Individualized and time-variant model for the functional link between thermoregulation and sleep onset

This study makes use of control system model identification techniques to examine the relationship between thermoregulation and sleep regulation. Specifically, data-based mechanistic (DBM) modelling is used to formulate and experimentally test the hypothesis, put forth by Gilbert et al., that there exists a connection between distal heat loss and sleepiness. Six healthy sleepers each spent three nights and the following day in the sleep laboratory: an adaptation, a cognitive arousal and a neutral testing day. In the cognitive arousal condition, a visit of a television camera crew took place and subjects were asked to be interviewed. During each of the three 25-min driving simulator tasks per day, the distal-to-proximal gradient and the electroencephalogram are recorded. It is observed from these experimental data that there exists a feedback connection between thermoregulation and sleep. In addition to providing experimental evidence in support of the Gilbert et al. (2004) hypothesis, the authors propose that the nature of the feedback connection is determined by the nature of sleep/wake state (i.e. NREM sleep versus unwanted sleepiness in active subjects). Besides this, an individualized and time-variant model for the linkage between thermoregulation and sleep onset is presented. This compact model feeds on real-time data regarding distal heat loss and sleepiness and contains a physically meaningful parameter that delivers an individual- and time-depending quantification of a well known biological features in the field of thermoregulation: the thermoregulatory error signal T(hypo)(t)-T(set)(t). A validation of these physical/biological features emphasizes the reliability and power of DBM in describing individual differences related to the sleep process.     

Effects of cognitive arousal and physiological arousal on sleep perception

STUDY OBJECTIVES: Two experiments were conducted to investigate the effect of presleep arousal on sleep perception. Experiment 1 examined the link between presleep cognitive arousal and distorted perception of sleep and compared the relative effect of anxious and neutral cognitive arousal on sleep perception. Experiment 2 compared the relative effect of anxious cognitive arousal and physiological arousal on sleep perception. DESIGN: Participants completed a nap session. Just prior to the nap, the participants were randomly assigned to 1 of 3 groups to receive different arousal manipulations. They were then allowed to go to sleep and were asked to report their sleep perception upon waking. SETTING: Sleep laboratory. PARTICIPANTS: Fifty-four healthy good sleepers in each experiment. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Self-reported sleep, actigraphy-defined sleep, and the discrepancy between them were indexed. In Experiment 1, participants who were experimentally manipulated to experience anxious cognitive arousal during the presleep period reported longer sleep-onset latency. Both the Anxious Cognitive Arousal Group and the Neutral Cognitive Arousal Group exhibited a greater discrepancy between self-reported and actigraphy-defined sleep, relative to participants who received no manipulation. In Experiment 2, participants who were experimentally manipulated to experience anxious cognitive arousal or physiological arousal during the presleep period reported longer sleep-onset latency and shorter total sleep time, and both groups exhibited a greater discrepancy between the self-reported and actigraphy-defined sleep, relative to participants who received no manipulation. CONCLUSIONS: Results suggest that both presleep cognitive arousal and presleep physiological arousal contribute to distorted perception of sleep.     

Prospective comparison of subjective arousal during the pre-sleep period in primary sleep-onset insomnia and normal sleepers

Psychophysiological insomnia (PI) is the most common insomnia subtype, representing 12-15% of all sleep centre referrals. Diagnostic guidelines describe PI as an intrinsic sleep disorder involving both hyperarousal and learned sleep-preventing associations. Whilst evidence for the first component is reasonably compelling, evidence for learned (conditioned) sleep effects is markedly lacking. Indeed, to date no study has attempted to capture directly the conditioned arousal effect assumed to characterize the disorder. Accordingly, the present study explored variations in subjective arousal over time in 15 PI participants (sleep onset type) and 15 normal sleepers (NS). Self-report measures of cognitive arousal, somatic arousal and sleepiness were taken at three time points: 3 h before bedtime (early to mid-evening); 1 h before bedtime (late evening); and in the bedroom at lights out (bedtime) across four, 24-h cycles. Fluctuations in mean arousal and sleepiness values, and in day-to-day variation were examined using analyses of variance. Participants with PI were significantly more cognitive aroused and significantly less sleepy relative to NS, within the bedroom environment. These results support the tenet of conditioned mental arousal to the bedroom, although competing explanations cannot be ruled out. Results are discussed with reference to extant insomnia models.     

