Effects of sleep deprivation and time-of-day on selected physical abilities in off-road motorcycle riders

The aim of this study was to observe how the combined effects of time-of-day and sleep deprivation impact motocross riders’ physical abilities. Balance, flexibility and maximal anaerobic alactic power were tested across laboratory tests that required only one ability (stork stand test, sit-and-reach test, Abalakov test) or across field tests that concentrated on a particular ability (narrow board riding test, riding under a rod test, long jump riding test) to maximise the sensitivity of the assessments and the interpretability of findings. Eight motocross riders of confirmed level took part in test sessions set up at 0600 and 1800 hours following a normal night’s sleep and a night of sleep deprivation, i.e. after 1, 13, 23 and 35 waking hours. On the one hand, the results confirmed the influence of time-of-day on riders’ physical abilities, performances being better at 1800 hours than at 0600 hours after the normal night’s sleep. On the other hand, as far as sleep deprivation effects are concerned, the results seemed to differ on the basis of the ability under consideration and the type of test that had been set up. Performance in the field tests still presented a diurnal fluctuation, whereas this improvement over the day did not occur for the performance in the laboratory tests. It seems that compensation mechanisms between the various abilities brought into play are set up in order to moderate the effects of the lack of sleep when riding.     

Total sleep deprivation decreases saliva ghrelin levels in adolescents

Ghrelin, a regulator of food intake and energy expenditure, has been shown to be associated with insufficient sleep. The goal of the present study was to investigate the effect of a single night of total sleep deprivation on fasting saliva ghrelin and on nocturnal variation of saliva ghrelin concentration. A further aim of the study was to investigate the influence of body mass index on changes in saliva ghrelin levels. Altogether 35 adolescents (18 boys; age: 13.8 ± 1.14 years) were studied on two subsequent days (sleep and total sleep deprivation). Saliva samples were collected during the two experimental nights at 21:00 hours, 01:00 hours and 06:00 hours. Total-ghrelin concentration showed a continuous increase from the evening until 06:00 hours. This increase was blunted significantly (p = 0.003) by total sleep deprivation. Total-ghrelin level was significantly lower (p = 0.02) during total sleep deprivation at 06:00 hours (median 403.6 pg ml⁻¹; 95% confidence interval: 343.1–468.9 pg ml⁻¹) as compared with values during the sleep condition (median 471.2 pg ml⁻¹; 95% confidence interval: 205.4–1578.7 pg ml⁻¹). Acyl-ghrelin levels did not present any change at the three time points, and were not affected by total sleep deprivation. Stratifying the study population according to body mass index (normal weight and overweight/obese groups), the blunting effect of total sleep deprivation was more pronounced in the obese/overweight group (sleep: median 428.2 pg ml⁻¹; 95% confidence interval: 331.3–606.9 pg ml⁻¹ versus total sleep deprivation: median 333.1 pg ml⁻¹; 95% confidence interval: 261.5–412.9 pg ml⁻¹; p = 0.0479). Saliva total-ghrelin concentrations gradually increased during the night, and total sleep deprivation significantly blunted this increase. This blunting effect was mainly observed in subjects with overweight/obesity. The physiological and clinical implications of the present observation are to be clarified by further studies.     

The impact of caffeine consumption during 50 hr of extended wakefulness on glucose metabolism,self‐reported hunger and mood state

