Canadian public health messages relating to physical activity have historically focused on the prescription of purposeful exercise, most often assessing leisure-time physical activity (LTPA). Although LTPA contributes to total energy expenditure (TEE), a large part of the day remains neglected unless one also considers the energy expended outside of purposeful exercise. This paper reviews the potential impact of incidental (non-exercise or non-purposeful) physical activity and lifestyle-embedded activities (chores and incidental walking) upon TEE and indicators of health. Given that incidental movement occurs sporadically throughout the day, this form of energy expenditure is perhaps most vulnerable to increasingly ubiquitous mechanization and automation. The paper also explores the relationship of physical inactivity, including sleep, to physical activity, TEE, and health outcomes. Suggestions are provided for a more comprehensive physical activity recommendation that includes all components of TEE. Objective physical activity monitors with time stamps are considered as a better means to capture and examine human movements over the entire day.
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Article de synthese sur la fonction du sommeil chez l'animal. Son role dans la vie, sa neurophysiologie cellulaire et la neurobiologie clinique de ses desordres, sont discutes par l'auteur
STUDY OBJECTIVES: To investigate the effects of sleep extension over multiple weeks on specific measures of athletic performance as well as reaction time, mood, and daytime sleepiness. SETTING: Stanford Sleep Disorders Clinic and Research Laboratory and Maples Pavilion, Stanford University, Stanford, CA. PARTICIPANTS: Eleven healthy students on the Stanford University men's varsity basketball team (mean age 19.4 ± 1.4 years). INTERVENTIONS: Subjects maintained their habitual sleep-wake schedule for a 2-4 week baseline followed by a 5-7 week sleep extension period. Subjects obtained as much nocturnal sleep as possible during sleep extension with a minimum goal of 10 h in bed each night. Measures of athletic performance specific to basketball were recorded after every practice including a timed sprint and shooting accuracy. Reaction time, levels of daytime sleepiness, and mood were monitored via the Psychomotor Vigilance Task (PVT), Epworth Sleepiness Scale (ESS), and Profile of Mood States (POMS), respectively. RESULTS: Total objective nightly sleep time increased during sleep extension compared to baseline by 110.9 ± 79.7 min (P < 0.001). Subjects demonstrated a faster timed sprint following sleep extension (16.2 ± 0.61 sec at baseline vs. 15.5 ± 0.54 sec at end of sleep extension, P < 0.001). Shooting accuracy improved, with free throw percentage increasing by 9% and 3-point field goal percentage increasing by 9.2% (P < 0.001). Mean PVT reaction time and Epworth Sleepiness Scale scores decreased following sleep extension (P < 0.01). POMS scores improved with increased vigor and decreased fatigue subscales (P < 0.001). Subjects also reported improved overall ratings of physical and mental well-being during practices and games. CONCLUSIONS: Improvements in specific measures of basketball performance after sleep extension indicate that optimal sleep is likely beneficial in reaching peak athletic performance.
Sleep has numerous important physiological and cognitive functions that may be particularly important to elite athletes. Recent evidence, as well as anecdotal information, suggests that athletes may experience a reduced quality and/or quantity of sleep. Sleep deprivation can have significant effects on athletic performance, especially submaximal, prolonged exercise. Compromised sleep may also influence learning, memory, cognition, pain perception, immunity and inflammation. Furthermore, changes in glucose metabolism and neuroendocrine function as a result of chronic, partial sleep deprivation may result in alterations in carbohydrate metabolism, appetite, food intake and protein synthesis. These factors can ultimately have a negative influence on an athlete's nutritional, metabolic and endocrine status and hence potentially reduce athletic performance. Research has identified a number of neurotransmitters associated with the sleep-wake cycle. These include serotonin, gamma-aminobutyric acid, orexin, melanin-concentrating hormone, cholinergic, galanin, noradrenaline, and histamine. Therefore, nutritional interventions that may act on these neurotransmitters in the brain may also influence sleep. Carbohydrate, tryptophan, valerian, melatonin and other nutritional interventions have been investigated as possible sleep inducers and represent promising potential interventions. In this review, the factors influencing sleep quality and quantity in athletic populations are examined and the potential impact of nutritional interventions is considered. While there is some research investigating the effects of nutritional interventions on sleep, future research may highlight the importance of nutritional and dietary interventions to enhance sleep.
