Examination of Sleep and Injury Among College Football Athletes.

Burke, TM, Lisman, PJ, Maguire, K, Skeiky, L, Choynowski, JJ, CapaldiII, VF, Wilder, JN, Brager, AJ, and Dobrosielski, DA. Examination of sleep and injury among college football athletes. J Strength Cond Res 34(3): 609-616, 2020-The purpose of this study was to characterize subjective sleep metrics in collegiate football players at the start of the season, determine the relationship between preseason subjective sleep measures and in-season objective sleep characteristics, and examine the association between subjective and objective sleep metrics and incidence of time-loss injury during the competitive season. Ninety-four Division I football players completed 5 validated sleep-related questionnaires to assess sleep quality, insomnia severity, daytime sleepiness, sleep apnea risk, and circadian preference before the start of the season. Clinical thresholds for sleep questionnaires were used to determine risk of sleep disorders. Continuous wrist actigraphy was collected throughout the season to generalize sleep behaviors. Time-loss injury incidence data were recorded and used for analysis. Results indicated that 67.4% (60 of 89) of athletes scored above clinical threshold in at least 1 questionnaire to indicate sleep disorder risk. At the start of the season, players subjectively reported an average sleep duration of 7:16 ± 1:18 hours:minutes, which was in contrast to the 6:04 ± 0:41 hours:minutes measured through actigraphy during the season. Logistic regression models adjusted for age and body mass index revealed no significant associations between injury and subjective (odds ratio [OR] = 1.00; 95% confidence interval [CI] = 0.99-1.01) and objective (OR = 1.01; 95% CI = 0.99-1.02) sleep duration or measures attained from sleep questionnaires (ORs ranged from 1.01 to 2.87). Sleep metrics (quantity and quality) were not associated with increased risk of injury in this cohort of collegiate football players.

Game Times and Higher Winning Percentages of West Coast Teams of the National Football League Correspond With Reduced Prevalence of Regular Season Injury.

Brager, AJ and Mistovich, RJ. Game times and higher winning percentages of west coast teams of the National Football League correspond with reduced prevalence of regular season injury. J Strength Cond Res 31(2): 462-467, 2017-West coast teams of the National Football League are more statistically likely to win home night games against east coast opponents. The alignment of game times with daily rhythms of alertness is thought to contribute to this advantage. This study aims to determine whether rates of turnovers and injuries during the regular season, putative measures of mental and physical fatigue, impact winning percentages. Regular season schedules and rates of turnovers for each of the 32 teams were obtained from Pro-Football-Reference. We developed our own metric of injury risk for each position obtained from depth charts and regular season schedules. This metric compared cumulative weeks on injury reserve with cumulative time zone travel. West coast teams traveled 4 times as often as east coast teams. However, teams traveling eastward won twice as many games. There was no relationship between the extent and direction of travel and number of turnovers. Losing teams had more turnovers. The offensive and defensive lines in Central Time (CT) were placed on injury reserve 4 times as often as offensive and defensive lines in Pacific Time (PT). Injury prevalence in CT vs. PT was most prominent midseason. Plotting midseason game time relative to biological time revealed that PT teams play games closer to endogenous peaks in alertness, whereas CT teams play games closer to endogenous troughs in alertness. Overall, closer alignment of game time with the endogenous "alerting" signal may protect west coast teams from fatigue-related injuries and suggests for modified strength and conditioning programs.

Maternal Ube3a Loss Disrupts Sleep Homeostasis But Leaves Circadian Rhythmicity Largely Intact.

