Effects of Cumulative Sleep Loss and Two Nights' Recovery Sleep on Multiple-Task Performance

Author(s):  
Marja-Leena Haavisto ◽  
Jussi Virkkala ◽  
Mikko Härmä ◽  
Kiti Müller ◽  
Tarja Porkka-Heiskanen ◽  
...  

The present study investigated the effects of five days' cumulative sleep restriction and two nights' recovery sleep on multiple-task performance and subjective sleepiness in a controlled laboratory environment. A total of 21 volunteers participated, thirteen in the experimental group and eight in the control group. Compared to the control group, the sleepiness of the sleep-loss group gradually increased over the five days, but returned to the baseline level after an eight hour recovery sleep period. Multiple-task performance declined selectively in the memory, arithmetic and auditory subtasks, while visual monitoring results were not affected. After the eight hour recovery period, the performance of the sleep-restricted participants in the auditory subtask remained low, although the individuals themselves no longer reported sleepiness. Performance in the rest of the tasks returned to the baseline level. Thus the partial cumulative sleep loss selectively impaired cognitive performance in subtasks of a multiple-task environment, which simulated many ordinary working environments. This may be due to the slowing of the cognitive processing during sleep restriction, as well as decline in attention control.

2007 ◽  
Author(s):  
Marja-Leena Haavisto ◽  
Jussi Virkkala ◽  
Mikko Harma ◽  
Kiti Muller ◽  
Tarja Porkka-Heiskanen ◽  
...  

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 ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A56-A56
Author(s):  
Mark McCauley ◽  
Peter McCauley ◽  
Hans Van Dongen

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


SLEEP ◽  
2021 ◽  
Author(s):  
Christopher M Depner ◽  
Edward L Melanson ◽  
Robert H Eckel ◽  
Janine A Higgins ◽  
Bryan C Bergman ◽  
...  

Abstract Study Objectives Insufficient sleep is believed to promote positive energy balance (EB) and weight-gain. Increasing weekend sleep duration to “recover” from weekday sleep loss is common, yet little is known regarding how weekend recovery sleep influences EB. We conducted a randomized controlled trial to assess how: 1) 2 days and 8 days of insufficient sleep and 2) ad libitum weekend recovery sleep impact EB (energy intake [EI] – energy expenditure [EE]). Methods Following ten baseline days with 9h per night sleep opportunities, participants completed one of three 10-day experimental protocols with ad libitum EI: control (9h sleep opportunities; n=8; 23±5y [mean±SD]); sleep restriction (SR; 5h sleep opportunities; n=14; 25±5y); sleep restriction with weekend recovery sleep (SR+WR; 5 days insufficient sleep, 2 days ad libitum weekend recovery sleep, 3 days recurrent insufficient sleep; n=14; 27±4y). Results 24h EB increased (P < 0.001; main effect) by an average of 797.7±96.7 (±SEM) kcal during the 10-day experimental protocol versus baseline with no significant differences between groups. Percent change from baseline in 24h-EE was higher (P < 0.05) on day 2 of insufficient sleep (SR and SR+WR groups; 10±1%) versus adequate sleep (control group; 4±3%). Conclusions In this between-group study, the effects of adequate sleep and insufficient sleep, with or without or weekend recovery sleep, on 24h-EB were similar. Examining EB and body weight changes using within-subject cross-over designs and “free-living” conditions outside the laboratory (e.g., sleep extension) are needed to advance our understanding of the links between insufficient sleep, weekend recovery sleep and weight-gain.


2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Wessel M. A. van Leeuwen ◽  
Christer Hublin ◽  
Mikael Sallinen ◽  
Mikko Härmä ◽  
Ari Hirvonen ◽  
...  

