Circadian rhythms in human muscular efficiency: continuous physical exercise versus continuous rest. A crossover study

This study deals with the influence of time of day on neuromuscular efficiency in competitive cyclists during continuous exercise versus continuous rest. Knee extension torque was measured in ultradistance cyclists over a 24h period (13:00 to 13:00 the next day) in the laboratory. The subjects were requested to maintain a constant speed (set at 70% of their maximal aerobic speed obtained during a preliminary test) on their own bicycles, which were equipped with cyclosimulators. Every 4h, torque developed and myoelectric activity were estimated during maximal isometric voluntary contractions of knee extensors using an isokinetic dynamometer. Mesenteric temperature was monitored by telemetry. The same measures were also recorded while the subjects were resting awake until 13:00 the next day. During activity, torque changed within the 24h period (p < .005), with an acrophase at 19:10 and an amplitude of 7.8% around the mean of 70.7%. At rest, a circadian rhythm was observed in knee extensor torque (p < .05), with an acrophase at 19:30 and an amplitude of 6% around the mean of 92.3%. Despite the standardized conditions, the results showed that isometric maximal strength varied with time of day during both a submaximal exercise and at rest without prior exercise. The sine waves representing these two rhythms were correlated significantly. Although at rest the diurnal rhythm followed muscular activity (i.e., neurophysiological factors), during exercise, this rhythm was thought to stem more from fluctuations in the contractile state of muscle.     

Circadian clock resetting by sleep deprivation without exercise in Syrian hamsters: dark pulses revisited

Circadian rhythms in Syrian hamsters can be phase shifted by procedures that stimulate wheel running ("exercise") in the mid-subjective day (the hamster's usual sleep period). The authors recently demonstrated that keeping hamsters awake by gentle handling, without continuous running, is sufficient to mimic this effect. Here, the authors assessed whether wakefulness, independent of wheel running, also mediates phase shifts to dark pulses during the midsubjective day in hamsters free-running in constant light (LL). With running wheels locked during a 3 h dark pulse on day 3 of LL, hamsters (N = 16) averaged only 43+/-15 min of spontaneous wake time and phase shifted only 24+/-43 min. When wheels were open during a dark pulse, two hamsters remained awake, ran continuously, and showed phase advance shifts of 7.3 h and 8.7 h, respectively, whereas the other hamsters were awake <60 min and shifted only 45+/-38 min. No animals stayed awake for 3 h without running. Additional time in LL (10 and 20 days) did not potentiate the waking or phase shift response to dark pulses. When all hamsters were sleep deprived with wheels locked during a dark pulse, phase advance shifts averaged 261+/-110 min and ranged up to 7.3 h. These shifts are large compared to those previously observed in response to the 3 h sleep deprivation procedure. Additional tests revealed that this potentiated shift response is dependent on LL prior to sleep deprivation but not LL after sleep deprivation. A final sleep deprivation test showed that a small part of the potentiation may be due to suppression of spontaneous wheel running by LL. These results indicate that some correlate of waking, other than continuous running, mediates the phase-shifting effect of dark pulses in the mid-subjective day. The mechanism by which LL potentiates shifting remains to be determined. The lack of effect of subsequent LL on the magnitude of shifts to sleep deprivation in the dark suggests that LL reduces responsivity to light by processes that take >3 h of dark to reverse.     

Circadian rhythm of serotonin binding in rat brain--II. Influence of sleep deprivation and imipramine

Sleep deprivation (SD) modified the circadian rhythm of specific high affinity serotonin (5-HT) binding to rat brain membranes. In control rats a 24-hr rhythm was evident with a trough at 1000-1200 and a nadir at 0000. During the last 26 hr of a 49 hr SD period, trough and peak values were delayed by 4-6 hr. The 24-hr mean binding was significantly (P less than 0.001) different from that of controls. If sleep deprivation was followed by recovery sleep (RS), the normal rhythm of 5-HT binding was obtained already within 1 hr after SD. The effects of SD and RS were ascertained by plasma ACTH and corticosterone assay. No significant change in the hormone rhythms were observed through the mean plasma level of ACTH and corticosterone were enhanced to about 180 and 150%, respectively. Chronic treatment with the antidepressant imipramine resulted in a decrease of the 24-hr mean 5-HT binding by about 50% and a 2-hr delay of peak and trough values. Imipramine treatment decreased the peak value of 5-HT concentration at 1000 to about 65% and appears to abolish the rhythm of 5-HT concentration.     