Sleep spindles are an electroencephalographic (EEG) hallmark of non-rapid eye movement (NREM) sleep and are believed to mediate many sleep-related functions, from memory consolidation to cortical development. Spindles differ in location, frequency, and association with slow waves, but whether this heterogeneity may reflect different physiological processes and potentially serve different functional roles remains unclear. Here we used a unique opportunity to record intracranial depth EEG and single-unit activity in multiple brain regions of neurosurgical patients to better characterize spindle activity in human sleep. We find that spindles occur across multiple neocortical regions, and less frequently also in the parahippocampal gyrus and hippocampus. Most spindles are spatially restricted to specific brain regions. In addition, spindle frequency is topographically organized with a sharp transition around the supplementary motor area between fast (13-15 Hz) centroparietal spindles often occurring with slow-wave up-states, and slow (9-12 Hz) frontal spindles occurring 200 ms later on average. Spindle variability across regions may reflect the underlying thalamocortical projections. We also find that during individual spindles, frequency decreases within and between regions. In addition, deeper NREM sleep is associated with a reduction in spindle occurrence and spindle frequency. Frequency changes between regions, during individual spindles, and across sleep may reflect the same phenomenon, the underlying level of thalamocortical hyperpolarization. Finally, during spindles neuronal firing rates are not consistently modulated, although some neurons exhibit phase-locked discharges. Overall, anatomical considerations can account well for regional spindle characteristics, while variable hyperpolarization levels can explain differences in spindle frequency.
Sleep is a physiological process involving different biological systems, from molecular to organ level; its integrity is essential for maintaining health and homeostasis in human beings. Although in the past sleep has been considered a state of quiet, experimental and clinical evidences suggest a noteworthy activation of different biological systems during sleep. A key role is played by the autonomic nervous system (ANS), whose modulation regulates cardiovascular functions during sleep onset and different sleep stages. Therefore, an interest on the evaluation of autonomic cardiovascular control in health and disease is growing by means of linear and non-linear heart rate variability (HRV) analyses. The application of classical tools for ANS analysis, such as HRV during physiological sleep, showed that the rapid eye movement (REM) stage is characterized by a likely sympathetic predominance associated with a vagal withdrawal, while the opposite trend is observed during non-REM sleep. More recently, the use of non-linear tools, such as entropy-derived indices, have provided new insight on the cardiac autonomic regulation, revealing for instance changes in the cardiovascular complexity during REM sleep, supporting the hypothesis of a reduced capability of the cardiovascular system to deal with stress challenges. Interestingly, different HRV tools have been applied to characterize autonomic cardiac control in different pathological conditions, from neurological sleep disorders to sleep disordered breathing (SDB). In summary, linear and non-linear analysis of HRV are reliable approaches to assess changes of autonomic cardiac modulation during sleep both in health and diseases. The use of these tools could provide important information of clinical and prognostic relevance.
Molecules involved in innate immunity affect sleep and circadian oscillators and vice versa. Sleep-inducing inflammatory molecules are activated by increased waking activity and pathogens. Pathologies that alter inflammatory molecules, such as traumatic brain injury, cancer, cardiovascular disease, and stroke often are associated with disturbed sleep and electroencephalogram power spectra. Moreover, sleep disorders, such as insomnia and sleep disordered breathing, are associated with increased dysregulation of inflammatory processes. Inflammatory molecules in both the central nervous system and periphery can alter sleep. Inflammation can also modulate cerebral vascular hemodynamics which is associated with alterations in electroencephalogram power spectra. However, further research is needed to determine the interactions of sleep regulatory inflammatory molecules and circadian clocks. The purpose of this review is to: 1) describe the role of the inflammatory cytokines interleukin-1 beta and tumor necrosis factor-alpha and nucleotide-binding domain and leucine-rich repeat protein-3 inflammasomes in sleep regulation, 2) to discuss the relationship between the vagus nerve in translating inflammatory signals between the periphery and central nervous system to alter sleep, and 3) to present information about the relationship between cerebral vascular hemodynamics and the electroencephalogram during sleep.
