Partial Sleep Deprivation Condition Research Articles

The influence of acute partial sleep deprivation on liking, choosing and consuming high- and low-energy foods

A wealth of cross-sectional studies found a link between sleep deprivation and food-related outcomes like energy intake and BMI. Recent experimental studies suggest that this link is causal. However, the mechanisms through which sleep deprivation influences intake remain unclear. Here, we tested two prevailing hypotheses: that sleep deprivation leads to 1) increased food reward sensitivity and 2) decreased food-related self-control.In a within-subject study (n = 60 normal-weight females), we compared outcome measures under normal sleep and partial sleep deprivation conditions. Our outcome measures were 1) proxies for food reward sensitivity – liking of high and low energy foods, 2) binary food choices ranging in level of self-control conflict, and 3) intake of high and low energy foods. Eye-movements during food choice were measured with an eye-tracker to gain insights in implicit food choice processes.Food reward sensitivity outcomes showed a lower liking of low energy foods after partial sleep deprivation. More high energy foods were chosen after partial sleep deprivation independent of the level of self-control conflict. Intake of high energy foods was higher in the partial sleep deprivation condition. Lastly, the number of gaze switches between high and low energy foods, an implicit measure of conflict in choice, was lower in the high-conflict trials after sleep deprivation than after a normal night sleep.To conclude, the increased intake of high energy foods after sleep deprivation may be driven by a decreased liking of low energy foods, rather than an increased liking of high energy foods. Further, sleep deprivation may affect self-control conflict detection as indicated by a lower number of gaze switches between food options.

Sleep loss does not aggravate the deteriorating effect of hypoglycemia on neurocognitive function in healthy men

Sleep deprivation (SD) impairs neurocognitive functions. Assuming that this effect is mediated by reduced cerebral glucose supply due to prolonged wakefulness inducing a progressive depletion of cerebral glycogen stores, we hypothesized that short-term sleep loss amplifies the deteriorating effects of acute hypoglycemia on neurocognitive functions. Seven healthy men were tested in a randomized and balanced order on 3 different conditions spaced 2 weeks apart. After a night of total SD (total SD), 4.5h of sleep (partial SD) and a night with 7h of regular sleep (regular sleep), subjects were exposed to a stepwise hypoglycemic clamp experiment. Reaction time (RT) and auditory evoked brain potentials (AEP) were assessed during a euglycemic baseline period and at the end of the clamp (blood glucose at 2.5mmol/l). During the euglycemic baseline, amplitude of the P3 component of the AEP was lower after total SD than after partial SD (9.2+/-3.2microV vs. 16.6+/-2.9microV; t(6)=3.2, P=0.02) and regular sleep (20.2+/-2.1microV; t(6)=18.8, P<0.01). Reaction time was longer after total SD in comparison to partial SD (367+/-45ms vs. 304+/-36ms; t(6)=2.7, P=0.04) and to regular sleep (322+/-36ms; t(6)=2.41, P=0.06) while there was no difference between partial SD and regular sleep condition (t(6)=0.60, P=0.57). Hypoglycemia decreased P3 amplitude by 11.2+/-4.1microV in the partial SD condition (t(6)=2.72, P=0.04) and by 9.3+/-0.7microV in the regular sleep condition (t(6)=12.51, P<0.01), but did not further reduce P3 amplitude after total SD (1.8+/-3.9microV; t(6)=0.46, P=0.66). Thus, at the end of hypoglycemia P3 amplitudes were similar across the 3 conditions (F(2,10)=0.89, P=0.42). RT generally showed a similar pattern with a significant prolongation due to hypoglycemia after partial SD (+42+/-12ms; t(6)=3.39, P=0.02) and regular sleep (+37+/-10ms; t(6)=3.53, P=0.01), but not after total SD (+15+/-16; t(6)=0.97, P=0.37), resulting in similar values at the end of hypoglycemia (F(1,6)=1.01, P=0.36). One night of total SD deteriorates neurocognitive function as reflected by indicators of attentive stimulus processing, but does not synergistically aggravate the impairing influence of acute hypoglycemia. The findings are not consistent with the view that neurocognitive deteriorations after SD result from challenged cerebral glucose metabolism.