Effects of sustained manual work and partial sleep deprivation on muscular strength and endurance

In a military field artillery trial, the effects of 8 days of sustained manual work and partial sleep loss on isometric right hand grip strength and upper and lower body anaerobic power (using the Wingate test) was investigated in 25 healthy young male soldiers. During the trial, the physical activity of each subject was essentially identical except that an experimental group (n = 18) manually handled a large quantity of artillery shells (weighing 45 kg) and charges (13 kg), whilst a control group (n = 7) merely simulated manual handling activities and did no lifting or loading of shells. The daily amount of sleep obtained by each group was similar (3 to 4 hours), as were their activity patterns and food and fluid intake. Isometric right hand grip strength for both groups fell progressively during the trial and did not return to pre-trial levels during 3 days of recovery. At the end of the 8 day trial, there were statistically significant reductions in the body weight (1.9%, p less than 0.001), % body fat (7.1%, p less than 0.001) and upper body mean power (7.3%, p less than 0.01) of the experimental group but not in the controls. Lower body peak and mean power were significantly increased at the end of the trial in both the experimental (14.7%, p less than 0.001 and 17.0%, p less than 0.001 respectively) and control (14.3%, p less than 0.01 and 15.0%, p less than 0.05 respectively) groups. Lower body power decrease was significantly increased (18.1%, p less than 0.05) in the experimental group but not in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circadian rhythm sleep disorders: An update

Sleep and Biological Rhythms - The primary symptom of circadian rhythm sleep disorders (CRSDs) is the inability to sleep during the desired sleep time. CRSDs are divided into two broad classes: (i)...     

Circadian gene variants influence sleep and the sleep electroencephalogram in humans

The sleep electroencephalogram (EEG) is highly heritable in humans and yet little is known about the genetic basis of inter-individual differences in sleep architecture. The aim of this study was to identify associations between candidate circadian gene variants and the polysomnogram, recorded under highly controlled laboratory conditions during a baseline, overnight, 8 h sleep opportunity. A candidate gene approach was employed to analyze single-nucleotide polymorphisms from five circadian-related genes in a two-phase analysis of 84 healthy young adults (28 F; 23.21 ± 2.97 years) of European ancestry. A common variant in Period2 (PER2) was associated with 20 min less slow-wave sleep (SWS) in carriers of the minor allele than in noncarriers, representing a 22% reduction in SWS duration. Moreover, spectral analysis in a subset of participants (n = 37) showed the same PER2 polymorphism was associated with reduced EEG power density in the low delta range (0.25–1.0 Hz) during non-REM sleep and lower slow-wave activity (0.75–4.5 Hz) in the early part of the sleep episode. These results indicate the involvement of PER2 in the homeostatic process of sleep. Additionally, a rare variant in Melatonin Receptor 1B was associated with longer REM sleep latency, with minor allele carriers exhibiting an average of 65 min (87%) longer latency from sleep onset to REM sleep, compared to noncarriers. These findings suggest that circadian-related genes can modulate sleep architecture and the sleep EEG, including specific parameters previously implicated in the homeostatic regulation of sleep.     

Mood, alertness, and performance in response to sleep deprivation and recovery sleep in experienced shiftworkers versus non-shiftworkers

Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5 h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean ± SD: 35.7 ± 7.2 and 32.5 ± 6.2 yrs, respectively) and body mass index (BMI) (28.7 ± 3.8 and 26.6 ± 3.4 kg/m(2), respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8 h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8 h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8 h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5 h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a decrease in subjective alertness and PVT performance during and following the sleep deprivation night. Subjective sleepiness and most aspects of PVT performance returned to baseline levels after a nap and recovery sleep. The mechanisms underlying the observed differences between shiftworkers and non-shiftworkers require further study, but may be related to the absence of shiftwork the week prior to and during the laboratory study as well as selection into and out of shiftwork.     

Structural fluctuations in the steady state of muscular contraction.

Recent studies of the intensity fluctuation spectra of coherent light scattered from striated muscle have demonstrated the existence of large scale fluctuations in position and polarizability at the level of the myofibrillar sarcomere and its major structural subunits during the steady state of contraction. The existence of these fluctuations implies a fluctuating driving force. Various possible fluctuating motions of the thick and thin filaments, A and I bands, and entire sarcomeres are described. The magnitude of the fluctuating forces associated with the making and breaking of cross bridges is estimated. A mechanical model is proposed for coupling structural elements of a single sarcomere to one another and for coupling myofibrillar sarcomeres to one another. It is shown that the fluctuating force generated by the spontaneous making and breaking of cross bridges in conjunction with the model accounts for some of the features of the observed intensity fluctuation spectra.     

Circadian rhythms and sleep in human aging

This issue of Chronobiology International is dedicated to the age-related changes in circadian rhythms as they occur in humans. It seems timely to give an overview of the knowledge and hypotheses on these changes now that we enter a century in which the number and percentage of elderly in the population will be unprecedented. Although we should take care not to follow the current tendency to think of old age as a disease—ignoring the fine aspects of being old—there is definitely an age-related increase in the risk of a number of conditions that are at least uncomfortable.

Circadian rhythms have been attributed adaptive values that usually go unnoticed, but can surface painfully clear when derangements occur. Alterations in the regulation of circadian rhythms are thought to contribute to the symptoms of a number of conditions for which the risk is increased in old age (e.g., sleep disturbances, dementia, and depression). A multidisciplinary approach to investigate the mechanisms of age-related changes in circadian regulation eventually may result in treatment strategies that will improve the quality of life of the growing number of elderly.