Sleep is essential for effective cognitive functioning. Loosing even a few hours of sleep can have detrimental effects on a wide variety of cognitive processes such as attention, language, reasoning, decision making, learning and memory. While sleep is necessary to ensure normal healthy cognitive functioning, it can also enhance performance beyond the boundaries of the normal condition. This article discusses the enhancing potential of sleep, mainly focusing on the domain of learning and memory. Sleep is known to facilitate the consolidation of memories learned before sleep as well as the acquisition of new memories to be learned after sleep. According to a widely held model this beneficial effect of sleep relies on the neuronal reactivation of memories during sleep that is associated with sleep-specific brain oscillations (slow oscillations, spindles, ripples) as well as a characteristic neurotransmitter milieu. Recent research indicates that memory processing during sleep can be boosted by (i) cueing memory reactivation during sleep; (ii) stimulating sleep-specific brain oscillations; and (iii) targeting specific neurotransmitter systems pharmacologically. Olfactory and auditory cues can be used, for example, to increase reactivation of associated memories during post-learning sleep. Intensifying neocortical slow oscillations (the hallmark of slow wave sleep (SWS)) by electrical or auditory stimulation and modulating specific neurotransmitters such as noradrenaline and glutamate likewise facilitates memory processing during sleep. With this evidence in mind, this article concludes by discussing different methodological caveats and ethical issues that should be considered when thinking about using sleep for cognitive enhancement in everyday applications.
Sleep quality decreases with aging and thus sleep complaints are prevalent in older adults, particularly for those with cognitive impairment and dementia. For older adults, emerging evidence suggests poor sleep quality increases risk of developing cognitive impairment and dementia. Given the aging population-and the impending economic burden associated with increasing numbers of dementia patients-there is pressing need to improve sleep quality among older adults. As such, research efforts have increased focus on investigating the association between age-related sleep changes and cognitive decline in older adults. Sleep quality is a complex construct to evaluate empirically, and yet the Pittsburg Sleep Quality Index (PSQI) is commonly used in studies as their only measure of sleep quality. Furthermore, the PSQI may not be the best sleep quality measure for older adults, due to its reliance on the cognitive capacity to reflect on the past month. Further study is needed to determine the PSQI's validity among older adults. Thus, the current study examined sleep quality for 78 community dwelling adults 55+ to determine the PSQI's predictive validity for objective sleep quality (as measured by actigraphy). We compared two subjective measures of sleep quality-the PSQI and Consensus Sleep Diary (CSD)-with actigraphy (MotionWatch 8©; camntech). Our results suggest perceived sleep quality is quite different from objective reality, at least for adults 55+. Importantly, we show this difference is unrelated to age, gender, education, or cognitive status (assessed using standard screens). Previous studies have shown the PSQI to be a valuable tool for assessing subjective sleep quality; however, our findings indicate for older adults the PSQI should not be used as a substitute for actigraphy, or vice versa. Hence, we conclude best practice is to include both subjective and objective measures when examining sleep quality in older adults (i.e., the PSQI, CSD, and actigraphy).
Spontaneous discharge of norepinephrine-containing locus coeruleus (NE-LC) neurons was examined during the sleep-walking cycle (S-WC) in behaving rats. Single unit and multiple unit extracellular recordings yielded a consistent set of characteristic discharge properties. (1) Tonic discharge co-varied with stages of the S-WC, being highest during waking, lower during slow wave sleep, and virtually absent during paradoxical sleep. (2) Discharge anticipated S-WC stages as well as phasic cortical activity, such as spindles, during slow wave sleep. (3) Discharge decreased within active waking during grooming and sweet water consumption. (4) Bursts of impulses accompanied spontaneous or sensory-evoked interruptions of sleep, grooming, consumption, or other such ongoing behavior. (5) These characteristic discharge properties were topographically homogeneous for recordings throughout the NE-LC. (6) Phasic robust activity was synchronized markedly among neurons in multiple unit populations. (7) Field potentials occurred spontaneously in the NE-LC and were synchronized with bursts of unit activity from the same electrodes. (8) Field potentials became dissociated from unit activity during paradoxical sleep, exhibiting their highest rates in the virtual absence of impulses. These results are generally consistent with previous proposals that the NE-LC system is involved in regulating cortical and behavioral arousal. On the basis of the present data and those described in the following report (Aston-Jones, G., and F. E. Bloom (1981) J. Neurosci.1: 887-900), we conclude that these neurons may mediate a specific function within the general arousal framework. In brief, the NE-LC system may globally bias the responsiveness of target neurons and thereby influence overall behavioral orientation.