The impact of driver sleepiness on fixation‐related brain potentials

The effects of driver sleepiness are often quantified as deteriorated driving performance, increased blink durations and high levels of subjective sleepiness. Driver sleepiness has also been associated with increasing levels of electroencephalogram (EEG) power, especially in the alpha range. The present exploratory study investigated a new measure of driver sleepiness, the EEG fixation‐related lambda response. Thirty young male drivers (23.6 ± 1.7 years old) participated in a driving simulator experiment in which they drove on rural and suburban roads in simulated daylight versus darkness during both the daytime (full sleep) and night‐time (sleep deprived). The results show lower lambda responses during night driving and with longer time on task, indicating that sleep deprivation and time on task cause a general decrement in cortical responsiveness to incoming visual stimuli. Levels of subjective sleepiness and line crossings were higher under the same conditions. Furthermore, results of a linear mixed‐effects model showed that low lambda responses are associated with high subjective sleepiness and more line crossings. We suggest that the fixation‐related lambda response can be used to investigate driving impairment induced by sleep deprivation while driving and that, after further refinement, it may be useful as an objective measure of driver sleepiness.     

Effects of moderate sleep deprivation and low-dose alcohol on driving simulator performance and perception in young men

STUDY OBJECTIVE: To determine the combined effects of sleep restriction and low-dose alcohol on driving simulator performance, EEG, and subjective levels of sleepiness and performance in the mid-afternoon. DESIGN: Repeated measures with 4 experimental conditions. Normal sleep without alcohol, sleep restriction alone (4 hours) and sleep restriction in combination with 2 different low blood alcohol concentrations (0.025 g/dL and 0.035 g/dL). SETTING: Sleep Laboratory, Adelaide Institute for Sleep Health. PARTICIPANTS: Twenty-one healthy young men, aged 18-30 years, mean (+/-SD) = 22.5(+/-3.7) years, BMI = 25(+/-6.7) kg/m2; all had normal sleep patterns and were free of sleep disorders. MEASUREMENTS: Participants completed a 70-minute simulated driving session, commencing at 14:00. Driving parameters included steering deviation, braking reaction time, and number of collisions. Alpha and theta EEG activity and subjective driving performance and sleepiness were also measured throughout the driving task. RESULTS: All measures were significantly affected by time. Steering deviation increased significantly when sleep restriction was combined with the higher dose alcohol. This combination also resulted in a significant increase in alpha/theta EEG activity throughout the drive, as well as greater subjective sleepiness and negative driving performance ratings compared to control or sleep restriction alone. DISCUSSION: These data indicate that combining low-dose alcohol with moderate sleep restriction results in significant decrements to subjective alertness and performance as well as to some driving performance and EEG parameters. This highlights the potential risks of driving after consumption of low and legal doses of alcohol when also sleep restricted.     

Physiological arousal and attention during a week of continuous sleep restriction

Waking brain physiology underlying deficits from continuous sleep restriction (CSR) is not well understood. Fourteen good sleepers participated in a 21-day protocol where they slept their usual amount in a baseline week, had their time in bed restricted by 33% in a CSR week, and slept the desired amount in a recovery week. Participants slept at home, completing diaries and wearing activity monitors to verify compliance. Each day participants completed an RT task and mood and sleepiness ratings every 3 h. Laboratory assessment of electrophysiology and performance took place at the end of baseline, three times throughout the CSR week, and at the beginning of recovery. Participants reported less sleep during CSR which was confirmed by activity monitors. Correspondingly, well-being and neurobehavioural performance was impaired. Quantitative EEG analysis revealed significantly reduced arousal between the 1st and 7th days of restriction and linear effects at anterior sites (Fp2, Fz, F8, T8). At posterior sites (P4, P8), reductions occurred only later in the week between the 4th and 7th nights of restriction. Both the immediate linear decline in arousal and precipitous drop later in the week were apparent at central sites (C4, Cz). Thus, frontal regions were affected immediately, while parietal regions showed maintenance of function until restriction was more severe. The P300 ERP component showed evidence of reduced attention by the 7th day of restriction (at Pz, P4). EEG and ERPs deficits were more robust in the right-hemisphere, which may reflect greater vulnerability to sleep loss in the non-dominant hemisphere.     