Individuals with Angelman syndrome (AS) suffer sleep disturbances that severely impair quality of life. Whether these disturbances arise from sleep or circadian clock dysfunction is currently unknown. Here, we explored the mechanistic basis for these sleep disorders in a mouse model of Angelman syndrome (Ube3a(m-/p+) mice). Genetic deletion of the maternal Ube3a allele practically eliminates UBE3A protein from the brain of Ube3a(m-/p+) mice, because the paternal allele is epigenetically silenced in most neurons. However, we found that UBE3A protein was present in many neurons of the suprachiasmatic nucleus--the site of the mammalian circadian clock--indicating that Ube3a can be expressed from both parental alleles in this brain region in adult mice. We found that while Ube3a(m-/p+) mice maintained relatively normal circadian rhythms of behavior and light-resetting, these mice exhibited consolidated locomotor activity and skipped the timed rest period (siesta) present in wild-type (Ube3a(m+/p+)) mice. Electroencephalographic analysis revealed that alterations in sleep regulation were responsible for these overt changes in activity. Specifically, Ube3a(m-/p+) mice have a markedly reduced capacity to accumulate sleep pressure, both during their active period and in response to forced sleep deprivation. Thus, our data indicate that the siesta is governed by sleep pressure, and that Ube3a is an important regulator of sleep homeostasis. These preclinical findings suggest that therapeutic interventions that target mechanisms of sleep homeostasis may improve sleep quality in individuals with AS. SIGNIFICANCE STATEMENT: Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by loss of expression of the maternal copy of the UBE3A gene. Individuals with AS have severe sleep dysfunction that affects their cognition and presents challenges to their caregivers. Unfortunately, current treatment strategies have limited efficacy due to a poor understanding of the mechanisms underlying sleep disruptions in AS. Here we demonstrate that abnormal sleep patterns arise from a deficit in accumulation of sleep drive, uncovering the Ube3a gene as a novel genetic regulator of sleep homeostasis. Our findings encourage a re-evaluation of current treatment strategies for sleep dysfunction in AS, and suggest that interventions that promote increased sleep drive may alleviate sleep disturbances in individuals with AS.

The Negative Effects of Travel on Student Athletes Through Sleep and Circadian Disruption.

Collegiate athletes must satisfy the academic obligations common to all undergraduates, but they have the additional structural and social stressors of extensive practice time, competition schedules, and frequent travel away from their home campus. Clearly such stressors can have negative impacts on both their academic and athletic performances as well as on their health. These concerns are made more acute by recent proposals and decisions to reorganize major collegiate athletic conferences. These rearrangements will require more multi-day travel that interferes with the academic work and personal schedules of athletes. Of particular concern is additional east-west travel that results in circadian rhythm disruptions commonly called jet lag that contribute to the loss of amount as well as quality of sleep. Circadian misalignment and sleep deprivation and/or sleep disturbances have profound effects on physical and mental health and performance. We, as concerned scientists and physicians with relevant expertise, developed this white paper to raise awareness of these challenges to the wellbeing of our student-athletes and their co-travelers. We also offer practical steps to mitigate the negative consequences of collegiate travel schedules. We discuss the importance of bedtime protocols, the availability of early afternoon naps, and adherence to scheduled lighting exposure protocols before, during, and after travel, with support from wearables and apps. We call upon departments of athletics to engage with sleep and circadian experts to advise and help design tailored implementation of these mitigating practices that could contribute to the current and long-term health and wellbeing of their students and their staff members.

Nightmare disorder in active-duty US military personnel.

STUDY OBJECTIVES: Military personnel experience high rates of traumatic experiences. Despite this, few studies have examined the presence of nightmare disorder in military personnel. The primary aim of this study was to examine diagnoses of nightmare disorder across the 4 largest branches of the active-duty US military. DESIGN & PARTICIPANTS: Data and service branch densities used to derive the expected rates of diagnoses of nightmare disorder were drawn from the Defense Medical Epidemiology Database. The branches examined included all active-duty services members in the US Army, Navy, Marine Corps, and Air Force, who served between 2016 and 2021. Single-sample chi-square goodness of fit tests were conducted to examine within-variable differences for military relevant variables. RESULTS: Between 2016 and 2019, the incidence rates of nightmare disorder (per 10,000 service members) in the US Department of Defense ranged from 11.3 in 2016 to a low of 6.9 in 2018. Service members who were classified as non-white, female, over the age of 35, married, in the Army, and/or a noncommissioned officer, were diagnosed at greater rates relative to their representation in the military population (p < .001). CONCLUSION: Our findings of higher than expected rates of nightmare disorder in older, senior service members as well as those in the Army align with the known precipitant of nightmares, and trauma. However, the reason for the finding that female and Black service members have higher than expected rates is not readily apparent.

