scholarly journals Interindividual differences in attentional vulnerability moderate cognitive performance during sleep restriction and subsequent recovery in healthy young men

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gina Marie Mathew ◽  
Stephen M. Strayer ◽  
Kelly M. Ness ◽  
Margeaux M. Schade ◽  
Nicole G. Nahmod ◽  
...  

AbstractWe investigated whether interindividual attentional vulnerability moderates performance on domain-specific cognitive tasks during sleep restriction (SR) and subsequent recovery sleep. Fifteen healthy men (M ± SD, 22.3 ± 2.8 years) were exposed to three nights of baseline, five nights of 5-h time in bed SR, and two nights of recovery sleep. Participants completed tasks assessing working memory, visuospatial processing, and processing speed approximately every two hours during wake. Analyses examined performance across SR and recovery (linear predictor day or quadratic predictor day2) moderated by attentional vulnerability per participant (difference between mean psychomotor vigilance task lapses after the fifth SR night versus the last baseline night). For significant interactions between day/day2 and vulnerability, we investigated the effect of day/day2 at 1 SD below (less vulnerable level) and above (more vulnerable level) the mean of attentional vulnerability (N = 15 in all analyses). Working memory accuracy and speed on the Fractal 2-Back and visuospatial processing speed and efficiency on the Line Orientation Task improved across the entire study at the less vulnerable level (mean − 1SD) but not the more vulnerable level (mean + 1SD). Therefore, vulnerability to attentional lapses after SR is a marker of susceptibility to working memory and visuospatial processing impairment during SR and subsequent recovery.

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A34-A35
Author(s):  
G M Mathew ◽  
S M Strayer ◽  
K Ness ◽  
O M Buxton ◽  
A Chang

Abstract Introduction We investigated whether individuals with more lapses on the psychomotor vigilance task (PVT) after sleep restriction (SR) demonstrated poorer working memory compared to those with fewer PVT lapses. Methods Fifteen healthy men (22.3±2.8 years) participated in a 10-night inpatient protocol with three nights of 10-hour baseline time in bed (TIB), five nights of SR (5-hour TIB), then two recovery (10-hour TIB) nights. Participants completed the Visual Object Learning Task (VOLT) and Fractal 2-Back (F2B; visual n-back) measuring working memory and the PVT (Joggle Research® battery) approximately every two hours during wake. During the VOLT, participants indicated whether presented images had been shown previously. Outcomes included number of misses and false alarms. During the F2B, participants tapped the screen when an image appeared that had been shown 2 images previously. Outcomes included sensitivity and specificity. Median split of mean PVT lapses after the last night of SR was used to categorize participants into “vulnerable” (n=8) versus “resistant” (n=7) groups. Outcomes were analyzed in mixed models with the predictor day*vulnerability, excluding the first three baseline days to preclude practice effects. Results There was a significant interaction between day and attentional vulnerability for VOLT misses (p<.001); misses increased linearly across days in vulnerable (b=.18, p<.001) but not resistant (p=.956) participants. There was no interaction between day and vulnerability for VOLT false alarms, which did not change across days. There was a significant interaction between day and attentional vulnerability for F2B sensitivity (p=.002); sensitivity increased linearly across days in resistant (b=.02, p<.001) but not in vulnerable (p=.273) participants. There was no interaction between day and vulnerability for F2B specificity, which did not change across days. Conclusion Performance on the VOLT decreased in vulnerable participants only; performance on the F2B improved in resistant participants likely due to practice effects not seen in vulnerable participants. Findings indicate vulnerability to attentional lapses after SR is a marker of vulnerability to working memory decrements. Support This study was funded by grant UL1TR000127 from the Clinical and Translational Science Institute (Chang PI) and the College of Health and Human Development at the Pennsylvania State University.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A42-A42
Author(s):  
M Kaizi-Lutu ◽  
C Jones ◽  
A Mange ◽  
M Basner ◽  
D F Dinges