This study identifies the effects of sleep restriction and subsequent recovery sleep on glucose homeostasis, serum leptin levels, and feelings of subjective satiety. Twenty-three healthy young men were allocated to a control group (CON) or an experimental (EXP) group. After two nights of 8 h in bed (baseline, BL), EXP spent 4 h in bed for five days (sleep restriction, SR), followed by two nights of 8 h (recovery, REC). CON spent 8 h in bed throughout the study. Blood samples were taken after the BL, SR, and REC period. In EXP, insulin and insulin-to-glucose ratio increased after SR. IGF-1 levels increased after REC. Leptin levels were elevated after both SR and REC; subjective satiety remained unaffected. No changes were observed in CON. The observed increase of serum IGF-1 and insulin-to-glucose ratio indicates that sleep restriction may result in an increased risk to develop type 2 diabetes.


1992 ◽  
Vol 36 (1) ◽  
pp. 12-16 ◽  
Author(s):  
Kenneth J. Sarno ◽  
Christopher D. Wickens

The goal of the present study was to evaluate three workload models, VACP (Aldrich, Szabo, and Bierbaum, 1988), TLAP (Parks and Boucek, 1988), and WINDEX (North & Riley, 1988), in terms of how well they account for task performance results gathered from a laboratory experiment. The models are discussed in terms of their treatment of five timesharing issues: 1) the nature of workload components (mutually exclusive or partially overlapping); 2) the utility of distinguishing between cognitive processing codes; 3) classifying voice response (psychomotor function or separate component; 4) qualitative vs. quantitative coding of task demands; and 5) the utility of an overload red-line. A correlational analysis was performed on model predictions versus actual performance for 16 different task loading conditions, to evaluate each of the three workload models. All three models did a good job of predicting performance differences across conditions, accounting for between 61% and 77% of the variance, with the TLAP model providing the best prediction. In addition, a hybrid model was developed (using the “optimal” assumptions concerning the five timesharing issues) which accounted for 85% of the variance. The results are discussed in terms of the viability of the assumptions made by each of the models with respect to the five timesharing issues.


SLEEP ◽  
2021 ◽  
Author(s):  
Michael G Smith ◽  
Grace C Wusk ◽  
Jad Nasrini ◽  
Pamela Baskin ◽  
David F Dinges ◽  
...  

Abstract Chronic sleep loss is associated with escalating declines in vigilant attention across days of sleep restriction. However, studies exceeding 2 weeks of chronic sleep loss are scarce, and the cognitive performance outcomes assessed are limited. We assessed the effects of 6 weeks of chronic sleep restriction on a range of cognitive domains in 15 high-performing individuals (38.5 ± 8.2 years, 6 women) confined to small space in groups of 4. Sleep opportunities were limited to 5 h on weekdays and 8 h on weekends. Individual sleep–wake patterns were recorded with actigraphy. Neurobehavioral performance was assessed in evenings with Cognition, a computerized battery of ten tests assessing a range of cognitive domains. There were some small to moderate effects of increasing sleep debt relative to pre-mission baseline, with decreases in accuracy across cognitive domains (standardized β = –0.121, p = 0.001), specifically on tests of spatial orientation (β = –0.289, p = 0.011) and vigilant attention (β = –0.688, p < 0.001), which were not restored by two nights of weekend recovery sleep. Cognitive and subjective decrements occurred despite occasional daytime napping in breach of study protocol, evening testing around the circadian peak, and access to caffeine before 14:00. Sensorimotor speed, spatial learning and memory, working memory, abstraction and mental flexibility, emotion identification, abstract reasoning, cognitive throughput, and risk decision making were not significantly affected by sleep debt. Taken together with modest lower subjective ratings of happiness and healthiness, these findings underline the importance of sufficient sleep, on both an acute and chronic basis, for performance in selected cognitive domains and subjective wellbeing in operationally relevant environments.


2019 ◽  
Author(s):  
Jeremi K. Ochab ◽  
Jerzy Szwed ◽  
Katarzyna Oleś ◽  
Anna Bereś ◽  
Dante R. Chialvo ◽  
...  