Caffeine is known for its capacity to mitigate performance decrements. The metabolic side‐effects are less well understood. This study examined the impact of cumulative caffeine doses on glucose metabolism, self‐reported hunger and mood state during 50 hr of wakefulness. In a double‐blind laboratory study, participants were assigned to caffeine (n = 9, 6M, age 21.3 ± 2.1 years; body mass index 21.9 ± 1.6 kg/m²) or placebo conditions (n = 8, 4M, age 23.0 ± 2.8 years; body mass index 21.8 ± 1.6 kg/m²). Following a baseline sleep (22:00 hours–08:00 hours), participants commenced 50 hr of sleep deprivation. Meal timing and composition were controlled throughout the study. Caffeine (200 mg) or placebo gum was chewed for 5 min at 01:00 hours, 03:00 hours, 05:00 hours and 07:00 hours during each night of sleep deprivation. Continual glucose monitors captured interstitial glucose 2 hr post‐breakfast, at 5‐min intervals. Hunger and mood state were assessed at 10:00 hours, 16:30 hours, 22:30 hours and 04:30 hours. Caffeine did not affect glucose area under the curve (p = 0.680); however, glucose response to breakfast significantly increased after 2 nights of extended wakefulness compared with baseline (p = 0.001). There was a significant main effect of day, with increased tiredness (p < 0.001), mental exhaustion (p < 0.001), irritability (p = 0.002) and stress (p < 0.001) on the second day of extended wake compared with day 1. Caffeine attenuated the rise in tiredness (p < 0.001), mental exhaustion (p = 0.044) and irritability (p = 0.018) on day 1 but not day 2. Self‐reported hunger was not affected by sleep deprivation or caffeine. These data confirm the effectiveness of caffeine in improving performance under conditions of sleep deprivation by reducing feelings of tiredness, mental exhaustion and irritability without exacerbating glucose metabolism and feelings of hunger.     

Electrophysiological correlates of cognition improve with nap during sleep deprivation

The efficacy of a 30-min nap as a countermeasure in the reduction of cognitive decline following 24 h of sleep deprivation (SD) on subjective sleepiness scales, event-related potential (ERP) P300, and contingent negative variation (CNV) was evaluated. The experiment was performed in three sessions on different days between 7 and 8 a.m. on nine normal, healthy males, of age 25–30 years: Session 1. Baseline recordings; Session 2, after one night’s total sleep deprivation, and; Session 3, after 1 week of Session 1, following one night’s sleep deprivation along with a 30-min nap opportunity between 1.00 and 3.00 a.m. Subjective sleepiness scores increased after SD as compared to baseline, but reduced significantly after nap (P < 0.05). There was an increase in P3 peak latency of ERP following SD (16%, P < 0.01), which was reduced with nap (10.7%, P < 0.05).There was an increase in CNV M1 peak latency after SD (18%) which decreased with the use of nap (12.5%) (P < 0.01). The CNV reaction time increased following SD (39.3%) and decreased with the use of nap (24%) (P < 0.01). No significant effects on ERP N1, P1, N2 latencies, P2 and P3 amplitudes and CNV N1, P3, M2 peak latencies and M1, and M2 amplitudes were observed. It was concluded that a 30-min nap, between 1.00 and 3.00 a.m. during night SD, reduces the cognitive decline following 24 h of SD in terms of its electro-physiological correlates. The study is of applied value in optimization of cognitive performance in professions demanding night work schedules.     

Length polymorphism in the Period 3 gene is associated with sleepiness and maladaptive circadian phase in night‐shift workers

The objective of the current study was to determine if night‐shift workers carrying the five‐repeat variant of the Period 3 gene show elevated levels of nocturnal sleepiness and earlier circadian phase compared with homozygotes for the four‐repeat allele. Twenty‐four permanent night‐shift workers were randomly selected from a larger study. Participants took part in an observational laboratory protocol including an overnight multiple sleep latency test and half‐hourly saliva collection for calculation of dim‐light melatonin onset. Period 3^–/5 shift workers had significantly lower multiple sleep latency test during overnight work hours compared with Period 3^4/4 workers (3.52 ± 23.44 min versus 10.39 ± 6.41 min, P = 0.003). We observed no significant difference in sleepiness during early morning hours following acute sleep deprivation. Long‐allele carriers indicated significantly higher sleepiness on the Epworth Sleepiness Scale administered at 17:00 hours (12.08 ± 2.55 versus 8.00 ± 1.94, P < 0.001). We observed a significantly earlier melatonin onset in Period 3^–/5 individuals compared with Period 3^4/4 shift workers (20:44 ± 6:37 versus 02:46 ± 4:58, P = 0.021). Regression analysis suggests that Period 3 genotype independently predicts sleepiness even after controlling for variations in circadian phase, but we were unable to link Period 3 to circadian phase when controlling for sleepiness. Period 3^–/5 shift workers showed both subjective and objective sleepiness in the pathological range, while their Period 3^4/4 counterparts showed sleepiness within normal limits. Period 3^–/5 night workers also show a mean circadian phase 6 h earlier (i.e. less adapted) than Period 3^4/4 workers. Because Period 3^–/5 workers have maladaptive circadian phase as well as pathological levels of sleepiness, they may be at greater risk for occupational and automotive accidents. We interpret these findings as a call for future research on the role of Period 3 in sleepiness and circadian phase, especially as they relate to night work.     