Abstract Introduction Chronic sleep restriction negatively effects working memory. Recovery sleep following sleep restriction partially restores working memory performance. This study examines the impact of chronic sleep restriction and subsequent recovery sleep dose on the N-Back Task (N-Back), a valid measure of working memory. Methods N=223 participants (29.9±6.9 years; 48.4% female), completed two baseline nights of 8h time in bed (TIB), followed by five nights of 4h TIB, and were then randomized to a sleep dose of 0, 2, 4, 6, 8, 10, or 12 h TIB. A subset of participants (n=73) were re-exposed to another five nights of 4h TIB. Participants completed the three versions of the N-Back (i.e. 1-Back, 2-Back, and B-back) every two hours during wakefulness and daily averages were computed. Mixed effects and linear regression models were used to assess the impact of sleep restriction and the sleep dose response on percent correct on the N-Back corrected for baseline. Results N=219 participants had valid working memory data. The 2-Back (β =-4.5%; P<0.0001) and the 3-Back (β =-12.5%; P<0.0001) were more difficult than the 1-Back. Working memory performance declined across days of sleep restriction for all N-Backs: 1-Back (β =-1.10%; P<0.0001), 2-Back (β =-0.99%; P<0.0001), and 3-Back (β =-1.10%; P<0.0001). The sleep dose analysis revealed a positive association with N-Back performance for all N-Back versions, 1-Back (β =0.99%; P=0.0002), 2-Back (β =1.46%; P<0.0001), and 3-Back (β =1.43%; P<0.0001). Re-exposure to only one night of 4h TIB following recovery sleep resulted in performance decrements equal to performance prior to recovery sleep for all N-Back versions (Ps>0.41). Conclusion These data indicate that working memory is adversely impacted by sleep restriction, and that sufficient recovery sleep, possibly across consecutive days, is necessary to maintain optimal working memory performance. Support Funded by National Institute of Health NIH R01NR004281 and National Space and Biomedical Research Institute NSRBI NCC 5–98


SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel

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.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A110-A110
Author(s):  
A Mange ◽  
C W Jones ◽  
M Kaizi-Lutu ◽  
M Basner ◽  
D F Dinges

Abstract Introduction Fatigue is one contributor to mood disturbance observed following sleep restriction; however, the contribution of other factors remains unclear. This study examined contributions to mood disturbance resulting from sleep restriction beyond that of fatigue, evaluated the benefit of recovery sleep, and assessed whether recovery sleep buffered the re-emergence of mood disturbance upon re-exposure to sleep restriction. Methods N=223 healthy participants (48% female; n=108) approximately 30-years-old (SD=6.89, range=22–45 years) completed two baseline nights of 8h time in bed (TIB), followed by five nights of 4h TIB, and were then then randomized to one of 7 sleep recovery opportunities (i.e., 0, 2, 4, 6, 8, 10, or 12 hours TIB). Following the sleep period, a subset of participants (n=72) were re-exposed to five consecutive nights of 4h TIB. The profile of mood states (POMS) was completed every 2h during wakefulness and daily averages were calculated. The POMS total mood disturbance (TMD) score without the fatigue subscale (i.e., mood disturbance = TMD - fatigue) was the primary outcome to isolate changes in mood disturbance beyond fatigue. Individual growth curve models were applied to the trajectory of mood disturbance. General linear models were used to evaluate the dose-response function of mood disturbance after recovery sleep. Results Mood disturbance (absent the POMS fatigue scale) increased with each day of sleep restriction (β=1.550 per day; P<0.0001), and decreased with longer recovery sleep durations in a dose-dependent manner (β=-1.614 for every 2h increase; P<0.0001). The benefits of recovery sleep were abated by the second night of 4h sleep during re-exposure, where mood disturbance was slightly higher than that observed before recovery, but this difference was not statistically significant (β=0.046; P=0.85). Conclusion The study findings suggest that fatigue is not the only contributor to mood disturbance following sleep restriction. Recovery sleep attenuates mood disturbance in a dose-dependent manner, albeit transiently. Candidate pathways linking sleep restriction and mood include the immune system and the dynamics of sleep physiology. Support This work was funded by National Institute of Health NIH R01NR004281 and National Space and Biomedical Research Institute NSRBI NCC 5–98.


Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2694
Author(s):  
Andrea M. Spaeth ◽  
Namni Goel ◽  
David F. Dinges

Sleep restriction (SR) reliably increases caloric intake. It remains unknown whether such intake cumulatively increases with repeated SR exposures and is impacted by the number of intervening recovery sleep opportunities. Healthy adults (33.9 ± 8.9y; 17 women, Body Mass Index: 24.8 ± 3.6) participated in a laboratory protocol. N = 35 participants experienced two baseline nights (10 h time-in-bed (TIB)/night; 22:00–08:00) followed by 10 SR nights (4 h TIB/night; 04:00–08:00), which were divided into two exposures of five nights each and separated by one (n = 13), three (n = 12), or five (n = 10) recovery nights (12 h TIB/night; 22:00–10:00). Control participants (n = 10) were permitted 10 h TIB (22:00–08:00) on all nights. Food and drink consumption were ad libitum and recorded daily. Compared to baseline, sleep-restricted participants increased daily caloric (+527 kcal) and saturated fat (+7 g) intake and decreased protein (−1.2% kcal) intake during both SR exposures; however, intake did not differ between exposures or recovery conditions. Similarly, although sleep-restricted participants exhibited substantial late-night caloric intake (671 kcal), such intake did not differ between exposures or recovery conditions. By contrast, control participants showed no changes in caloric intake across days. We found consistent caloric and macronutrient intake increases during two SR exposures despite varying intervening recovery nights. Thus, energy intake outcomes do not cumulatively increase with repeated restriction and are unaffected by recovery opportunities.


2017 ◽  
Vol 16 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Wessel M. A. van Leeuwen ◽  
Mikael Sallinen ◽  
Jussi Virkkala ◽  
Harri Lindholm ◽  
Ari Hirvonen ◽  
...  

2010 ◽  
Vol 12 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Norah S. Simpson ◽  
Siobhan Banks ◽  
David F. Dinges

Study Objectives: We evaluated the effects of sleep restriction on leptin levels in a large, diverse sample of healthy participants, while allowing free access to food. Methods: Prospective experimental design. After 2 nights of baseline sleep, 136 participants (49% women, 56% African Americans) received 5 consecutive nights of 4 hours time in bed (TIB). Additionally, one subset of participants received 2 additional nights of either further sleep restriction (n = 27) or increased sleep opportunity (n = 37). Control participants (n = 9) received 10 hr TIB on all study nights. Plasma leptin was measured between 10:30 a.m. and 12:00 noon following baseline sleep, after the initial sleep-restriction period, and after 2 nights of further sleep restriction or recovery sleep. Results: Leptin levels increased significantly among sleep-restricted participants after 5 nights of 4 hr TIB (Z = -8.43, p < .001). Increases were significantly greater among women compared to men (Z = -4.77, p < .001) and among participants with higher body mass index (BMI) compared to those with lower (Z = -2.09, p = .036), though participants in all categories (sex, race/ethnicity, BMI, and age) demonstrated significant increases. There was also a significant effect of allowed TIB on leptin levels following the 2 additional nights of sleep restriction (p < .001). Participants in the control condition showed no significant changes in leptin levels. Conclusions: These findings suggest that sleep restriction with ad libitum access to food significantly increases morning plasma leptin levels, particularly among women.