Although diverse topics are addressed in this issue, the possible mechanisms by which a deranged circadian timing system may be involved in sleep disturbances receives the most attention. This seems appropriate in view of the numerous studies that have addressed this relation in the last decade and also because of the high frequency and strong impact of sleep disturbances in the elderly. This introduction to the special issue first briefly addresses the impact of disturbed sleep in the elderly to show that the development of therapeutic methods other than the currently available pharmacological treatments should be given high priority. I believe that chronobiological insights may play an important role in the development of rational therapeutical methods.(Chronobiology International, 17(3), 233-243, 2000)     

Neurophysiologic aspects of sleep deprivation in depression

Study of EEG in 45 patients, suffering from endogenic and psychogenic depression, in the state of rest, in mental and emotional loads, SGR, orienting reaction and night sleep before and after a course of sleep deprivation has shown that neurophysiological shifts in the cycle alertness-sleep have one direction. The weakening of depression was accompanied by rather unidirected alterations of neurophysiological relations, which testified to the normalization of biological periods of the organism.     

Changes in brain glycogen after sleep deprivation vary with genotype

Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by approximately 40% in the cortex of B6 mice, while glycogen significantly decreased by 20-38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis.     

Circadian preference and sleep-wake regularity: associations with self-report sleep parameters in daytime-working adults

The aim of this study was to explore how interindividual differences in circadian type (morningness) and sleep timing regularity might be related to subjective sleep quality and quantity. Self-report circadian phase preference, sleep timing, sleep quality, and sleep duration were assessed in a sample of 62 day-working adults (33.9% male, age 23?48 yrs). The Pittsburgh Sleep Quality Index (PSQI) measured subjective sleep quality and the Sleep Timing Questionnaire (STQ) assessed habitual sleep latency and minutes awake after sleep onset. The duration, timing, and stability of sleep were assessed using the STQ separately for work-week nights (Sunday?Thursday) and for weekend nights (Friday and Saturday). Morningness-eveningness was assessed using the Composite Scale of Morningness (CSM). Daytime sleepiness was measured using the Epworth Sleepiness Scale (ESS). A morning-type orientation was associated with longer weekly sleep duration, better subjective sleep quality, and shorter sleep-onset latency. Stable weekday rise-time correlated with better self-reported sleep quality and shorter sleep-onset latency. A more regular weekend bedtime was associated with a shorter sleep latency. A more stable weekend rise-time was related to longer weekday sleep duration and lower daytime sleepiness. Increased overall regularity in rise-time was associated with better subjective sleep quality, shorter sleep-onset latency, and higher weekday sleep efficiency. Finally, a morning orientation was related to increased regularity in both bedtimes and rise-times. In conclusion, in daytime workers, a morning-type orientation and more stable sleep timing are associated with better subjective sleep quality. (Author correspondence: asoehner@berkeley.edu ).     

The effects of two types of sleep deprivation on visual working memory capacity and filtering efficiency

Sleep deprivation has adverse consequences for a variety of cognitive functions. The exact effects of sleep deprivation, though, are dependent upon the cognitive process examined. Within working memory, for example, some component processes are more vulnerable to sleep deprivation than others. Additionally, the differential impacts on cognition of different types of sleep deprivation have not been well studied. The aim of this study was to examine the effects of one night of total sleep deprivation and 4 nights of partial sleep deprivation (4 hours in bed/night) on two components of visual working memory: capacity and filtering efficiency. Forty-four healthy young adults were randomly assigned to one of the two sleep deprivation conditions. All participants were studied: 1) in a well-rested condition (following 6 nights of 9 hours in bed/night); and 2) following sleep deprivation, in a counter-balanced order. Visual working memory testing consisted of two related tasks. The first measured visual working memory capacity and the second measured the ability to ignore distractor stimuli in a visual scene (filtering efficiency). Results showed neither type of sleep deprivation reduced visual working memory capacity. Partial sleep deprivation also generally did not change filtering efficiency. Total sleep deprivation, on the other hand, did impair performance in the filtering task. These results suggest components of visual working memory are differentially vulnerable to the effects of sleep deprivation, and different types of sleep deprivation impact visual working memory to different degrees. Such findings have implications for operational settings where individuals may need to perform with inadequate sleep and whose jobs involve receiving an array of visual information and discriminating the relevant from the irrelevant prior to making decisions or taking actions (e.g., baggage screeners, air traffic controllers, military personnel, health care providers).     

Metabolic states in athletes during alternate intense muscular activity

The dynamics of metabolic states in athletes during alternate intense muscular activity was studied. In a laboratory, highly trained athletes (cyclists and speed skaters) performed tests on a bicycle ergometer at the level of the critical power and maximal oxygen consumption. In two additional series of experiments, each of the subjects performed tests at the level of critical power with initial acceleration of 28% of the maximal duration of the 45- and 108-s exercises. During the exercise when the subjects worked at critical power, a succession of metabolic phases was observed: the initial lag period, rapid exponential growth to the level of critical power, subsequent maintenance of the critical power, and, finally, functional disorders of aerobic metabolism, along with increasing local fatigue. We found that a short (no more than 10 s) initial acceleration at the level of power equal to the 45-s maximal exercise is the most efficient for performance at the level of critical power maintenance; this acceleration stimulates the development of aerobic metabolism and does not lead to depletion of anaerobic resources or considerable local exhaustion at the end of the performance.