The night before night shift: Chronotype impacts total sleep and rapid eye movement sleep during a strategically delayed sleep

Transition to night shift may be improved by strategically delaying the main sleep preceding a first night shift. However, the effects of delayed timing on sleep may differ between chronotypes. Therefore, the study aim was to compare the impacts of chronotype on sleep quality and architecture during a normally timed sleep opportunity and a delayed sleep opportunity. Seventy-two (36 female, 36 male) healthy adults participated in a laboratory study. Participants were provided with a normally timed sleep opportunity (23:00–08:00) and a delayed sleep opportunity (03:00–12:00) over two consecutive nights in a sleep laboratory. Sleep was monitored by polysomnography (PSG), and chronotype was determined from dim light melatonin onset (DLMO). A tertile split of DLMO defined early (20:24 ± 0:42 h), intermediate (21:31 ± 0:12 h), and late chronotype (22:56 ± 0:54 h) categories. Although there was no main effect of chronotype on any sleep measure, early chronotypes obtained less total sleep with delayed sleep than with normally timed sleep (p = 0.044). Intermediate and late chronotypes obtained more rapid eye movement (REM) sleep with delayed sleep than with normally timed sleep (p = 0.013, p = 0.012 respectively). Wake was more elevated for all chronotypes in the later hours of the delayed sleep opportunity than at the start of the sleep opportunity. Strategically delaying the main sleep preceding a first night shift appears to benefit intermediate and late chronotypes (i.e., more REM sleep), but not early chronotypes (i.e., less total sleep). Circadian processes appear to elevate wakefulness for all chronotypes in the later stages of a delayed sleep opportunity.     

Ankle dexterity remains intact in patients with incomplete spinal cord injury in contrast to stroke patients

The present study assessed the influence of visual feedback on stance stability and soleus H-reflex excitability. The centre of pressure (COP) displacement was measured in upright stance on a rigid surface (stable surface) and on a spinning top (unstable surface) while subjects either received “normal” visual feedback (without laser pointer = WLP) or pointed with a laser pointer on a target on the wall (LP). In order to verify that laser pointing influenced visual feedback, two additional experiments were conducted: (1) Subjects performed a finger reaction task which was thought to increase attention and cognitive demands without alteration of the visual feedback. (2) The effect of laser pointing on the wall was compared with pointing at a board, which was attached to the subjects themselves. In this case, the laser point could not serve as a reference for sway because the board moved in synchrony with the body. On stable and unstable surface, COP displacement was reduced in the LP compared to the WLP task (−17 cm ± 6, P < 0.05; −14 cm ± 6, P < 0.05). Conversely, H-reflexes were greater in the LP condition (stable: +20 μV ± 30, not significant; unstable +115 μV ± 40, P < 0.05). Stance stability and H-reflex modulation were negatively correlated (R ² = −0.5; P < 0.001). The finger reaction task did neither influence COP displacement nor H-reflexes. Pointing at the body-fixed target did not alter COP displacement. These findings suggest that postural sway can be reduced by a handheld laser pointer targeting on an external reference point. It is argued that altered visual input was responsible for modulating the H-reflex.     