2015 ◽  
Vol 47 ◽  
pp. 93-99 ◽  
Author(s):  
Julie Lasselin ◽  
Javaid-ur Rehman ◽  
Torbjorn Åkerstedt ◽  
Mats Lekander ◽  
John Axelsson

2019 ◽  
Vol 316 (6) ◽  
pp. R697-R703 ◽  
Author(s):  
Kelly M. Ness ◽  
Stephen M. Strayer ◽  
Nicole G. Nahmod ◽  
Anne-Marie Chang ◽  
Orfeu M. Buxton ◽  
...  

Chronic inadequate sleep is associated with increased risk of cardiometabolic diseases. The mechanisms involved are poorly understood but involve changes in insulin sensitivity, including within adipose tissue. The aim of this study was to assess the effects of sleep restriction on nonesterified fatty acid (NEFA) suppression profiles in response to an intravenous glucose tolerance test (IVGTT) and to assess whether 2 nights of recovery sleep (a “weekend”) is sufficient to restore metabolic health. We hypothesized that sleep restriction impairs both glucose and lipid metabolism, specifically adipocyte insulin sensitivity, and the dynamic lipemic response of adipocyte NEFA release during an IVGTT. Fifteen healthy men completed an inpatient study of 3 baseline nights (10 h of time in bed/night), followed by 5 nights of 5 h of time in bed/night and 2 recovery nights (10 h of time in bed/night). IVGTTs were performed on the final day of each condition. Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity P = 0.002; acute insulin response to glucose P = 0.23). The disposition index was suppressed by sleep restriction and did not recover after recovery sleep ( P < 0.0001 and P = 0.01, respectively). Fasting NEFAs were not different from baseline in either the restriction or recovery conditions. NEFA rebound was significantly suppressed by sleep restriction ( P = 0.01) but returned to baseline values after recovery sleep. Our study indicates that sleep restriction impacts NEFA metabolism and demonstrates that 2 nights of recovery sleep may not be adequate to restore glycemic health.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A114-A114
Author(s):  
R K Yuan ◽  
K Zitting ◽  
N Vujovic ◽  
W Wang ◽  
O Buxton ◽  
...  

Abstract Introduction Sleep loss negatively impacts many aspects of neurobehavioral performance, including sustained attention and reaction times. However, the time course of recovery from chronic sleep restriction (CSR) is not well understood. To explore this, we assessed the effects of 3 weeks of CSR followed by 1 week of recovery on psychomotor vigilance task (PVT) performance in healthy adults. Methods 8 healthy adults (27–71; 4f) participated in a 37-day inpatient study. The study consisted of 6 baseline (BL) days with 8–16 h time-in-bed, followed by 3 weeks of CSR (5-5.6h time-in-bed at night), and 1 week of recovery (RC; 8-10h time-in-bed). Sustained attention was assessed by 10-minute visual PVTs administered every 2h starting ~5h after wake (~4/day). Linear and generalized linear mixed models were used to compare average reaction times (RT) and number of lapses, respectively, from the last 3 days of baseline, CSR, and recovery. Results Average RT was almost twice as long at the end of CSR compared to baseline (p&lt;0.0001). Moreover, it remained significantly slower than baseline by roughly 173ms, even after 1 week of recovery (p&lt;0.0001). Similarly, there was a threefold increase in the number of lapses at the end of CSR compared to baseline (p&lt;0.0001) which remained elevated after one week of recovery (p&lt;0.0001). Conclusion One week of recovery sleep of 8-10 h/night following 3 weeks of chronic sleep restriction was insufficient for full recovery of sustained attention as assessed by PVT reaction time and number of lapses. This suggests that chronic sleep restriction has consequences on neurobehavioral performance that do not fully dissipate within one week. Support Study supported by P01AG009975 and conducted in the Brigham and Women’s Hospital Center for Clinical Investigation, part of Harvard Clinical and Translational Science Center supported by UL1TR001102. KMZ supported by a fellowship from the Finnish Cultural Foundation. RKY supported by T32HL007901 and F32HL143893. NV supported by T32HL007901 and F32AG051325.


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