ABSTRACTThe duration of sleep, wakefulness and dynamic changes in human performance are determined by neural and genetic mechanisms. Sleep deprivation and chronic restriction of sleep cause perturbations of circadian rhythmicity and degradation of waking alertness as reflected in attention, cognitive efficiency and memory. In this work we report on multiple neurobehavioral correlates of sleep loss in healthy adults in an unprecedented study comprising 21 consecutive days divided into periods of 4 days of regular life (a baseline), 10 days of chronic partial sleep restriction and 7 days of recovery. Throughout the whole experiment we continuously measured the spontaneous locomotor activity by means of actigraphy with 1-minute resolution in two acquisition modes (frequency and intensity of movement). Moreover, on daily basis the subjects were undergoing EEG measurements (64-electrodes with 500 Hz sampling frequency): resting state with eyes open and closed (RS; 8 minutes long each) followed by Stroop task (ST; 22 minutes). Altogether we analyzed actigraphy (distributions of rest and activity durations), behavioral measures (accuracy and reaction times from Stroop task) and EEG (amplitudes, latencies and scalp maps of event-related potentials from Stroop task and power spectra from resting states). The actigraphy measures clearly indicate rapid changes after sleep restriction onset, confirming our former investigations — the novel insight is a slow and incomplete relaxation to the original locomotor behavior. The pattern of partial recovery appears also in accuracy (in ST) and power of delta rhythm (in RS). The impact of sleep loss is also evident in reaction times (in ST), yet followed by complete recovery, and finally in ERP amplitudes and latencies, which however did not return to the baseline at all. The results indicate that short periods (a few days) of recovery sleep subsequent to prolonged periods of sleep restriction are overall insufficient to recover fully.


2017 ◽  
Vol 114 (16) ◽  
pp. 4243-4248 ◽  
Author(s):  
David Elmenhorst ◽  
Eva-Maria Elmenhorst ◽  
Eva Hennecke ◽  
Tina Kroll ◽  
Andreas Matusch ◽  
...  

Adenosine and functional A1adenosine receptor (A1AR) availability are supposed to mediate sleep–wake regulation and cognitive performance. We hypothesized that cerebral A1AR availability after an extended wake period decreases to a well-rested state after recovery sleep. [18F]CPFPX positron emission tomography was used to quantify A1AR availability in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep. Data were additionally compared with A1AR values after 8 h of baseline sleep from an earlier dataset. Polysomnography, cognitive performance, and sleepiness were monitored. Recovery from sleep deprivation was associated with a decrease in A1AR availability in several brain regions, ranging from 11% (insula) to 14% (striatum). A1AR availabilities after recovery did not differ from baseline sleep in the control group. The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to sleep deprivation correlated negatively with the decrease in A1AR availability. Sleep deprivation resulted in a higher A1AR availability in the human brain. The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode. Individuals with a large increase in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase. This pattern implies that differences in endogenous adenosine and A1AR availability might be causal for individual responses to sleep loss.


SLEEP ◽  
2020 ◽  
Vol 43 (10) ◽  
Author(s):  
Sally Loomis ◽  
Andrew McCarthy ◽  
Derk-Jan Dijk ◽  
Gary Gilmour ◽  
Raphaelle Winsky-Sommerer

Abstract Study Objectives Sleep restriction (SR) leads to performance decrements across cognitive domains but underlying mechanisms remain largely unknown. The impact of SR on performance in rodents is often assessed using tasks in which food is the reward. Investigating how the drives of hunger and sleep interact to modulate performance may provide insights into mechanisms underlying sleep loss-related performance decrements. Methods Three experiments were conducted in male adult Wistar rats to assess: (1) effects of food restriction on performance in the simple response latency task (SRLT) across the diurnal cycle (n = 30); (2) interaction of food restriction and SR (11 h) on SRLT performance, sleep electroencephalogram, and event-related potentials (ERP) (n = 10–13); and (3) effects of food restriction and SR on progressive ratio (PR) task performance to probe the reward value of food reinforcement (n = 19). Results Food restriction increased premature responding on the SRLT at the end of the light period of the diurnal cycle. SR led to marked impairments in SRLT performance in the ad libitum-fed group, which were absent in the food-restricted group. After SR, food-restricted rats displayed a higher amplitude of cue-evoked ERP components during the SRLT compared with the ad libitum group. SR did not affect PR performance, while food restriction improved performance. Conclusions Hunger may induce a functional resilience to negative effects of sleep loss during subsequent task performance, possibly by maintaining attention to food-related cues.


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