Reestablishment of individual sleep structure during a single 14‐h recovery sleep episode after 58 h of wakefulness

Sleep structure is highly stable within individuals but different between individuals. The present study investigated robustness of the individual sleep structure to extended total sleep deprivation. Seventeen healthy men spent a baseline night (23:00–07:00 hours), 58 h of sleep deprivation and a 14‐h recovery night (17:00–07:00 hours) in the laboratory. Intraclass correlation coefficients showed that the agreement between baseline and recovery with respect to the proportion of the different sleep stages increased as a function of recovery sleep duration. High values were reached for most of the sleep stages at the end of 14 h of recovery sleep (intraclass correlation coefficients between 0.38 and 0.76). If sleep duration of the recovery night is extended to 14 h, sleep stage distribution resembles that of a baseline night underlining the robustness of the individual sleep structure.     

Sleep deprivation increases formation of false memory

Retrieving false information can have serious consequences. Sleep is important for memory, but voluntary sleep curtailment is becoming more rampant. Here, the misinformation paradigm was used to investigate false memory formation after 1 night of total sleep deprivation in healthy young adults (N = 58, mean age ± SD = 22.10 ± 1.60 years; 29 males), and 7 nights of partial sleep deprivation (5 h sleep opportunity) in these young adults and healthy adolescents (N = 54, mean age ± SD = 16.67 ± 1.03 years; 25 males). In both age groups, sleep‐deprived individuals were more likely than well‐rested persons to incorporate misleading post‐event information into their responses during memory retrieval (P < 0.050). These findings reiterate the importance of adequate sleep in optimal cognitive functioning, reveal the vulnerability of adolescents' memory during sleep curtailment, and suggest the need to assess eyewitnesses' sleep history after encountering misleading information.     

Emotional working memory during sustained wakefulness

In the present study we investigated whether one night of sleep deprivation can affect working memory (WM) performance with emotional stimuli. Twenty‐five subjects were tested after one night of sleep deprivation and after one night of undisturbed sleep at home. As a second aim of the study, to evaluate the cumulative effects of sleep loss and of time‐of‐day changes on emotional WM ability, the subjects were tested every 4 h, from 22:00 to 10:00 hours, in four testing sessions during the sleep deprivation period (deprivation sessions: D1, D2, D3 and D4). Subjects performed the following test battery: Psychomotor Vigilance Task, 0‐back task, 2‐back task and an ‘emotional 2‐back task’ with neutral, positive and negative emotional pictures selected from the International Affective Picture System. Results showed lower accuracy in the emotional WM task when the participants were sleep‐deprived relative to when they had slept, suggesting the crucial role of sleep for preserving WM ability. In addition, the accuracy for the negative pictures remains stable during the sessions performed from 22:00 to 06:00 hours (D1, D2 and D3), while it drops at the D4 session, when the participants had accumulated the longest sleep debt. It is suggested that, during sleep loss, attentional and WM mechanisms may be sustained by the higher arousing characteristics of the emotional (negative) stimuli.     

Slow oscillating transcranial direct current stimulation during sleep has a sleep‐stabilizing effect in chronic insomnia: a pilot study

Recent evidence suggests that lack of slow‐wave activity may play a fundamental role in the pathogenesis of insomnia. Pharmacological approaches and brain stimulation techniques have recently offered solutions for increasing slow‐wave activity during sleep. We used slow (0.75 Hz) oscillatory transcranial direct current stimulation during stage 2 of non‐rapid eye movement sleeping insomnia patients for resonating their brain waves to the frequency of sleep slow‐wave. Six patients diagnosed with either sleep maintenance or non‐restorative sleep insomnia entered the study. After 1 night of adaptation and 1 night of baseline polysomnography, patients randomly received sham or real stimulation on the third and fourth night of the experiment. Our preliminary results show that after termination of stimulations (sham or real), slow oscillatory transcranial direct current stimulation increased the duration of stage 3 of non‐rapid eye movement sleep by 33 ± 26 min (P = 0.026), and decreased stage 1 of non‐rapid eye movement sleep duration by 22 ± 17.7 min (P = 0.028), compared with sham. Slow oscillatory transcranial direct current stimulation decreased stage 1 of non‐rapid eye movement sleep and wake time after sleep‐onset durations, together, by 55.4 ± 51 min (P = 0.045). Slow oscillatory transcranial direct current stimulation also increased sleep efficiency by 9 ± 7% (P = 0.026), and probability of transition from stage 2 to stage 3 of non‐rapid eye movement sleep by 20 ± 17.8% (P = 0.04). Meanwhile, slow oscillatory transcranial direct current stimulation decreased transitions from stage 2 of non‐rapid eye movement sleep to wake by 12 ± 6.7% (P = 0.007). Our preliminary results suggest a sleep‐stabilizing role for the intervention, which may mimic the effect of sleep slow‐wave‐enhancing drugs.     

