Biomedical subjects

C Cajochen

Publications and source records attributed to C Cajochen.

32 records · Page 2Linked to original sources

PubMed1997

The hypothermic effect of late evening melatonin does not block the phase delay induced by concurrent bright light in human subjects.

This constant routine study (n = 9 men) compared the phase delay of the circadian system induced by a single pulse of evening light (5000 lx at 2100-2400 h) in the presence or absence of exogenous melatonin (5 mg p.o. at 2040 h). On the treatment day, light and melatonin protracted and accelerated, respectively, the evening decline in core body temperature (CBT). Subjective sleepiness ratings showed parallel shifts, the earlier the decline in CBT, the sleepier. On the post-treatment day, light induced a phase delay in the mid-range crossing time of CBT decline independent of whether melatonin was co-administered or not. Subjective sleepiness was delayed in parallel. The phase delay of the circadian system by evening light appears to be independent of an immediate hyperthermic effect and is not mediated by melatonin.

Adult↗

PubMed1997

Early evening melatonin and S-20098 advance circadian phase and nocturnal regulation of core body temperature.

The phase-shifting capacity and thermoregulatory effects of a single oral administration at 18 h of melatonin (5 mg) or S-20098, a melatonin agonist (5 or 100 mg), was investigated in eight healthy young men in a double-blind placebo crossover design. The unmasking conditions of a shortened constant-routine protocol (mini-CR) were used to collect evening phase markers of physiological parameters. In comparison to placebo, all three drug administrations induced an earlier dim-light melatonin onset (DLMO), an earlier increase in distal skin temperature, and an earlier decrease in core body temperature (CBT), heart rate, and proximal skin temperature. This indicates that administration at 18 h of both melatonin and S-20098 (more pronounced with 100 than 5 mg) induced an earlier regulation of the endogenous circadian nocturnal decline in CBT. On the posttreatment day a second mini-CR revealed persistent significantly phase-advanced circadian rhythms as estimated by DLMO, as well as by the midrange crossing time of CBT and heart rate decline. There were no significant differences between the two doses of S-20098. The data suggest that, in addition to immediate thermoregulatory changes, a phase advance of the circadian system had occurred and that the phase advance could still be measured on the posttreatment day.

Acetamides↗

PubMed1997

Melatonin and S-20098 increase REM sleep and wake-up propensity without modifying NREM sleep homeostasis.

The pineal hormone melatonin has been implicated in the circadian regulation of sleep. In a crossover design, we investigated the effect of acute administration of 5 mg melatonin and a melatonin agonist (S-20098, 5 and 100 mg) in healthy young men when given 5 h before bedtime on sleep structure and electroencephalogram (EEG) power density. Each trial comprised a baseline, a treatment, and a posttreatment sleep episode. Relative to the placebo condition, all treatments phase advanced the core body temperature rhythm [Kräuchi, K., C. Cajochen, D. Möri, C. Hetsch, and A. Wirz-Justice. Sleep Res. 24: 526, 1995; and Kräuchi, K., C. Cajochen, D. Möri, and A. Wirz-Justice. Am. J. Physiol. 272 (Regulatory Integrative Comp. Physiol. 41): R1178-1188, 1997]. Rapid eye movement (REM) sleep was increased after both melatonin and S-20098. This increase in REM sleep was most pronounced in the first REM sleep episode. On the posttreatment night after melatonin and S-20098 administration, more wakefulness was present in the latter one-half of the sleep episode. EEG power density between 0.25 and 20 Hz during either non-REM (NREM) or REM sleep did not differ from placebo. Thus a single early evening dose of melatonin or the agonist S-20098 increases REM sleep propensity and advances sleep termination while, at the same time, the EEG in NREM sleep remains unaffected.

Acetamides↗

PubMed1997

A relationship between heat loss and sleepiness: effects of postural change and melatonin administration.

Both the pineal hormone melatonin (Mel) and postural changes have thermoregulatory sequelae. The purpose of the study was to evaluate their relationship to subjective sleepiness. Eight healthy young men were investigated under the unmasking conditions of a constant routine protocol. Heart rate, rectal temperature (Tre), skin temperatures (foot, Tfo; and stomach), and subjective sleepiness ratings were continuously recorded from 1000 to 1700. Mel (5 mg po) was administered at 1300, a time when Mel should not phase shift the circadian system. Both the postural change at 1000 from upright to a supine position (lying down in bed) and Mel administration at 1300 reduced Tre and increased Tfo in parallel with increased sleepiness. These findings suggest that under comfortable ambient temperature conditions, heat loss via the distal skin regions (e.g., feet) is a key mechanism for induction of sleepiness as core body temperature declines.

Adult↗

PubMed1997

Melatonin and the circadian regulation of sleep initiation, consolidation, structure, and the sleep EEG.