Good sleep is essential for optimal performance, yet few studies have examined the sleep/wake behaviour of elite athletes. The aim of this study was to assess the impact of early-morning training on the amount of sleep obtained by world-class swimmers. A squad of seven swimmers from the Australian Institute of Sport participated in this study during 14 days of high-intensity training in preparation for the 2008 Olympic Games. During these 14 days, participants had 12 training days, each starting with a session at 06:00 h, and 2 rest days. For each day, the amount of sleep obtained by participants was determined using self-report sleep diaries and wrist-worn activity monitors. On nights that preceded training days, participants went to bed at 22:05 h (s=00:52), arose at 05:48 h (s=00:24) and obtained 5.4 h (s=1.3) of sleep. On nights that preceded rest days, participants went to bed at 00:32 h (s=01:29), arose at 09:47 h (s=01:47) and obtained 7.1 h (s=1.2) of sleep. Mixed model analyses revealed that on nights prior to training days, bedtimes and get-up times were significantly earlier (p<0.001), time spent in bed was significantly shorter (p<0.001) and the amount of sleep obtained was significantly less (p<0.001), than on nights prior to rest days. These results indicate that early-morning training sessions severely restrict the amount of sleep obtained by elite athletes. Given that chronic sleep restriction of <6 h per night can impair psychological and physiological functioning, it is possible that early-morning schedules actually limit the effectiveness of training.
Obstructive sleep apnea syndrome (OSAS) is a common breathing disorder in sleep in which the airways narrow or collapse during sleep, causing obstructive sleep apnea. The prevalence of OSAS continues to rise worldwide, particularly in middle-aged and elderly individuals. The mechanism of upper airway collapse is incompletely understood but is associated with several factors, including obesity, craniofacial changes, altered muscle function in the upper airway, pharyngeal neuropathy, and fluid shifts to the neck. The main characteristics of OSAS are recurrent pauses in respiration, which lead to intermittent hypoxia (IH) and hypercapnia, accompanied by blood oxygen desaturation and arousal during sleep, which sharply increases the risk of several diseases. This paper first briefly describes the epidemiology, incidence, and pathophysiological mechanisms of OSAS. Next, the alterations in relevant signaling pathways induced by IH are systematically reviewed and discussed. For example, IH can induce gut microbiota (GM) dysbiosis, impair the intestinal barrier, and alter intestinal metabolites. These mechanisms ultimately lead to secondary oxidative stress, systemic inflammation, and sympathetic activation. We then summarize the effects of IH on disease pathogenesis, including cardiocerebrovascular disorders, neurological disorders, metabolic diseases, cancer, reproductive disorders, and COVID-19. Finally, different therapeutic strategies for OSAS caused by different causes are proposed. Multidisciplinary approaches and shared decision-making are necessary for the successful treatment of OSAS in the future, but more randomized controlled trials are needed for further evaluation to define what treatments are best for specific OSAS patients.
Post-traumatic stress disorder (PTSD) is accompanied by disturbed sleep and an impaired ability to learn and remember extinction of conditioned fear. Following a traumatic event, the full spectrum of PTSD symptoms typically requires several months to develop. During this time, sleep disturbances such as insomnia, nightmares, and fragmented rapid eye movement sleep predict later development of PTSD symptoms. Only a minority of individuals exposed to trauma go on to develop PTSD. We hypothesize that sleep disturbance resulting from an acute trauma, or predating the traumatic experience, may contribute to the etiology of PTSD. Because symptoms can worsen over time, we suggest that continued sleep disturbances can also maintain and exacerbate PTSD. Sleep disturbance may result in failure of extinction memory to persist and generalize, and we suggest that this constitutes one, non-exclusive mechanism by which poor sleep contributes to the development and perpetuation of PTSD. Also reviewed are neuroendocrine systems that show abnormalities in PTSD, and in which stress responses and sleep disturbance potentially produce synergistic effects that interfere with extinction learning and memory. Preliminary evidence that insomnia alone can disrupt sleep-dependent emotional processes including consolidation of extinction memory is also discussed. We suggest that optimizing sleep quality following trauma, and even strategically timing sleep to strengthen extinction memories therapeutically instantiated during exposure therapy, may allow sleep itself to be recruited in the treatment of PTSD and other trauma and stress-related disorders.