Respiratory sinus arrhythmia during sleep in children with upper airway obstruction

Upper airway obstruction during adulthood is associated with cardiovascular morbidity; cardiovascular consequences of childhood upper airway obstruction are less well established. This study aimed at investigating the effect of childhood upper airway obstruction on respiratory sinus arrhythmia as a measure of cardiac vagal modulation during night‐time sleep. Overnight polysomnography was conducted in 40 healthy children (20 M; age: 7.5 ± 2.6 years; body mass index percentile: 60.7 ± 26.4%) and 40 children with upper airway obstruction (24 M; age: 7.5 ± 2.7 years; body mass index percentile: 65.8 ± 31.9%). We used the phase‐averaging technique to compute respiratory sinus arrhythmia amplitude and phase delay. To study sleep stage effects and the effect of upper airway obstruction, respiratory sinus arrhythmia was measured during all artefact‐free sleep episodes, and after exclusion of respiratory events. A significant increase in respiratory sinus arrhythmia amplitude and phase delay was observed during stage 4 sleep as compared with rapid eye movement sleep in both groups (amplitude: controls = 0.10 ± 0.03 versus 0.07 ± 0.02 s, P < 0.01, respectively, and upper airway obstruction = 0.07 ± 0.03 versus 0.05 ± 0.03 s, P < 0.05, respectively; phase delay: controls = 3.1 ± 0.1 versus 3.0 ± 0.1 rad, P < 0.05, respectively, and upper airway obstruction = 3.13 ± 0.04 versus 3.04 ± 0.08 rad, P < 0.01, respectively). A significant association between respiratory sinus arrhythmia and apnea/hypopnea index was observed during stage 2 sleep in children with upper airway obstruction. Compared with healthy controls, a significant decrease in respiratory sinus arrhythmia amplitude during stage 2 sleep was observed in children with upper airway obstruction (0.09 ± 0.03 versus 0.06 ± 0.03 s, P < 0.05). However, this difference was not apparent when respiratory events were excluded from analysis. Importantly, respiratory sinus arrhythmia showed a strong negative correlation with body mass index. In conclusion, night‐time respiratory sinus arrhythmia in children is sleep stage dependent and normal during quiet sleep in children with relatively mild upper airway obstruction.     

Motor sequence consolidation: constrained by critical time windows or competing components

Skill improvements may develop between practice sessions during memory consolidation. Skill enhancement within an egocentric coordinate frame develops over wake, whereas skill enhancement in an allocentric coordinate frame develops over a night of sleep. We tested whether both types of improvement could develop over two different 24-h intervals: 8 am to 8 am or from 8 pm to 8 pm. We found that for each 24 h interval, only one type of skill improvement was seen. Despite passing through wake and a night of sleep participants only showed skill improvements commensurate with either a night of sleep or a day awake. The nature of the off-line skill enhancement was determined by when consolidation occurred within the normal sleep–wake cycle. We conclude that motor sequence consolidation is constrained either by having critical time windows or by a competitive interaction in which improvements within one co-ordinate frame actively block improvements from developing in the alternative co-ordinate frame.     