Cocaine modulates pathways for photic and nonphotic entrainment of the mammalian SCN circadian clock.

Cocaine abuse is highly disruptive to circadian physiological and behavioral rhythms. The present study was undertaken to determine whether such effects are manifest through actions on critical photic and nonphotic regulatory pathways in the master circadian clock of the mouse suprachiasmatic nucleus (SCN). Impairment of SCN photic signaling by systemic (intraperitoneal) cocaine injection was evidenced by strong (60%) attenuation of light-induced phase-delay shifts of circadian locomotor activity during the early night. A nonphotic action of cocaine was apparent from its induction of 1-h circadian phase-advance shifts at midday. The serotonin receptor antagonist, metergoline, blocked shifting by 80%, implicating a serotonergic mechanism. Reverse microdialysis perfusion of the SCN with cocaine at midday induced 3.7 h phase-advance shifts. Control perfusions with lidocaine and artificial cerebrospinal fluid had little shifting effect. In complementary in vitro experiments, photic-like phase-delay shifts of the SCN circadian neuronal activity rhythm induced by glutamate application to the SCN were completely blocked by cocaine. Cocaine treatment of SCN slices alone at subjective midday, but not the subjective night, induced 3-h phase-advance shifts. Lidocaine had no shifting effect. Cocaine-induced phase shifts were completely blocked by metergoline, but not by the dopamine receptor antagonist, fluphenazine. Finally, pretreatment of SCN slices for 2 h with a low concentration of serotonin agonist (to block subsequent serotonergic phase resetting) abolished cocaine-induced phase shifts at subjective midday. These results reveal multiple effects of cocaine on adult circadian clock regulation that are registered within the SCN and involve enhanced serotonergic transmission.

Non-rapid eye movement sleep determines resilience to social stress.

Resilience, the ability to overcome stressful conditions, is found in most mammals and varies significantly among individuals. A lack of resilience can lead to the development of neuropsychiatric and sleep disorders, often within the same individual. Despite extensive research into the brain mechanisms causing maladaptive behavioral-responses to stress, it is not clear why some individuals exhibit resilience. To examine if sleep has a determinative role in maladaptive behavioral-response to social stress, we investigated individual variations in resilience using a social-defeat model for male mice. Our results reveal a direct, causal relationship between sleep amount and resilience-demonstrating that sleep increases after social-defeat stress only occur in resilient mice. Further, we found that within the prefrontal cortex, a regulator of maladaptive responses to stress, pre-existing differences in sleep regulation predict resilience. Overall, these results demonstrate that increased NREM sleep, mediated cortically, is an active response to social-defeat stress that plays a determinative role in promoting resilience. They also show that differences in resilience are strongly correlated with inter-individual variability in sleep regulation.

To many of us, it may seem obvious that sleep is restorative: we feel better after a good night's rest. However, exactly how sleep benefits the brain and body remains poorly understood. One clue may lie in neuropsychiatric disorders: these conditions ­ such as depression and anxiety ­ are often accompanied by disrupted sleep. Additionally, these neuropsychiatric disorders are frequently caused or worsened by stress, which can also interfere with sleep. This close association between stress and sleep has led some to hypothesize that sleep serves to overcome the adverse effects of stress on the brain, but this hypothesis remains largely untested. One type of stress that is common to all mammals is social stress, defined as stress caused by social interactions. This means that mice and other rodents can be subjected to social stress in the laboratory to test hypotheses about the effects of stress on the brain. Importantly, in both animals and humans, there are individual differences in resilience, or the ability to overcome the adverse effects of stress. Based on this information, Bush et al. set out to establish whether sleep can regulate resilience to social stress in mice. When the mice were gently kept awake during their normal sleep time, resilience decreased and so the mice were less able to overcome the negative effects of stress. Conversely, increasing sleep, by activating an area of the brain responsible for initiating sleep, increased the mice's resilience to social stress. Thus, Bush et al. showed that changes in sleep do lead to changes in resilience. To find out whether resilience can be predicted by changes in sleeping patterns, Bush et al. studied how both resilient mice and those susceptible to stress slept before and after social stress. Resilient mice would often sleep more after social stress; meanwhile, few changes were observed in susceptible mice. Surprisingly, sleep quality also predicted resilience, with resilient mice sleeping better than susceptible mice even before exposure to social stress. To determine whether the differences in sleep that predict resilience can be detected as brain activity, Bush et al. placed electrodes in two regions of the prefrontal cortex ­ a part of the brain important for decision-making and social behaviors ­ to measure how mice recovered lost sleep. This experiment revealed that the changes in sleep that predict resilience are prominent in the prefrontal cortex. Overall, Bush et al. reveal that sleeping more and sleeping better promote resilience to social stress. Furthermore, the results suggests that lack of sleep may lead to increased risk of stress-related psychiatric conditions. Humans are one of the few species that choose to deprive themselves of sleep: Bush, et al. provide evidence that this choice may have significant consequences on mental health. Furthermore, this work creates a new model that lays the groundwork for future studies investigating how sleep can overcome stress on the brain.