Temporal profile of prolonged, night-time driving performance: breaks from driving temporarily reduce time-on-task fatigue but not sleepiness

Breaks are often used by drivers to counteract sleepiness and time-on-task fatigue during prolonged driving. We examined the temporal profile of changes in driving performance, electroencephalogram (EEG) activity and subjective measures of sleepiness and fatigue during prolonged nocturnal driving in a car simulator. In addition, the study examined the impact of regular breaks from driving on performance, sleepiness and fatigue. Healthy volunteers (n=12, 23-45 years) maintained a regular sleep-wake pattern for 14 days and were then in a laboratory from 21:00 to 08:30 hours. The driving simulator scene was designed to simulate monotonous night-time rural driving. Participants drove 4 × 2-h test sessions, with a break from driving of 1 h between each session. During the break participants performed tests assessing sleepiness and fatigue, and psychomotor performance (~30 mins), and then were permitted to sit quietly. They were monitored for wakefulness, and not permitted to nap or ingest caffeine. EEG was recorded during the driving task, and subjective assessments of sleepiness and fatigue were obtained at the start and completion of each session. We found that driving performance deteriorated (2.5-fold), EEG delta, theta and alpha activity increased, and subjective sleepiness and fatigue ratings increased across the testing period. Driving performance and fatigue ratings improved following the scheduled breaks from driving, while the breaks did not affect EEG activity and subjective sleepiness. Time-on-task effects increased through the testing period, indicating that these effects are exacerbated by increasing sleepiness. Breaks from driving without sleep temporarily ameliorate time-on-task fatigue, but provide little benefit to the sleepy driver.     

Sleep latency testing as a time course measure of state arousal

The purpose of this study was to determine how long the effects of a brief period of physiological arousal persisted using repeated sleep latency testing and measurement of heart rate. Thirteen normal sleeping young adults spent two non-consecutive nights and the following days in the laboratory. On each day, subjects had five sleep latency measurements - at 09:00, 09:30, 10:00, 10:30, and 11:00 hours. The 09:00 test was a premanipulation baseline. Following this nap, subjects either walked for 5 min (on one day) or rested in bed for 10 min (on another day) prior to the 09:30 hours sleep latency test. Significant increases in sleep latency were found at 09:30, 10:00, and 11:00 hours following the single 5-min walk as compared with resting in bed (mean sleep latency after the walk was 11.7 min compared with 7.1 min for the resting condition). Heart rate was significantly higher throughout all of the postmanipulation naps following the walk. The elevated sleep latency is probably secondary to the changes in underlying physiological arousal as measured in this study by heart rate.     

The influence of pre-sleep cognitive arousal on sleep onset processes

Cognitive hyperarousal, resulting in enhanced cognitive activation, has been cited as an important contributor to the development and preservation of insomnia. To further understand this process, our study examined the effects of acutely-induced pre-sleep cognitive hyperarousal on sleep onset processes in healthy volunteers. Following an adaptation night, 15 subjects slept two nights in our sleep laboratory: one reference night and another one with cognitive arousal induction, in a counterbalanced order. In the cognitive arousal condition, subjects worked through half an hour of cognitive tasks without interference of an emotional component prior to retiring to bed. Objective sleep onset latency was significantly prolonged in the cognitive arousal condition compared to the reference condition. Significantly more high frequency activity was recorded during the first and second deep-sleep period. Moreover, differences in heart rate and proximal temperature during and after sleep onset were observed in the nights after the cognitive induction. Pre-sleep cognitive activation successfully induced a significant cognitive load and activation in our subjects to influence subsequent sleep (onset) processes.     

Efficacy of a 'functional energy drink' in counteracting driver sleepiness

Driver sleepiness is a major cause of serious road crashes. Coffee is often used as an effective countermeasure to driver sleepiness. However, the caffeine levels in coffee are variable, whereas certain proprietary "functional energy drinks" (FEDs) contain known levels of caffeine (and other ingredients). We investigated the effectiveness of a well-known FED in reducing sleepiness in drivers. Twelve healthy young adults drove an instrumented car simulator between 14:00 and 17:00 h. Their sleepiness was enhanced by sleep restriction to 5 h the night before. Following a pretreatment 30-min drive and at the beginning of a 30-min break, participants were given double-blind 250-ml FED (containing sucrose, glucose, 80-mg caffeine, taurine, glucuronolactone and vitamins) vs. a control drink with the same volume and same taste but without caffeine, taurine and glucuronolactone. Two hours of continuous driving ensued. Lane drifting, subjective sleepiness and the electroencephalogram (EEG) were monitored throughout. Compared with the control, the FED significantly reduced sleep-related driving incidents and subjective sleepiness for the first 90 min of the drive. There was a trend for the EEG to reflect less sleepiness during this period. It was concluded that the FED is beneficial in reducing sleepiness and sleep-related driving incidents under conditions of afternoon monotonous driving following sleep restriction the night before.     