Evidence of break-points in breathing pattern at the gas-exchange thresholds during incremental cycling in young, healthy subjects

The present study investigated whether ‘break-points’ in breathing pattern correspond to the first ( G_\textEX1 G_{{{\text{EX}}_{1} }} ) and second gas-exchange thresholds ( G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} ) during incremental cycling. We used polynomial spline smoothing to detect accelerations and decelerations in pulmonary gas-exchange data, which provided an objective means of ‘break-point’ detection without assumption of the number and shape of said ‘break-points’. Twenty-eight recreational cyclists completed the study, with five individuals excluded from analyses due to low signal-to-noise ratios and/or high risk of ‘pseudo-threshold’ detection. In the remaining participants (n = 23), two separate and distinct accelerations in respiratory frequency (f _R) during incremental work were observed, both of which demonstrated trivial biases and reasonably small ±95% limits of agreement (LOA) for the G_\textEX1 G_{{{\text{EX}}_{1} }} (0.2 ± 3.0 ml O₂ kg⁻¹ min⁻¹) and G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} (0.0 ± 2.4 ml O₂ kg⁻¹ min⁻¹), respectively. A plateau in tidal volume (V _T) data near the G_\textEX1 G_{{{\text{EX}}_{1} }} was identified in only 14 individuals, and yielded the most unsatisfactory mean bias ±LOA of all comparisons made (−0.4 ± 5.3 ml O₂ kg⁻¹ min⁻¹). Conversely, 18 individuals displayed V _T-plateau in close proximity to the G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} evidenced by a mean bias ± LOA of 0.1 ± 3.1 ml O₂ kg⁻¹ min⁻¹. Our findings suggest that both accelerations in f _R correspond to the gas-exchange thresholds, and a plateau (or decline) in V _T at the G_{\textEX 2} G_{{{\text{EX}}_{ 2} }} is a common (but not universal) feature of the breathing pattern response to incremental cycling.     

Cardiac function and arteriovenous oxygen difference during exercise in obese adults

The purpose of this study was to assess cardiac function and arteriovenous oxygen difference (a-vO₂ difference) at rest and during exercise in young, normal-weight (n = 20), and obese (n = 12) men and women who were matched for age and fitness level. Participants were assessed for body composition, peak oxygen consumption (VO_2peak), and cardiac variables (thoracic bioimpedance)—cardiac index (CI), cardiac output (Q), stroke volume (SV), heart rate (HR), and ejection fraction (EF)—at rest and during cycling exercise at 65% of VO_2peak. Differences between groups were assessed with multivariate ANOVA and mixed-model ANOVA with repeated measures controlling for sex. Absolute VO_2peak and VO_2peak relative to fat-free mass (FFM) were similar between normal-weight and obese groups (Mean ± SEE 2.7 ± 0.2 vs. 3.3 ± 0.3 l min⁻¹, p = 0.084 and 52.4 ± 1.5 vs. 50.9 ± 2.3 ml kg FFM⁻¹ min⁻¹, p = 0.583, respectively). In the obese group, resting Q and SV were higher (6.7 ± 0.4 vs. 4.9 ± 0.1 l min⁻¹, p < 0.001 and 86.8 ± 4.3 vs. 65.8 ± 1.9 ml min⁻¹, p < 0.001, respectively) and EF lower (56.4 ± 2.2 vs. 65.5 ± 2.2%, p = 0.003, respectively) when compared with the normal-weight group. During submaximal exercise, the obese group demonstrated higher mean CI (8.8 ± 0.3 vs. 7.7 ± 0.2 l min⁻¹ m⁻², p = 0.007, respectively), Q (19.2 ± 0.9 vs. 13.1 ± 0.3 l min⁻¹, p < 0.001, respectively), and SV (123.0 ± 5.6 vs. 88.9 ± 4.1 ml min⁻¹, p < 0.001, respectively) and a lower a-vO₂ difference (10.4 ± 1.0 vs. 14.0 ± 0.7 ml l00 ml⁻¹, p = 0.002, respectively) compared with controls. Our study suggests that the ability to extract oxygen during exercise may be impaired in obese individuals.     