Keeping an eye on circadian time in clinical research and medicine.

BACKGROUND: Daily rhythms are observed in humans and almost all other organisms. Most of these observed rhythms reflect both underlying endogenous circadian rhythms and evoked responses from behaviours such as sleep/wake, eating/fasting, rest/activity, posture changes and exercise. For many research and clinical purposes, it is important to understand the contribution of the endogenous circadian component to these observed rhythms. CONTENT: The goal of this manuscript is to provide guidance on best practices in measuring metrics of endogenous circadian rhythms in humans and promote the inclusion of circadian rhythms assessments in studies of health and disease. Circadian rhythms affect all aspects of physiology. By specifying minimal experimental conditions for studies, we aim to improve the quality, reliability and interpretability of research into circadian and daily (i.e., time-of-day) rhythms and facilitate the interpretation of clinical and translational findings within the context of human circadian rhythms. We describe protocols, variables and analyses commonly used for studying human daily rhythms, including how to assess the relative contributions of the endogenous circadian system and other daily patterns in behaviours or the environment. We conclude with recommendations for protocols, variables, analyses, definitions and examples of circadian terminology. CONCLUSION: Although circadian rhythms and daily effects on health outcomes can be challenging to distinguish in practice, this distinction may be important in many clinical settings. Identifying and targeting the appropriate underlying (patho)physiology is a medical goal. This review provides methods for identifying circadian effects to aid in the interpretation of published work and the inclusion of circadian factors in clinical research and practice.

Acamprosate-responsive brain sites for suppression of ethanol intake and preference.

Acamprosate suppresses alcohol intake and craving in recovering alcoholics; however, the central sites of its action are unclear. To approach this question, brain regions responsive to acamprosate were mapped using acamprosate microimplants targeted to brain reward and circadian areas implicated in alcohol dependence. mPer2 mutant mice with nonfunctional mPer2, a circadian clock gene that gates endogenous timekeeping, were included, owing to their high levels of ethanol intake and preference. Male wild-type (WT) and mPer2 mutant mice received free-choice (15%) ethanol/water for 3 wk. The ethanol was withdrawn for 3 wk and then reintroduced to facilitate relapse. Four days before ethanol reintroduction, mice received bilateral blank or acamprosate-containing microimplants releasing ∼50 ng/day into reward [ventral tegmental (VTA), peduculopontine tegmentum (PPT), and nucleus accumbens (NA)] and circadian [intergeniculate leaflet (IGL) and suprachiasmatic nucleus (SCN)] areas. The hippocampus was also targeted. Circadian locomotor activity was measured throughout. Ethanol intake and preference were greater in mPer2 mutants than in wild-type (WT) mice (27 g·kg(-1)·day(-1) vs. 13 g·kg(-1)·day(-1) and 70% vs. 50%, respectively; both, P < 0.05). In WTs, acamprosate in all areas, except hippocampus, suppressed ethanol intake and preference (by 40-60%) during ethanol reintroduction. In mPer2 mutants, acamprosate in the VTA, PPT, and SCN suppressed ethanol intake and preference by 20-30%. These data are evidence that acamprosate's suppression of ethanol intake and preference are manifest through actions within major reward and circadian sites.