CNS arousal and neurobehavioral performance in a short-term sleep restriction paradigm

Few studies have investigated waking electrophysiological measures of arousal during sleep restriction. This study examined electroencephalogram (EEG) activity and performance during a 96-hour laboratory protocol where participants slept a baseline night (8 h), were randomly assigned to 3-, 5-, or 8-hour sleep groups for the next two nights sleep restriction (SR1, SR2), and then slept a recovery night (8 h). There were dose-dependent deficits on measures of mood, sleepiness, and reaction time that were apparent during this short-term bout of sleep restriction. The ratio of alpha to theta EEG recorded at rest indicated dose-dependent changes in CNS arousal. At 9:00 hours, both the 3- and 5-hour groups showed EEG slowing (sleepiness) during restriction, with the 3-hour group exhibiting greater deficits. Later in the day at 13:00 hours, the 5-hour group no longer exhibited EEG slowing, but the extent of slowing was more widespread across the scalp for the 3-hour group. High-frequency EEG, a measure of effort, was greater on the mornings following sleep restriction. The 5-hour group had increased beta EEG at central-parietal sites following both nights of restriction, whereas the 3-hour group had increased beta and gamma EEG at occipital regions following the first night only. Short-term sleep restriction leads to deficits in performance as well as EEG slowing that correspond to the amount and duration of sleep loss. High-frequency EEG may be a marker of effort or compensation.     

Evening administration of melatonin and bright light: Interactions on the EEG during sleep and wakefulness

Both the pineal hormone melatonin and light exposure are considered to play a major role in the circadian regulation of sleep. In a placebo- controlled balanced cross-over design, we investigated the acute effects of exogenous melatonin (5 mg p.o. at 20.40 hours) with or without a 3-h bright light exposure (5000 lux from 21.00 hours–24.00 hours) on subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in healthy young men. The acute effects of melatonin, bright light and their interaction were measured on the first day (treatment day), possible circadian phase shifts were assessed on the post-treatment day. On the treatment day, the evening rise in subjective sleepiness was accelerated after melatonin and protracted during bright light exposure. These effects were also reflected in specific changes of EEG power density in the theta/alpha range during wakefulness. Melatonin shortened and bright light increased sleep latency. REMS latency was reduced after melatonin administration but bright light had no effect. Slow-wave sleep and slow-wave activity during the first non-rapid eye movement (NREMS) episode were suppressed after melatonin administration and rebounded in the second NREMS episode, independent of whether light was co-administered or not. Self rated sleep quality was better after melatonin administration whereas the awakening process was rated as more difficult after bright light. On the post-treatment day after evening bright light, the rise in sleepiness and the onset of sleep were delayed, independent of whether melatonin was co-administered or not. Thus, although acute bright light and melatonin administration affected subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in a additive manner, the phase shifting effect of a single evening bright light exposure could not be blocked by exogenous melatonin     

What is the moment of sleep onset for insomniacs?

Subjective estimates of sleep latency were compared with three EEG-assessed measures of sleep onset: (a) the traditional one, i.e., the first epoch that is scored as stage 2 sleep; (b) the beginning of the first 15 min of uninterrupted stage 2 sleep; and (c) the beginning of the first 30 min of uninterrupted stage 2 sleep. A total of 56 insomniacs and 10 good sleepers were studied for 3 nights each in the laboratory. The traditional measure of sleep latency agreed best with the subjective estimates of good sleepers. Most insomniacs, however, were best able to estimate their sleep latency when the 15-min criterion was used. We suggest that for most insomniacs the subjective experience of being asleep occurs later in the EEG-defined transition from waking to sleeping than it does for good sleepers.     