PER3 and ADORA2A polymorphisms impact neurobehavioral performance during sleep restriction

The objective of the study was to determine whether ADORA2A or PER3 polymorphisms contribute to individual responsivity to sleep restriction. Nineteen healthy adults (ages 18–39, 11 males, 8 females) underwent sleep restriction (SR) which consisted of seven nights of 3 h time in bed (TIB) (04:00–07:00). SR was preceded by seven in‐laboratory nights of 10 h TIB (21:00–07:00) and followed by three nights of 8 h TIB (23:00–07:00). Volunteers underwent psychomotor vigilance, objective alertness, and subjective sleepiness assessments throughout. Volunteers were genotyped for the PER3 VNTR polymorphism (PER3^4/4 n = 7; PER3^4/5 n = 10; PER3^5/5 n = 2) and the ADORA2A c.1083T>C polymorphism, (ADORA2A^C/T n = 9; ADORA2A^T/T n = 9; ADORA2A^C/C n = 1) using polymerase chain reaction (PCR). Separate mixed‐model anova s were used to assess contributions of ADORA2A and PER3 polymorphisms. Results showed that PER3^4/4 and ADORA2A^C/T individuals expressed greater behavioral resiliency to SR compared to PER^4/5and ADORA2A^T/T individuals. Our findings contrast with previously reported non‐significant effects for the PER3 polymorphism under a less challenging sleep restriction regimen (4 h TIB per night for five nights). We conclude that PER3 and ADORA2A polymorphisms become more behaviorally salient with increasing severity and/or duration of sleep restriction (based on psychomotor vigilance). Given the small sample size these results are preliminary and require replication.     

Lengthening of the photoperiod influences sleep characteristics before and during total sleep deprivation in rat

The photoperiod has been evidenced to influence sleep regulation in the rat. Nevertheless, lengthening of the photoperiod beyond 30 days seems to have little effect on the 24‐hr baseline level of sleep and the response to total sleep deprivation. We studied the effects of 12:12 (habitual) and 16:8 (long) light–dark photoperiods on sleep, locomotor activity and body core temperature, before and after 24 hr of total sleep deprivation. Eight rats were submitted for 14 days to light–dark 12:12 (lights on: 08:00 hours–20:00 hours) followed by total sleep deprivation, and then for 14 days to light–dark 16:8 (light extended to 24:00 hours) followed by total sleep deprivation. Rats were simultaneously recorded for electroencephalogram, locomotor activity and body core temperature for 24 hr before and after total sleep deprivation. At baseline before total sleep deprivation, total sleep time and non‐rapid eye movement sleep per 24 hr and during extended light hours (20:00 hours–24:00 hours) were higher (13% for total sleep time) after light–dark exposure compared with habitual photoperiod, while percentage delta power in non‐rapid eye movements and rapid eye movements were unchanged. Locomotor activity and body core temperature were lower, particularly during extended light hours (20:00 hours–24:00 hours). Following total sleep deprivation, total sleep time and non‐rapid eye movements were significantly lower after long photoperiod between 20:00 hours and 24:00 hours, and between 10:00 hours and 12:00 hours, and unchanged per 24 hr. The percentage delta power in non‐rapid eye movements was lower between 08:00 hours and 11:00 hours. Total sleep deprivation decreased locomotor activity and body core temperature after habitual photoperiod exposure only. Fourteen days under long photoperiod (light–dark 16:8) increased non‐rapid eye movements sleep, and decreased sleep rebound related to total sleep deprivation (lower non‐rapid eye movements duration and delta power). This may create a model of sleep extension for the rat that has been found to favour anabolism in the brain and the periphery.     