Low Levels of Alcohol Impair Driving Simulator Performance and Reduce Perception of Crash Risk in Partially Sleep Deprived Subjects

Partial sleep deprivation and alcohol consumption are a common combination, particularly among young drivers. We hypothesized that while low blood alcohol concentration (<0.05 g/dL) may not significantly increase crash risk, the combination of partial sleep deprivation and low blood alcohol concentration would cause significant performance impairment. Experimental Sleep Disorders Unit Laboratory 20 healthy volunteers (mean age 22.8 years; 9 men). Subjects underwent driving simulator testing at 1 am on 2 nights a week apart. On the night preceding simulator testing, subjects were partially sleep deprived (5 hours in bed). Alcohol consumption (2-3 standard alcohol drinks over 2 hours) was randomized to 1 of the 2 test nights, and blood alcohol concentrations were estimated using a calibrated Breathalyzer. During the driving task subjects were monitored continuously with electroencephalography for sleep episodes and were prompted every 4.5 minutes for answers to 2 perception scales-performance and crash risk. Mean blood alcohol concentration on the alcohol night was 0.035 +/- 0.015 g/dL. Compared with conditions during partial sleep deprivation alone, subjects had more microsleeps, impaired driving simulator performance, and poorer ability to predict crash risk in the combined partial sleep deprivation and alcohol condition. Women predicted crash risk more accurately than did men in the partial sleep deprivation condition, but neither men nor women predicted the risk accurately in the sleep deprivation plus alcohol condition. Alcohol at legal blood alcohol concentrations appears to increase sleepiness and impair performance and the detection of crash risk following partial sleep deprivation. When partially sleep deprived, women appear to be either more perceptive of increased crash risk or more willing to admit to their driving limitations than are men. Alcohol eliminated this behavioral difference.

Effect of sleep loss on C-Reactive protein, an inflammatory marker of cardiovascular risk

ObjectivesWe sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP) levels. BackgroundConcentrations of high-sensitivity CRP are predictive of future cardiovascular morbidity. In epidemiologic studies, short sleep duration and sleep complaints have also been associated with increased cardiovascular morbidity. Two studies were undertaken to examine the effect of acute total and short-term partial sleep deprivation on concentrations of high-sensitivity CRP in healthy human subjects. MethodsIn Experiment 1, 10 healthy adult subjects stayed awake for 88 continuous hours. Samples of high-sensitivity CRP were collected every 90 min for 5 consecutive days, encompassing the vigil. In Experiment 2, 10 subjects were randomly assigned to either 8.2 h (control) or 4.2 h (partial sleep deprivation) of nighttime sleep for 10 consecutive days. Hourly samples of high-sensitivity CRP were taken during a baseline night and on day 10 of the study protocol. ResultsThe CRP concentrations increased during both total and partial sleep deprivation conditions, but remained stable in the control condition. Systolic blood pressure increased across deprivation in Experiment 1, and heart rate increased in Experiment 2. ConclusionsBoth acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.

Sleepiness as Measured by Modified Multiple Sleep Latency Testing Varies as a Function of Preceding Activity

Many studies have examined the impact of varying levels of sleep loss or sleep disturbance upon the multiple sleep latency test (MSLT). Virtually no studies have examined the impact of level of physiologic arousal upon measured sleep tendency. In the current study, 12 normal-sleeping young adults took modified multiple sleep latency tests after either watching television for 15 minutes or after a 5-minute walk. This entire protocol was repeated on another week after subjects had been partially sleep deprived by reducing their time in bed by 50%. It was hypothesized that sleep latencies would be significantly shorter after watching television as compared to walking and after partial sleep loss as compared to normal sleep and that these effects would be independent. The results of the study supported all of these hypotheses. ANOVAs showed no significant interaction effects, but sleep latencies were 11.6 and 5.8 minutes following the walk and watching television respectively. Sleep latencies were 9.8 and 7.6 minutes following baseline and partial sleep-deprivation conditions. Heart rate, used as a measure of physiological arousal, was significantly elevated throughout naps following the walk as compared to naps following television viewing. On a theoretical level, these data imply that measured sleepiness is a combination of sleep drive and physiological arousal, and these effects appear to be independent. On a practical level, these data indicate that more care may be necessary in monitoring the activity levels of patients and subjects prior to MSLT evaluations, since physiological arousal may mask the measurement of sleep tendency. Knowledge of the role of arousal in modulating sleepiness can be important in many settings.