EEG arousal pattern in habitual snorers with and without obstructive sleep apnoea (OSA)

SUMMARY  This study evaluated the arousal pattern and sleep fragmentation in the sleep microstructure of heavy snorers and obstructive sleep apnoea (OSA) patients. Fifteen snorers [Group A, (A + H I) ≤ 10], 15 mild OSA (Group B, A + H I > 10 ≤ 30] and 15 moderate to severe OSA (Group C, A + H I > 30) were studied retrospectively analysing the number, duration and type of arousals according to scoring rules concerning definition (including delta bursts) and length (from 2 to 60 s) of phasic arousal events. The number of arousals per hour of sleep related to respiratory events was higher in Groups B and C, whilst in Group A there was a number of arousals not related to apnoea or hypopnoea. Daytime sleepiness, present in all three groups and measured by a subjective evaluation, correlated with both the number and EEG type of arousal, but not with the duration. Statistical analysis indicated that arousal index related to apnoea or hypopnoea was the best variable for determining the sleepiness risk in OSA and snorers. Sleep microstructure analysis seems a good scoring method for the detection of sleep fragmentation and arousals in relation to abnormal respiratory events.     

Auditory arousal thresholds of good sleepers and poor sleepers with and without flurazepam.

Auditory arousal thresholds of good (N = 12) and poor (N = 12) sleepers (sleep onset insomniacs) were obtained during stage 2, stage 4, and REM sleep at various times of the night. Despite claims of being "light" sleepers who are easily awakened by noise, poor sleeper auditory arousal thresholds were the same as those of good sleepers. Flurazepam (30 mg) increased the auditory arousal thresholds of poor sleepers (N = 6), but the increase was statistically significant only during the period of peak effect which occurred 1--2 hr after ingestion. Consistent with poor sleeper complaints of trouble falling asleep, the return to sleep (i.e., sleep latency) was significantly longer for poor than for good sleepers following stimulus arousals during the first stage 2 and first stage 4 periods of the night. Sleep latencies for good and poor sleepers did not differ significantly following subsequent arousals. The sleep latency following the first stage 2 stimulus arousal was significantly reduced in poor sleepers during flurazepam-induced sleep.     

Subjective sleepiness ratings: the effects of sleep deprivation, circadian rhythmicity and cognitive performance.

Computerized self-report sleepiness scales were administered before and after cognitive testing in a 72-hour sleep deprivation study. The cognitive test battery was administered every 2 hours and took approximately 1-1.25 hours. Two computerized measures of subjective sleepiness were used, one a visual analog scale, the other a Hebrew version of the Stanford sleepiness scale. The results indicated that both accumulated sleep loss, circadian and ultradian (2 cycles/day) factors were significant in determining subjective estimates of sleepiness. The extent of the differences between subjective sleepiness ratings before cognitive testing and after testing was dependent upon the phase of the circadian cycle. These differences were greatest at approximately 0200-0600 hours and least around 1000 hours. A second low point occurred at 1800-2000 hours. Analysis by complex demodulation of the individual subjects' sleepiness rating curves indicated that the amount of variance accounted for by the circadian component increased significantly after cognitive testing.     

Evaluation of activity-based techniques to identify transient arousal in respiratory sleep disorders

Daytime sleepiness and impaired cognitive function can be a consequence of recurrent transient arousal from sleep. Arousal is often associated with abrupt changes in the electroencephalogram (EEG), and such changes can be used as an index of sleep disturbance, but EEG analysis is laborious and requires trained observers. Possible alternative indices of arousal not reliant on EEG analysis were investigated. Recordings were made from 36 sleeping subjects who were being investigated for sleep-related breathing disorders. In each study awakenings and transient arousals according to EEG criteria were compared with activity in five potential indirect indicators of arousal: wrist movement, ankle movement, left and right tibial electromyogram, and phase change in ribcage-abdominal movement. The mean values of sensitivity to arousal ranged from only 25 to 45%. However, their high positive predictive accuracies (PPAs, 68 to 92%) indicated that activity, when present, was usually associated with arousal. Sensitivity to awakenings was higher (71–87%), though PPAs were lower (42 to 63%). For the indicator based on ribcage-abdominal phase, the number of periods of activity showed a significant relation to the number of arousals ( r =0.70, P <0.001). It can be concluded that phase changes in chest/abdomen movement are a useful indicator of arousal associated with obstructive apnoea and related conditions. Limb activity has much lower sensitivity for transient arousal, but may be of value in indicating periods of wakefulness.     

