Effects of Natural Between-Days Variation in Sleep on Elite Athletes’ Psychomotor Vigilance and Sport-Specific Measures of Performance

Performance capacity in athletes depends on the ability to recover from past exercise. While evidence suggests that athletic performance decreases following (partial) sleep deprivation and increases following sleep extension, it is unclear to which extent natural variation in sleep impacts performance. Sleep quantity and, for the first time, sleep stages were assessed among 98 elite athletes on three non-consecutive nights within a 7-day monitoring period, along with performance tests that were taken on standardized times each following morning. Performance assessment included psychomotor performance (10-minute psychomotor vigilance task) and sport-specific tests of fine (e.g., accuracy) and gross motor skills (e.g., endurance, power). Mixed-effects models were employed to assess the effect of sleep quantity (total sleep time (TST), sleep onset latency (SOL), wake after sleep onset, sleep efficiency) and sleep stage duration (light, deep, REM) on performance. Average TST was 7:30 ± 1:05 hours, with a mean variation of 57 minutes across days. Longer TSTs were associated with faster reaction times (p = 0.04). Analyses indicated small and inconsistent effects of sleep quantity (TST, SOL) and sleep staging (light sleep) on gross motor performance, and no effects on fine motor skill performance. Results indicate that natural variation in sleep quantity impacts psychomotor vigilance to a greater extent than athletic performance. Small or absent effects can be a consequence of the rather small variation in non-manipulated sleep. It is suggested that one night of compromised sleep may not be immediately problematic, but that more extreme sleep loss or accumulated sleep debt may have more severe consequences

Endogenous rhythm of absence epilepsy: Relationship with general motor activity and sleep-wake states

Contains fulltext : 99307.pdf (publisher's version ) (Open Access)The rhythms of spontaneously occurring seizures (spike-wave discharges, SWD) and motor activity, as well as the relationship between SWD and sleep-wake states were investigated in the WAG/Rij rat model of absence epilepsy. In order to establish whether SWD are controlled by external (Zeitgebers) or by endogenous factors such as circadian influences or the state of vigilance, the study was performed in entrained and constant dim light conditions. EEG and motor activity were recorded in the 12:12 light dark cycle and in constant dim light conditions. Circadian rhythmicity was found both for motor activity and the occurrence of SWD in conditions of entrainment. In constant dim light conditions also circadian rhythms emerged, however, the change in circadian parameters was opposite for the rhythm of SWD and motor activity. SWD were preceded mostly by passive wakefulness and by slow-wave sleep in both experimental conditions. It can be concluded that the rhythm of SWD seems to be generated and controlled by an endogenous mechanism distinct from that which controls the rhythm of motor activity. The relationship between SWD and sleep-wake states preceding their occurrences appeared to be unchanged, suggesting that the mechanism of generation of SWD is independent of the circadian timing system

Mammalian sleep may have no adaptive advantage over simple activity-rest cycles

Contains fulltext : 54549.pdf (publisher's version ) (Closed access)The adaptive value of sleep remains unknown in spite of the intense research performed throughout the last decades. However, few sleep researchers are aware of the difficulties posed by the blind acceptance of an extreme adaptationist viewpoint. Under this philosophy, every anatomical and functional detail present in a living being should have a positive adaptive value, a position that has been considered as rather doubtful. In this report, it is proposed that most of the physiological changes used for mammalian sleep definition could be mere by-products of other true adaptations, such as the ontogenetic and phylogenetic development of the nervous system. As a result, complex mammalian sleep could have no adaptive value over that of the simplest forms of rest-activity cycles present in all living forms. In addition, it is proposed that the absence of adaptive value should, by default, be the first option regarding the function of sleep. Besides, the burden of the proof should be always charged over the proponents of every particular adaptive function. As this proof has not been reached, it is the absence of function for sleep which should be taken for granted

Melatonin Improves Health Status and Sleep in Children With Idiopathic Chronic Sleep-Onset Insomnia: A Randomized Placebo-Controlled Trial

Contains fulltext : 63781.pdf (publisher's version ) (Closed access)Objective: To investigate the effect of melatonin treatment on health status and sleep in children with idiopathic sleep-onset insomnia. Method: A randomized, double-blind, placebo-controlled trial was conducted in a Dutch sleep center, involving 62 children, 6 to 12 years of age, who suffered more than 1 year from idiopathic chronic sleep-onset insomnia. Patients received either 5 mg melatonin or placebo at 7 pm. The study consisted of a 1-week baseline period, followed by a 4-week treatment. Health status was measured with the RAND General Health Rating Index (RAND-GHRI) and Functional Status II (FS-II) questionnaires. Lights-off time, sleep onset, and wake-up time were recorded in a diary, and endogenous dim light melatonin onset was measured in saliva. Results: The total scores of the RAND-GHRI and FS-II improved significantly more during melatonin treatment compared to placebo. The magnitude of change was much higher in the melatonin group than in the placebo group, with standardized response means for the RAND-GHRI of 0.69 versus 0.07 and for the FS-II of 1.61 versus 0.64. Melatonin treatment also significantly advanced sleep onset by 57 minutes, sleep offset by 9 minutes, and melatonin onset by 82 minutes, and decreased sleep latency by 17 minutes. Lights-off time and total sleep time did not change. Conclusions: Melatonin improves health status and advances the sleep-wake rhythm in children with idiopathic chronic sleep-onset insomnia. Chronic sleep-onset insomnia occurs in about 10% of the nondisabled school-aged population (Blader et al., 1997) and is associated with increased occurrence of fears, night wakening, and daytime fatigue (Blader et al., 1997; Dahl, 1996; Ring et al., 1998). Poor sleep severely impairs daytime functioning and overall well-being (Dahl, 1996; Wiggs and Stores, 1995) and is associated with impaired health status (Leger et al., 2001; Stein et al., 2001). Melatonin is a chronobiotic drug with soporific properties (Wirz-Justice and Armstrong, 1996). In adults suffering from delayed sleep phase syndrome, it advances the sleep-wake rhythm (Nagtegaal et al., 1998b) and improves quality of life (Nagtegaal et al., 2000). Jan and colleagues treated more than 100 mentally handicapped children with chronic sleep disorders successfully with 2.5 to 10 mg melatonin (Jan and O'Donnell, 1996). An earlier study (Smits et al., 2001) showed that melatonin advanced the sleep-wake rhythm and increased sleep duration in elementary school children with idiopathic chronic sleep-onset insomnia. During the follow-up period of that study, many parents reported that their child's behavior had considerably improved. Severe adverse events did not occur. In children, behavior and the effect of disease on behavior can be assessed with the Functional Status II (FS-II) questionnaire (Stein and Jessop, 1990). General health status can be measured with the RAND General Health Rating Index for children (RAND-GHRI) (Lewis et al., 1989). Because melatonin seemed to improve behavior in children with chronic sleep-onset insomnia, we performed another placebo-controlled study to assess the influence of melatonin on behavior, health status, and sleep pattern in these children