Acute ethanol disrupts photic and serotonergic circadian clock phase-resetting in the mouse.

BACKGROUND: Alcohol dependence is associated with impaired circadian rhythms and sleep. Ethanol administration disrupts circadian clock phase-resetting, suggesting a mode for the disruptive effect of alcohol dependence on the circadian timing system. In this study, we extend previous work in C57BL/6J mice to: (i) characterize the suprachiasmatic nucleus (SCN) pharmacokinetics of acute systemic ethanol administration, (ii) explore the effects of acute ethanol on photic and nonphotic phase-resetting, and (iii) determine if the SCN is a direct target for photic effects. METHODS: First, microdialysis was used to characterize the pharmacokinetics of acute intraperitoneal (i.p.) injections of 3 doses of ethanol (0.5, 1.0, and 2.0 g/kg) in the mouse SCN circadian clock. Second, the effects of acute i.p. ethanol administration on photic phase delays and serotonergic ([+]8-OH-DPAT-induced) phase advances of the circadian activity rhythm were assessed. Third, the effects of reverse-microdialysis ethanol perfusion of the SCN on photic phase-resetting were characterized. RESULTS: Peak ethanol levels from the 3 doses of ethanol in the SCN occurred within 20 to 40 minutes postinjection with half-lives for clearance ranging from 0.6 to 1.8 hours. Systemic ethanol treatment dose-dependently attenuated photic and serotonergic phase-resetting. This treatment also did not affect basal SCN neuronal activity as assessed by Fos expression. Intra-SCN perfusion with ethanol markedly reduced photic phase delays. CONCLUSIONS: These results confirm that acute ethanol attenuates photic phase-delay shifts and serotonergic phase-advance shifts in the mouse. This dual effect could disrupt photic and nonphotic entrainment mechanisms governing circadian clock timing. It is also significant that the SCN clock is a direct target for disruptive effects of ethanol on photic shifting. Such actions by ethanol could underlie the disruptive effects of alcohol abuse on behavioral, physiological, and endocrine rhythms associated with alcoholism.

Geographically based risk assessment of sleep disorders and disease states impacting medical readiness across active duty army installations from military medical databases in fiscal year 2017.

BACKGROUND: The impact of sleep disorders on active duty Soldiers' medical readiness is clinically significant. Sleep disorders often present high comorbidity with disease states impacting readiness ranging from obesity and drug dependence. Patient data generated from military health databases can be accessed to examine such relationships. The current study performed a risk assessment of sleep disorders, obesity, tobacco use, and substance abuse based on geographical distribution of active duty Army installations through a comprehensive analysis of the Office of the Army Surgeon General Health of the Force report, specifically for Fiscal Year 2017, which summarizes data collected during 2016. METHODS: Health incidences (percent active duty per installation) were queried from the Health of the Force Fiscal Year 2017 (n = 471,000; 85.5% male, >70% between 18 and 34). Nonparametric ranked tests identified active duty Army installations at low risk (green; <25% percentile relative to mean rank), moderate risk (amber; 25%-50% percentile relative to mean rank), and high risk (red; >75% percentile relative to mean rank). Pearson's correlations determined extent of generalized comorbidity of sleep disorders with obesity, tobacco use, and substance abuse across all installations. RESULTS: Large combat arms and training installations of the Southern U.S. were at highest risk for sleep disorder. Mean rank comparisons for sleep disorders versus obesity (P = .306), tobacco use (P = .378), and substance abuse (P = .591) did not differ for each installation. There was a high degree of generalized comorbidity of diagnosed sleep disorder with obesity (P < .001; r2 = 0.963), tobacco use (P < .001; r2 = 0.928), and substance abuse (P < .001; r2 = 0.968). CONCLUSIONS: These risk assessments mirror geographical risk data from civilian populations which is surprising because there is a large degree of inter-individual variability in geographical origin, race/ethnicity, and socioeconomic statuses within a single Army installation. Nevertheless, these data demonstrate strong geographical influences on medical readiness in active duty Soldiers comparable to civilian sectors.