Space agencies such as the National Aeronautics and Space Administration of the United States, the Russian Federal Space Agency, the European Space Agency, the China National Space Administration, the Japan Aerospace Exploration Agency, and Indian Space Research Organization, although differing in their local political agendas, have a common interest in promoting all applied sciences that may facilitate man's adaptation to life beyond the earth. One of man's most important adaptations has been the evolutionary development of sleep cycles in response to the 24 hour rotation of the earth. Less well understood has been man's biological response to gravity. Before humans ventured into space, many questioned whether sleep was possible at all in microgravity environments. It is now known that, in fact, space travelers can sleep once they leave the pull of the earth's gravity, but that the sleep they do get is not completely refreshing and that the associated sleep disturbances can be elaborate and variable. According to astronauts' subjective reports, the duration of sleep is shorter than that on earth and there is an increased incidence of disturbed sleep. Objective sleep recordings carried out during various missions including the Skylab missions, space shuttle missions, and Mir missions all support the conclusion that, compared to sleep on earth, the duration in human sleep in space is shorter, averaging about six hours. In the new frontier of space exploration, one of the great practical problems to be solved relates to how man can preserve "normal" sleep in a very abnormal environment. The challenge of managing fatigue and sleep loss during space mission has critical importance for the mental efficiency and safety of the crew and ultimately for the success of the mission itself. Numerous "earthly" examples now show that crew fatigue on ships, trucks, and long-haul jetliners can lead to inadequate performance and sometimes fatal consequences, a reality which has caused many space agencies to take the issue of sleep seriously.
Elite athletes are particularly susceptible to sleep inadequacies, characterised by habitual short sleep (<7 hours/night) and poor sleep quality (eg, sleep fragmentation). Athletic performance is reduced by a night or more without sleep, but the influence on performance of partial sleep restriction over 1-3 nights, a more real-world scenario, remains unclear. Studies investigating sleep in athletes often suffer from inadequate experimental control, a lack of females and questions concerning the validity of the chosen sleep assessment tools. Research only scratches the surface on how sleep influences athlete health. Studies in the wider population show that habitually sleeping <7 hours/night increases susceptibility to respiratory infection. Fortunately, much is known about the salient risk factors for sleep inadequacy in athletes, enabling targeted interventions. For example, athlete sleep is influenced by sport-specific factors (relating to training, travel and competition) and non-sport factors (eg, female gender, stress and anxiety). This expert consensus culminates with a sleep toolbox for practitioners (eg, covering sleep education and screening) to mitigate these risk factors and optimise athlete sleep. A one-size-fits-all approach to athlete sleep recommendations (eg, 7-9 hours/night) is unlikely ideal for health and performance. We recommend an individualised approach that should consider the athlete's perceived sleep needs. Research is needed into the benefits of napping and sleep extension (eg, banking sleep).
The transition from wakefulness to NREM sleep is associated with typical signs of brain electrical activity, characterized by prolonged periods of hyperpolarization and increased membrane conductance in thalamocortical (TC) neurons, with the consequence that incoming messages are inhibited and the cerebral cortex is deprived of signals from the outside world. There are three major oscillations during NREM sleep. Spindles are generated within the thalamus, due to thalamic reticular (RE) neurons that impose rhythmic inhibitory sequences onto TC neurons, but the widespread synchronization of this rhythm is governed by corticothalamic projections. There are two types of delta activity: clock-like waves generated in TC neurons by the interplay between two hyperpolarization-activated inward currents; and cortical waves that survive extensive thalamectomy. The hallmark of NREM sleep activity is the slow oscillation, generated intracortically, which has the virtue of grouping the other types of sleep activities, thus leading to a coalescence of different rhythms that can only be observed in intact-brain animals and humans. Far from being epiphenomena, with no functional role, NREM sleep oscillations, particularly spindles and their experimental model augmenting responses, produce synaptic plasticity in target cortical neurons and resonant activity in corticothalamic loops, as in "memory" processes. Upon brain arousal, spindles are blocked by inhibition of RE neurons, the spindles' pacemakers; clock-like delta rhythm is obliterated by depolarization of TC neurons; and the cortically generated slow oscillation is abolished by selective erasure of its hyperpolarizing components. Fast (beta and gamma) oscillations are roduced by the depolarizing effects of mesopontine cholinergic neurons acting on TC neurons and nucleus basalis neurons acting on cortical neurons.
