Ageing and the circadian and homeostatic regulation of human sleep during forced desynchrony of rest, melatonin and temperature rhythms.
1. The circadian timing system has been implicated in age-related changes in sleep structure, timing and consolidation in humans. 2. We investigated the circadian regulation of sleep in 13 older men and women and 11 young men by forced desynchrony of polysomnographically recorded sleep episodes (total, 482; 9 h 20 min each) and the circadian rhythms of plasma melatonin and core body temperature. 3. Stage 4 sleep was reduced in older people. Overall levels of rapid eye movement (REM) sleep were not significantly affected by age. The latencies to REM sleep were shorter in older people when sleep coincided with the melatonin rhythm. REM sleep was increased in the first quarter of the sleep episode and the increase of REM sleep in the course of sleep was diminished in older people. 4. Sleep propensity co-varied with the circadian rhythms of body temperature and plasma melatonin in both age groups. Sleep latencies were longest just before the onset of melatonin secretion and short sleep latencies were observed close to the temperature nadir. In older people sleep latencies were longer close to the crest of the melatonin rhythm. 5. In older people sleep duration was reduced at all circadian phases and sleep consolidation deteriorated more rapidly during the course of sleep, especially when the second half of the sleep episode occurred after the crest of the melatonin rhythm. 6. The data demonstrate age-related decrements in sleep consolidation and increased susceptibility to circadian phase misalignment in older people. These changes, and the associated internal phase advance of the propensity to awaken from sleep, appear to be related to the interaction between a reduction in the homeostatic drive for sleep and a reduced strength of the circadian signal promoting sleep in the early morning. (+info)
Time course of sleep inertia dissipation in human performance and alertness.
Alertness and performance on a wide variety of tasks are impaired immediately upon waking from sleep due to sleep inertia, which has been found to dissipate in an asymptotic manner following waketime. It has been suggested that behavioural or environmental factors, as well as sleep stage at awakening, may affect the severity of sleep inertia. In order to determine the time course of sleep inertia dissipation under normal entrained conditions, subjective alertness and cognitive throughput were measured during the first 4 h after habitual waketime from a full 8-h sleep episode on 3 consecutive days. We investigated whether this time course was affected by either sleep stage at awakening or behavioural/environmental factors. Sleep inertia dissipated in an asymptotic manner and took 2-4 h to near the asymptote. Saturating exponential functions fitted the sleep inertia data well, with time constants of 0.67 h for subjective alertness and 1.17 h for cognitive performance. Most awakenings occurred out of stage rapid eye movement (REM), 2 or 1 sleep, and no effect of sleep stage at awakening on either the severity of sleep inertia or the time course of its dissipation could be detected. Subjective alertness and cognitive throughput were significantly impaired upon awakening regardless of whether subjects got out of bed, ate breakfast, showered and were exposed to ordinary indoor room light (approximately 150 lux) or whether subjects participated in a constant routine (CR) protocol in which they remained in bed, ate small hourly snacks and were exposed to very dim light (10-15 lux). These findings allow for the refinement of models of alertness and performance, and have important implications for the scheduling of work immediately upon awakening in many occupational settings. (+info)
Modelling and exploring human sleep with event history analysis.
In this paper we propose the use of statistical models of event history analysis for investigating human sleep. These models provide appropriate tools for statistical evaluation when sleep data are recorded continuously over time or on a fine time grid, and are classified into sleep stages such as REM and nonREM as defined by Rechtschaffen and Kales (1968). In contrast to conventional statistical procedures, event history analysis makes full use of the information contained in sleep data, and can therefore provide new insights into non-stationary properties of sleep. Probabilities of or intensities for transitions between sleep stages are the basic quantities for characterising sleep processes. The statistical methods of event history analysis aim at modelling and estimating these intensities as functions of time, taking into account individual sleep history and assessing the influence of factors of interest, such as hormonal secretion. In this study we suggest the use of non-parametric approaches to reveal unknown functional forms of transition intensities and to explore time-varying and non-stationary effects. We then apply these techniques in a study of 30 healthy male volunteers to assess the mean population intensity and the effects of plasma cortisol concentration on the transition between selected sleep stages as well as the influence of elapsed time in a current REM period on the intensity for a transition to nonREM. The most interesting findings are that (a) the intensity of the nonREM-to-REM transitions after sleep onset in young men shows a periodicity which is similar to that of nonREM/REM cycles; (b) 30-45 min after sleep onset, young men reveal a great propensity to pass from light sleep (stages 1 or 2) into slow-wave sleep (SWS) (stages 3 or 4); (c) high cortisol levels imposed additional impulses on the transition intensity of (i) wake to sleep around 2 h after sleep onset, (ii) nonREM to REM around 6 h later, (iii) stage 1 or stage 2 sleep to SWS around 2, 4 and 6 h later and (iv) SWS to stage 1 or stage 2 sleep about 2 h later. Moreover, high cortisol concentrations at the beginning of REM periods favoured the change to nonREM sleep, whereas later their influence on a nonREM change became weak and weaker. As sleep data are also available as event-oriented data in many studies in sleep research, event history analysis applied additionally to conventional statistical procedures, such as regression analysis or analysis of variance, could help to acquire more information and knowledge about the mechanisms behind the sleep process. (+info)
Heart period and heart period variability during sleep on the MIR space station.