Self-Reported Sleep Need, Subjective Resilience, and Cognitive Performance Following Sleep Loss and Recovery Sleep.

OBJECTIVE: Individuals vary in response to sleep loss: some individuals are "vulnerable" and demonstrate cognitive decrements following insufficient sleep, while others are "resistant" and maintain baseline cognitive capability. Physiological markers (e.g., genetic polymorphisms) have been identified that can predict relative vulnerability. However, a quick, cost-effective, and feasible subjective predictor tool has not been developed. The objective of the present study was to determine whether two factors-"subjective sleep need" and "subjective resilience"-predict cognitive performance following sleep deprivation. METHODS: Twenty-seven healthy, sleep-satiated young adults participated. These individuals were screened for sleep disorders, comorbidities, and erratic sleep schedules. Prior to 40 hours of in-laboratory total sleep deprivation, participants were questioned on their subjective sleep need and completed a validated resilience scale. During and after sleep deprivation, participants completed a 5-minute psychomotor vigilance test every 2 hours. RESULTS: Both subjective resilience and subjective sleep need individually failed to predict performance during sleep loss. However, these two measures interacted to predict performance. Individuals with low resilience and low sleep need had poorer cognitive performance during sleep loss. However, in individuals with medium or high resilience, psychomotor vigilance test performance was not predicted by subjective sleep need. Higher resilience may be protective against sleep loss-related neurobehavioral impairments in the context of subjective sleep need. CONCLUSIONS: Following sleep loss (and recovery sleep), trait resilient individuals may outperform those with lower resiliency on real-world tasks that require continuous attention. Future studies should determine whether the present findings generalize to other, operationally relevant tasks and additional cognitive domains.

Chronic ethanol disrupts circadian photic entrainment and daily locomotor activity in the mouse.

BACKGROUND: Chronic ethanol abuse is associated with disrupted circadian rhythms and sleep. Ethanol administration impairs circadian clock phase-resetting, suggesting a mode for the disruptive effect of alcohol abuse on circadian timing. Here, we extend previous studies to explore the effects of chronic forced ethanol on photic phase-resetting, photic entrainment, and daily locomotor activity patterns in C57BL/6J mice. METHODS: First, microdialysis was used to characterize the circadian patterns of ethanol uptake in the suprachiasmatic (SCN) circadian clock and correlate this with systemic ethanol levels and episodic drinking of 10 or 15% ethanol. Second, the effects of chronic forced ethanol drinking and withdrawal on photic phase-delays of the circadian activity rhythm were assessed. Third, the effects of chronic ethanol drinking on entrainment to a weak photic zeitgeber (1 minute of 25 lux intensity light per day) were assessed. This method was used to minimize any masking actions of light that could mask ethanol effects on clock entrainment. RESULTS: Peak ethanol levels in the SCN and periphery occurred during the dark phase and coincided with the time when light normally induces phase-delays in mice. These delays were dose-dependently inhibited by chronic ethanol and its withdrawal. Chronic ethanol did not impede re-entrainment to a shifted light cycle but affected entrainment under the weak photic zeitgeber and disrupted the daily pattern of locomotor activity. CONCLUSIONS: These results confirm that chronic ethanol consumption and withdrawal markedly impair circadian clock photic phase-resetting. Ethanol also disturbs the temporal structure of nighttime locomotor activity and photic entrainment. Collectively, these results suggest a direct action of ethanol on the SCN clock.

Environmental modulation of alcohol intake in hamsters: effects of wheel running and constant light exposure.