BACKGROUND: Information on sleep quality and insomnia symptomatology among elite athletes remains poorly systematised in the sports science and medicine literature. The extent to which performance in elite sport represents a risk for chronic insomnia is unknown. OBJECTIVES: The purpose of this systematic review was to profile the objective and experienced characteristics of sleep among elite athletes, and to consider relationships between elite sport and insomnia symptomatology. METHODS: Studies relating to sleep involving participants described on a pre-defined continuum of 'eliteness' were located through a systematic search of four research databases: SPORTDiscus, PubMed, Science Direct and Google Scholar, up to April 2016. Once extracted, studies were categorised as (1) those mainly describing sleep structure/patterns, (2) those mainly describing sleep quality and insomnia symptomatology and (3) those exploring associations between aspects of elite sport and sleep outcomes. RESULTS: The search returned 1676 records. Following screening against set criteria, a total of 37 studies were identified. The quality of evidence reviewed was generally low. Pooled sleep quality data revealed high levels of sleep complaints in elite athletes. Three risk factors for sleep disturbance were broadly identified: (1) training, (2) travel and (3) competition. CONCLUSION: While acknowledging the limited number of high-quality evidence reviewed, athletes show a high overall prevalence of insomnia symptoms characterised by longer sleep latencies, greater sleep fragmentation, non-restorative sleep, and excessive daytime fatigue. These symptoms show marked inter-sport differences. Two underlying mechanisms are implicated in the mediation of sport-related insomnia symptoms: pre-sleep cognitive arousal and sleep restriction.
Correctly identifying sleep stages is important in diagnosing and treating sleep disorders. This paper proposes a joint classification-and-prediction framework based on convolutional neural networks (CNNs) for automatic sleep staging, and, subsequently, introduces a simple yet efficient CNN architecture to power the framework. Given a single input epoch, the novel framework jointly determines its label (classification) and its neighboring epochs' labels (prediction) in the contextual output. While the proposed framework is orthogonal to the widely adopted classification schemes, which take one or multiple epochs as contextual inputs and produce a single classification decision on the target epoch, we demonstrate its advantages in several ways. First, it leverages the dependency among consecutive sleep epochs while surpassing the problems experienced with the common classification schemes. Second, even with a single model, the framework has the capacity to produce multiple decisions, which are essential in obtaining a good performance as in ensemble-of-models methods, with very little induced computational overhead. Probabilistic aggregation techniques are then proposed to leverage the availability of multiple decisions. To illustrate the efficacy of the proposed framework, we conducted experiments on two public datasets: Sleep-EDF Expanded (Sleep-EDF), which consists of 20 subjects, and Montreal Archive of Sleep Studies (MASS) dataset, which consists of 200 subjects. The proposed framework yields an overall classification accuracy of 82.3% and 83.6%, respectively. We also show that the proposed framework not only is superior to the baselines based on the common classification schemes but also outperforms existing deep-learning approaches. To our knowledge, this is the first work going beyond the standard single-output classification to consider multitask neural networks for automatic sleep staging. This framework provides avenues for further studies of different neural-network architectures for automatic sleep staging.
STUDY OBJECTIVE: Animal data suggest that Δ(9)-TetraHydroCannabinol (Δ(9)THC) stabilizes autonomic output during sleep, reduces spontaneous sleep-disordered breathing, and blocks serotonin-induced exacerbation of sleep apnea. On this basis, we examined the safety, tolerability, and efficacy of dronabinol (Δ(9)THC), an exogenous Cannabinoid type 1 and type 2 (CB1 and CB2) receptor agonist in patients with Obstructive Sleep Apnea (OSA). DESIGN AND SETTING: Proof of concept; single-center dose-escalation study of dronabinol. PARTICIPANTS: Seventeen adults with a baseline Apnea Hypopnea Index (AHI) ≥15/h. Baseline polysomnography (PSG) was performed after a 7-day washout of Continuous Positive Airway Pressure treatment. INTERVENTION: Dronabinol was administered after baseline PSG, starting at 2.5 mg once daily. The dose was increased weekly, as tolerated, to 5 mg and finally to 10 mg once daily. MEASUREMENTS AND RESULTS: Repeat PSG assessments were performed on nights 7, 14, and 21 of dronabinol treatment. Change in AHI (ΔAHI, mean ± SD) was significant from baseline to night 21 (-14.1 ± 17.5; p = 0.007). No degradation of sleep architecture or serious adverse events was noted. CONCLUSION: Dronabinol treatment is safe and well-tolerated in OSA patients at doses of 2.5-10 mg daily and significantly reduces AHI in the short-term. These findings should be confirmed in a larger study in order to identify sub-populations with OSA that may benefit from cannabimimetic pharmacologic therapy.