The long-term acclimation of cardiac rhythms to microgravity was studied in four astronauts aboard the Russian space station MIR during wakefulness and sleep. Sleep polygraphies were obtained between the third and the 30th day in space and, in addition, prior to mission on the ground. From each of the sleep polygraphies, beat-to-beat intervals of cardiac rhythms were determined. The response of heart period and heart period variability to the stimulus microgravity was tested during sleep across sleep stages and during waking. A lengthening of heart period by about 100 ms was found in space compared to measurements on the ground. The slowing of heart rate was more pronounced for non-REM sleep than for REM sleep. A systematic change in heart period in relation to the duration of the stay in space could not be detected. An analysis of heart period variability in the high frequency (respiratory sinus arrhythmia) band supports the hypothesis that the decrease of heart rate under microgravity is produced by an increase in parasympathetic activity. Testing the response of cardiac rhythms to microgravity across distinct behavioural states seems to be a powerful tool to investigate the cardiovascular system. (+info)
Sino-aortic denervation augments the increase in blood pressure seen during paradoxical sleep in the rat.
Using a computer assisted telemetric system, we have re-examined the effect of sino-aortic denervation (SAD) on the changes in arterial blood pressure (AP) and heart rate (HR) during sleep in the rat suitably recovered from the operation. Eight 1 hourly polygraphic recordings were performed 4 weeks after the initial SAD surgery. In the SAD rats, the increase in AP during paradoxical sleep (PS) was much larger than that in sham-operated rats. HR in the SAD rats increased on-going from slow-wave sleep to PS, but it showed no change in sham-operated rats. The present study suggests that chronic SAD causes the enhanced AP increase during PS concomitantly with the persistent hypertension and tachycardia across sleep-wake states. (+info)
Prediction of sleep-disordered breathing by unattended overnight oximetry.
Between January 1994 and July 1997, 793 patients suspected of having sleep-disordered breathing had unattended overnight oximetry in their homes followed by laboratory polysomnography. From the oximetry data we extracted cumulative percentage time at SaO2 < 90% (CT90) and a saturation variability index (delta Index, the sum of the differences between successive readings divided by the number of readings - 1). CT90 was weakly correlated with polysomnographic apnea/hypopnea index (AHI). (Spearman rho = 0.36, P < 0.0001) and with delta Index (rho = 0.71, P < 0.0001). delta Index was more closely correlated with AHI (rho = 0.59, P < 0.0001). In a multivariate model, only delta Index was significantly related to AHI, the relationship being AHI = 18.8 delta Index + 7.7. The 95% CI for the coefficient were 16.2, 21.4, and for the constant were 5.8, 9.7. The sensitivity of a delta Index cut-off of 0.4 for the detection of AHI > or = 15 was 88%, for detection of AHI > or = 20 was 90% and for the detection of AHI > or = 25 was 91%. The specificity of delta Index > or = 0.4 for AHI > or = 15 was 40%. In 113 further patients, oximetry was performed simultaneously with laboratory polysomnography. Under these circumstances delta Index was more closely correlated with AHI (rho = 0.74, P < 0.0001), as was CT90 (rho = 0.58, P < 0.0001). Sensitivity of delta Index > or = 0.4 for detection of AHI > or = 15 was not improved at 88%, but specificity was better at 70%. We concluded that oximetry using a saturation variability index is sensitive but nonspecific for the detection of obstructive sleep apnea, and that few false negative but a significant proportion of false positive results arise from night-to-night variability. (+info)
The relationship between 6-sulphatoxymelatonin and polysomnographic sleep in good sleeping controls and wake maintenance insomniacs, aged 55-80 years.
The pineal hormone, melatonin, is reported to possess hypnotic properties. This has led to an investigation of the relationship between the endogenous melatonin rhythm and sleep. However, this relationship has yet to be fully examined in aged insomniacs and controls. From media advertisements, 16 good sleeping controls (11F, 5M) and 16 sleep maintenance insomniacs (11F, 5M), aged over 55 years, were recruited to participate in a study involving four nights of polysomnographically (PSG) measured sleep followed by a 26 h constant routine. During the constant routine, 2 h urine samples were collected and analysed for the melatonin metabolite, 6-sulphatoxymelatonin (aMT.6S). This was used to determine total melatonin excretion. As well, the following circadian melatonin parameters were calculated from fifth order polynomial curve fitting analyses, the goodness of the polynomial curve fit, peak melatonin concentration, the phase of the melatonin rhythm, and melatonin and sleep rhythm synchrony. Apart for one control, all subjects showed significant circadian melatonin rhythms. Although insomniacs showed a greater amount of wakefulness, less sleep in total, and lower sleep efficiency, no significant group differences were observed in any of the melatonin parameters. In addition, while subjects with more reliable melatonin curve fits showed shorter sleep latencies and higher sleep efficiencies, correlational analyses revealed no other significant relationships between any melatonin and PSG sleep parameters. Overall, the present results suggest that neither melatonin amplitude nor phase are related to sleep quality in the aged. (+info)
Sleep-disordered breathing in a predominantly African-American pediatric population.
The goal of this study was to characterize sleep and respiratory parameters in children with sleep-disordered breathing (SDB) as compared to children without SDB. Data are from 198 children and adolescents referred for sleep center evaluation, 128 of whom were diagnosed with SDB. In children with SDB, obesity (> 95% wgt for age) was more common than being severely underweight (< 5% wgt for age), but only the older children with SDB were heavier than age-matched normal sleepers. Children with SDB had increased EEG arousals; sleep architecture was not otherwise significantly different from the non-SDB group. African-American children with SDB had significantly greater oxygen desaturation with obstructive events compared to Caucasian and Latino children. It appears that the role of obesity as a risk factor for obstructive sleep apnea (OSA) increases in children above the age of 8-years. Additionally, African-American children with SDB may be at increased risk for hypoxemia and cardiovascular consequences of SDB. (+info)