BACKGROUND: Alcohol abuse leads to marked disruptions of circadian rhythms, and these disturbances in themselves can increase the drive to drink. Circadian clock timing is regulated by light, as well as by nonphotic influences such as food, social interactions, and wheel running. We previously reported that alcohol markedly disrupts photic and nonphotic modes of circadian rhythm regulation in Syrian hamsters. As an extension of this work, we characterize the hedonic interrelationship between wheel running and ethanol (EtOH) intake and the effects of environmental circadian disruption (long-term exposure to constant light [LL]) on the drive to drink. METHODS: First, we tested the effect of wheel running on chronic free-choice consumption of a 20% (v/v) EtOH solution and water. Second, the effect of this alcohol drinking on wheel running in alcohol-naive animals was investigated. Third, we assessed the influence of LL, known to suppress locomotor activity and cause circadian rhythm disruption, on EtOH consumption and wheel-running behavior. RESULTS: Inhibitory effects of wheel running on EtOH intake and vice versa were observed. Exposure to LL, while not affecting EtOH intake, induced rhythm splitting in 75% of the animals. Notably, the splitting phenotype was associated with lower levels of EtOH consumption and preference prior to, and throughout, the period of LL exposure. CONCLUSIONS: These results are evidence that exercise may offer an efficacious clinical approach to reducing EtOH intake. Also, predisposition for light-induced (or other) forms of circadian disruption may modulate the drive to drink.

Effect of cognitive load and emotional valence of distractors on performance during sleep extension and subsequent sleep deprivation.

STUDY OBJECTIVES: The purpose of the present study was to assess the extent to which sleep extension followed by sleep deprivation impacts performance on an attentional task with varying cognitive and attentional demands that influence decisions. METHODS: Task performance was assessed at baseline, after 1 week of sleep extension, and after 40 h of total sleep deprivation. RESULTS: One week of sleep extension resulted in improved performance, particularly for high cognitive load decisions regardless of the emotional salience of attentional distractors. Those who extended sleep the most relative to their habitual sleep duration showed the greatest improvement in general performance during sleep extension. However, a higher percentage of time spent in slow-wave sleep (SWS) on the last night of the sleep extension phase was negatively correlated with performance on more difficult high cognitive load items, possibly reflecting a relatively higher level of residual sleep need. Sleep deprivation generally resulted in impaired performance, with a nonsignificant trend toward greater performance decrements in the presence of emotionally salient distractors. Performance overall, but specifically for high cognitive load decisions, during total sleep deprivation was negatively correlated with longer sleep and higher SWS percentage during subsequent recovery sleep. CONCLUSIONS: The present findings suggest two possibilities: those who performed relatively poorly during sleep deprivation were more vulnerable because (1) they utilized mental resources (i.e. accrued sleep debt) at a relatively faster rate during wakefulness, and/or (2) they failed to "pay down" pre-study sleep debt to the same extent as better-performing participants during the preceding sleep extension phase.

Posttraumatic Stress Disorder, Traumatic Brain Injury, Sleep, and Performance in Military Personnel.

Sleep disturbances, posttraumatic stress disorder, and traumatic brain injury are highly prevalent in military personnel and veterans. These disorders can negatively impact military performance. Although literature evaluating how posttraumatic stress disorder and traumatic brain injury directly impact military performance is limited, there is evidence supporting that these disorders negatively impact cognitive and social functioning. What is not clear is if impaired performance results from these entities individually, or a combination of each. Further research using standardized evaluations for the clinical disorders and metrics of military performance is required to assess the overall performance decrements related to these disorders.

Sleep in the United States Military.

The military lifestyle often includes continuous operations whether in training or deployed environments. These stressful environments present unique challenges for service members attempting to achieve consolidated, restorative sleep. The significant mental and physical derangements caused by degraded metabolic, cardiovascular, skeletomuscular, and cognitive health often result from insufficient sleep and/or circadian misalignment. Insufficient sleep and resulting fatigue compromises personal safety, mission success, and even national security. In the long-term, chronic insufficient sleep and circadian rhythm disorders have been associated with other sleep disorders (e.g., insomnia, obstructive sleep apnea, and parasomnias). Other physiologic and psychologic diagnoses such as post-traumatic stress disorder, cardiovascular disease, and dementia have also been associated with chronic, insufficient sleep. Increased co-morbidity and mortality are compounded by traumatic brain injury resulting from blunt trauma, blast exposure, and highly physically demanding tasks under load. We present the current state of science in human and animal models specific to service members during- and post-military career. We focus on mission requirements of night shift work, sustained operations, and rapid re-entrainment to time zones. We then propose targeted pharmacological and non-pharmacological countermeasures to optimize performance that are mission- and symptom-specific. We recognize a critical gap in research involving service members, but provide tailored interventions for military health care providers based on the large body of research in health care and public service workers.