Long sleepers sleep more and short sleepers sleep less: a comparison of older adults who sleep well

To determine some of the risks and benefits of being a long or short sleeper, psychological adjustment, lifestyle, and sleep parameters were investigated in 239 older adults. Responses of people who slept well and who were either long or short sleepers were studied on 48 variables investigating sleep parameters and sleep-related affect and beliefs; daytime fatigue and sleepiness; demographic factors, including age, sex, and income satisfaction; sleep lifestyle factors, including naps, bedtimes, arising times, and the regularity of these; general lifestyle factors, including regularity of mealtimes, overall daytime pleasantness, perceived busyness, diversity and valence of daily activities, and potentially stressful major life events. In addition, 14 variables evaluated aspects of psychological adjustment, including cognitive and somatic arousal, nocturnal tension, anxious, negative, unpleasant and worrying self-talk, depression, anxiety, overall psychopathology, neuroticism, and life satisfaction. Overall, the results indicate that short sleepers get up earlier, spend less time in bed, and have lower sleep efficiencies than their long sleeper counterparts. They eat breakfast earlier, and of course, they sleep less. Only one of the 14 psychological adjustment variables was significant. In view of the many differences between short and long sleepers described in prior research, the lack of differences observed between long and short sleepers is noteworthy.     

High intention to fall asleep causes sleep fragmentation

The aim of this study was to investigate the effects of intention to fall asleep on sleep quality in good sleepers using polysomnographic and subjective nap parameters. We hypothesized that high intention to sleep would lead to arousal, worsening sleep quality. A counterbalanced 2 × 2 experimental design with one intra‐individual (neutral versus motivating instruction) and one inter‐individual (instruction sequence) variable was used. Thirty‐three good sleepers (22 females; mean age: 24.1 ± 8.4 years) each attended two 1‐h daytime polysomnographic recording sessions in the laboratory. When providing motivating instruction, the experimenter insisted on the importance of falling asleep as quickly as possible and promised a financial reward. Compared with neutral instruction, motivating instruction was associated with increased waking after sleep onset, number of awakenings and arousal index during napping. No relationship between instruction and subjective nap appraisal was found. The effect of high intention on sleep fragmentation remained significant after controlling for habitual napping, depression, anxiety and sleepiness. Thus, our findings suggest that high intention to fall asleep worsened sleep quality, especially in terms of sleep fragmentation, in good sleepers.     

Performance and cardiovascular measures in normal adults with extreme MSLT scores and subjective sleepiness levels

STUDY OBJECTIVES: The purpose of this study was to determine the relationship of subjective and objective sleepiness across several nights. Extreme groups were chosen based upon both Multiple Sleep Latency Test (MSLT) findings and report of characteristic subjective sleepiness, and groups were compared across sleep, demographic, performance, and physiologic variables. DESIGN AND SETTING: Subjects spent 3 baseline nights and the following days in the laboratory. Standard polysomnographic recordings were made on each night. On each day, subjects had an MSLT, performance testing, and metabolic and heart rate observation periods. PARTICIPANTS: Participants were 50 adult normal sleepers. INTERVENTIONS: None. MEASUREMENT AND RESULTS: Those subjects with sleep latencies on the MSLT of more than 10 minutes following the adaptation night (Alert) were compared with 2 groups of subjects with sleep latencies on the MSLT of less than 7 minutes following the adaptation night. Subjects with MSLT < 7 were divided into those who reported subjective sleepiness during the day (subjective sleepiness > 1 SD above the mean for the entire group-Sleepy-Sleepy) and those who did not report subjective sleepiness (subjective sleepiness < 1 SD above the mean for the entire group--Sleepy-Alert). The Alert group maintained longer sleep latencies than the other groups and had improved performance on vigilance compared to the Sleepy-Sleepy group on all days and on some days compared to the Sleepy-Alert group. Vigilance was improved in the Sleepy-Alert group compared with the Sleepy-Sleepy group on all days. The Alert group had higher heart rate and increased low/high spectral heart rate power compared to both sleepy groups, and the Sleepy-Alert group had higher heart rate and increased low/high spectral heart rate power compared to the Sleepy-Sleepy group at some points. CONCLUSIONS: It was concluded that normal adults with short MSLT latencies differ from those with longer latencies on both cardiac and performance variables. Also, those individuals with short latencies can be divided into subgroups claiming subjective sleepiness or denying sleepiness. Those denying sleepiness have improved vigilance performance and greater heart rate and low/high spectral heart rate power compared to those with subjective sleepiness. Both the MSLT group differences and the subjective group differences imply that ability to maintain wakefulness and performance in sedentary situations may be related to innate ability to maintain physiologic arousal.