait individual differences in the magnitude of this SWS rebound effect. We sought to determine whether a single nucleotide polymorphism (SNP) of the ARC gene is associated with individual differences in SWS rebound following TSD. Methods 64 healthy normal sleepers (ages 27.2 ± 4.8y; 32 females) participated in one of two in-laboratory TSD studies. In each study, subjects had a baseline day with 10h sleep opportunity (TIB 22:00–08:00) which was followed by 38h TSD. The studies concluded with 10h recovery sleep opportunity (TIB 22:00–08:00). Baseline and recovery sleep were recorded polysomnographically and scored visually by a trained technician. Genomic DNA was extracted from whole blood. The ARC c.*742 + 58C>T non-coding SNP, rs35900184, was assayed using real-time PCR. Heterozygotes and T/T homozygotes were combined for analysis. The genotype effect on time in SWS was assessed using mixed-effects ANOVA with fixed effects for ARC genotype (C/C vs. T carriers), night (baseline vs. recovery), and their interaction, controlling for study. Results The genotype distribution in this sample – C/C: 41; C/T: 17; T/T: 6 – did not vary significantly from Hardy-Weinberg equilibrium. There was a significant interaction between ARC genotype and night (F1,62=7.27, p=0.009). Following TSD, T allele carriers exhibited 47.6min more SWS compared to baseline, whereas C/C homozygotes exhibited 62.3min more SWS compared to baseline. There was no significant difference in SWS between genotypes at baseline (F1,61=0.69, p=0.41). Conclusion ARC T allele carriers exhibited an attenuated SWS rebound following TSD compared to those homozygous for the C allele. This suggests that the ARC SNP is associated with trait individual differences related to sleep homeostasis, and may thus influence molecular mechanisms involved in long-term memory. Support (if any) ONR N00014-13-1-0302, NIH R21CA167691, and USAMRDC W81XWH-18-1-0100.


2017 ◽  
Vol 27 (4) ◽  
pp. e12633 ◽  
Author(s):  
Johanna M. Boardman ◽  
Bei Bei ◽  
Alix Mellor ◽  
Clare Anderson ◽  
Tracey L. Sletten ◽  
...  

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