Earlier shift in race pacing can predict future performance during a single-effort ultramarathon under sleep deprivation.

OBJECTIVE: We constructed research camps at single-effort ultramarathons (50 and 100 miles) in order to study human endurance capabilities under extreme sleep loss and stress. It takes > 24h, on average, to run 100 miles on minimal sleep, allowing us to construct 24h human performance profiles (HPP). METHODS: We collected performance data plotted across time (race splits) and distance (dropout rates; n=257), self-reported sleep and training patterns (n=83), and endpoint data on cardiovascular fitness/adaptation to total sleep deprivation and extreme exercise/stress (n=127). RESULTS: In general, we found that self-reported napping was higher for 100-miler versus 50-miler runners and that ultra-endurance racing may possibly pre-select for early morning risers. We also compared HPPs between the first 50 miles completed by all runners in order to examine amplitude and acrophase differences in performance using a cosinor model. We showed that even though all runners slowed down over time, runners who completed a 100-miler ultramarathon had an earlier acrophase shift in race pace compared to non-finishers. DISCUSSION: We were able to identify time-dependent predictions on overall performance under minimal sleep, warranting the ultramarathon athlete as a unique demographic for future study of sleep and chronobiological relationships in the real world.

TNFα G308A genotype, resilience to sleep deprivation, and the effect of caffeine on psychomotor vigilance performance in a randomized, double-blind, placebo-controlled, crossover study.

The TNFα G308A gene polymorphism has been reported to influence performance impairment during total sleep deprivation (TSD). We investigated this effect in a randomized, double-blind, crossover laboratory study of repeated exposure to 48 h TSD with caffeine administration at different doses. In a retrospective analysis, we replicated the finding that the A allele of TNFα G308A, found in 4 of 12 study participants, confers resilience to performance impairment during TSD. There was no evidence of an interaction of TNFα genotype with the beneficial effect of caffeine (200 or 300 mg) on performance during TSD, suggesting distinct underlying mechanisms.

Chronic ethanol attenuates circadian photic phase resetting and alters nocturnal activity patterns in the hamster.

Acute ethanol (EtOH) administration impairs circadian clock phase resetting, suggesting a mode for the disruptive effect of alcohol abuse on human circadian rhythms. Here, we extend this research by characterizing the chronobiological effects of chronic alcohol consumption. First, daily profiles of EtOH were measured in the suprachiasmatic nucleus (SCN) and subcutaneously using microdialysis in hamsters drinking EtOH. In both cases, EtOH peaked near lights-off and declined throughout the dark-phase to low day-time levels. Drinking bouts preceded EtOH peaks by approximately 20 min. Second, hamsters chronically drinking EtOH received a light pulse during the late dark phase [Zeitgeber time (ZT) 18.5] to induce photic phase advances. Water controls had shifts of 1.2 +/- 0.2 h, whereas those drinking 10% and 20% EtOH had much reduced shifts (0.5 +/- 0.1 and 0.3 +/- 0.1 h, respectively; P < 0.001 vs. controls). Third, incremental decreases in light intensity (270 lux to 0.5 lux) were used to explore chronic EtOH effects on photic entrainment and rhythm stability. Activity onset was unaffected by 20% EtOH at all light intensities. Conversely, the 24-h pattern of activity bouts was disrupted by EtOH under all light intensities. Finally, replacement of chronic EtOH with water was used to examine withdrawal effects. Water controls had photic phase advances of 1.1 +/- 0.3 h, while hamsters deprived of EtOH for 2-3 days showed enhanced shifts (2.1 +/- 0.3 h; P < 0.05 vs. controls). Thus, in chronically drinking hamsters, brain EtOH levels are sufficient to inhibit photic phase resetting and disrupt circadian activity. Chronic EtOH did not impair photic entrainment; however, its replacement with water potentiated photic phase resetting.