The homeostatic and circadian sleep recovery responses after total sleep deprivation in mice

Many studies on sleep deprivation effects lack data regarding the recovery period. We investigated the 2‐day homeostatic and circadian sleep recovery response to 24 h of total sleep deprivation (TSD) induced by brief rotation of an activity wheel. Eight mice were implanted with telemetry transmitters (DSI F40‐EET) that recorded simultaneously their electroencephalography (EEG), locomotor activity and temperature during 24 h of baseline (BSL), TSD and 2 days of recovery (D1 and D2). In a second experiment, two groups of five non‐implanted mice underwent TSD or ad libitum sleep, after which they were killed, adrenal glands were weighed and blood was collected for analysis of corticosterone concentration. During TSD mice were awake at least 97% of the time, with a consecutive sleep rebound during D1 that persisted during D2. This was characterized by increases of non‐rapid eye movement (NREM) sleep (44.2 ± 6.9% for D1 and 43.0 ± 7.7% for D2 versus 33.8 ± 9.2% for BSL) and the relative delta band power (179.2 ± 34.4% for D1 and 81.9 ± 11.2% for D2). Greater NREM and REM sleep amounts were observed during the ‘light’ periods. Temperature and locomotor activity characteristics were unchanged during D1 and D2 versus BSL. In non‐implanted mice, corticosterone levels as well as adrenal gland and overall body weights did not differ between TSD and ad libitum sleep groups. In conclusion, 24 h of TSD in an activity wheel without stress responses influence homeostatic sleep regulation with no effect on the circadian regulation over at least 2 days of recovery in mice.     

Measuring individual vulnerability to sleep loss—the CHICa scale

The aim of this project was to construct a psychometrically satisfying scale to describe subjective reactions to sleep deprivation. First, on the basis of a literature review, a list of items was generated which reflected the negatively affected mood and reduced wellbeing associated with sleep loss. Additionally, psychology students were asked to describe their cognitive and emotional symptoms following a night with curtailed sleep. As a result, 69 items were included in the experimental set. University students (n = 102, females, mean age 22.5 ± 1.9 years) completed the form several times during 1 week in June (while preparing for examinations) and on a free day in September; a total of 460 forms were collected. The final, 26‐item version of the scale was validated in a sleep deficit experiment lasting 1 week, conducted with 25 female participants (mean age 23.4 ± 1.9 years). Factor analysis showed 71.7% of total variance explained by four components: impaired thermoregulation (C for cold), disrupted appetite (H for hunger), affective problems (I for irritability) and lowered level of cognitive functioning (Ca for cognitive attenuation). A Polish version of the CHICa scale showed satisfactory psychometric properties. Cronbach's alpha of the subscales were between 0.90 and 0.95. All four subscales exhibited a significant increase with an experimental 3‐h daily sleep restriction over a period of 1 week; cognitive attenuation was the most symptomatic. Cognitive problems (reduced concentration, comprehension and accuracy) and a lack of energy seem to be the most specific subjective manifestations of the chronic sleep deficit state. CHICa may be helpful in research on inter‐and intra‐individual differences and on the efficacy of various counteractive treatments for the consequences of sleep deprivation.     

Daytime course of sleepiness in de novo Parkinson's disease patients

Normal subjects show an increase of sleepiness in the morning, early afternoon and before sleep. In the advanced stages of Parkinson's disease (PD) the mean level of sleepiness is quite high, while with respect to healthy subjects it seems to be unchanged in the early stages. The aim of this study was to evaluate the time–course of the sleepiness level during the wakefulness period in untreated patients with early‐stage Parkinson's disease. Eighteen Parkinson's disease patients who had never been treated before with dopaminergic drugs (male = 9, female = 9, age: 68.39 ± 1.89, mean ± standard error) and 18 healthy subjects (male = 9, female = 9, age: 67.22 ± 1.98) were recruited for this study. All subjects underwent continuous actigraphic recording for three consecutive days, during which they also completed the Karolinska Sleepiness Scale (KSS) once an hour throughout wakefulness. Our results showed a higher level of sleepiness in the patients than the controls in the hours following awakening and in the early afternoon, specifically at 08:00 and 14:00 hours (08:00 hours, PD patients, KSS: 3 ± 0.3 versus healthy subjects, KSS: 2 ± 0.2, P < 0.05; 14:00 hours, PD patients, KSS: 4.4 ± 0.5 versus healthy subjects, KSS: 3 ± 0.3, P < 0.05). We suggest that some daytime hours are sensitive windows showing the first increase of sleepiness which will spread later to the whole daytime.