The endogenous circadian rhythm of melatonin, driven by the suprachiasmatic nucleus, exhibits a close association with the endogenous circadian component of the sleep propensity rhythm and the endogenous circadian component of the variation in electroencephalogram (EEG) oscillations such as sleep spindles and slow waves. This association is maintained even when the sleep-wake cycle is desynchronized from the endogenous circadian rhythm of melatonin. Administration of melatonin during the day increases daytime sleep propensity as indexed by both the latency to sleep onset and sleep consolidation. The EEG during daytime sleep after melatonin administration exhibits characteristics reminiscent of the nocturnal sleep EEG, that is, increased sleep spindle activity and reduced slow-wave sleep and slow-wave activity, as detected by quantitative EEG analysis. Administration of higher doses of melatonin (5 mg or more) prior to nocturnal sleep results in an increase in rapid eye movement (REM) sleep. These data demonstrate that melatonin exerts effects on the main characteristics of human sleep, that is, latency to sleep onset, sleep consolidation, slow waves, sleep spindles, and REM sleep. There is a need for further studies using physiological doses and delivery systems that generate physiological plasma melatonin profiles to firmly establish the role of the endogenous circadian rhythm of melatonin in the circadian regulation of sleep.

Animals↗

PubMed1997

The acute soporific action of daytime melatonin administration: effects on the EEG during wakefulness and subjective alertness.

Melatonin has been reported to have soporific effects; following daytime administration, it induces sleepiness and reduces sleep onset latency. However, subjective sleepiness is masked by a variety of stimuli and behaviors; thus, it is important to be able to delineate objective psychophysiological sequelae of melatonin administration. Alertness decrements during wakefulness are correlated with augmented theta/alpha power in the waking electroencephalogram (EEG). This has been validated in a constant routine protocol. In a variety of experiments with melatonin administration (5 mg), the authors have shown that the EEG changes can be measured immediately, before any subjective soporific effects are recognized. These increases in theta/alpha power occur when melatonin is administered during the day (1300 or 1800 h) but are less visible when near the endogenous melatonin rise in the evening (2040 h). Importantly, both subjective and objective measures of sleepiness are suppressed when subjects change posture from supine to standing.

Animals↗

PubMed1996

Daytime melatonin administration enhances sleepiness and theta/alpha activity in the waking EEG.

It is still controversial whether the pineal hormone melatonin can be characterized as a hypnotic. We therefore measured subjective sleepiness and waking EEG power density in the range of 0.25-20 Hz after a single dose of melatonin (5 mg). During an 8 h mini-constant routine protocol, melatonin administered in a double blind cross-over design to healthy young men at 1300 h or 1800 h increased subjective sleepiness, as rated half-hourly on three different scales (Visual Analogue Scale, Akerstedt Sleepiness Symptoms Check List, Akerstedt Sleepiness Scale) and objective fatigue as evidenced by augmented waking EEG power density in the theta/alpha range (5.25-9 Hz). The increase in subjective sleepiness reached significance 40 min and 90 min after melatonin administration (at 1300 h and 1800 h, respectively) and lasted for 3 h (at 1300 h) and 5 h (at 1800 h). The increase in the theta/alpha frequencies of the waking EEG occurred immediately after melatonin ingestion and stayed significantly higher parallel to the higher sleepiness ratings. However, the EEG changes appeared before the subjective symptoms of sleepiness became manifest. There was a significant correlation between salivary melatonin levels and the timing of increased subjective sleepiness. Melatonin had no effects on mood.

Adult↗

PubMed1996

Homeostatic sleep regulation in habitual short sleepers and long sleepers.

Homeostatic sleep regulation in habitual short sleepers (sleep episode < 6 h, n = 9) and long sleepers (> 9 h, n = 7) was investigated by studying their sleep structure and sleep electroencephalogram (EEG) during baseline conditions and after prolonging their habitual waking time by 24 h. In each sleep episode, total sleep time was > 3 h longer in the long sleepers than in the short sleepers. Sleep deprivation decreased sleep latency and rapid eye movement (REM) density in REM sleep more in long sleepers than in short sleepers. The enhancement of EEG slow-wave activity (SWA; spectral power density in the 0.75-4.5 Hz range) in non-REM sleep after sleep loss was larger in long sleepers (47%) than in short sleepers (19%). This difference in the SWA response was predicted by the two-process model of sleep regulation on the basis of the different sleep durations. The results indicate that short sleepers live under a higher "non-REM sleep pressure" than long sleepers. However, the two groups do not differ with respect to the homeostatic sleep regulatory mechanisms.

Adult↗

PubMed1995

Power density in theta/alpha frequencies of the waking EEG progressively increases during sustained wakefulness.

Electroencephalogram (EEG) power density and self-rated fatigue were assessed in nine healthy women during a 40-hour period of sustained wakefulness under constant behavioral and environmental conditions (constant routine protocol). Waking EEG recordings were performed for 4 minutes after 3, 10, 27 and 34 hours of prior wakefulness. EEG power density in the 6.25- to 9.0-Hz frequency range progressively increased across the four recordings, suggesting an endogenous homeostatic component in the regulation of the theta/alpha frequencies under constant conditions. Subjective fatigue also exhibited an increasing component in the course of the constant routine protocol, with a clear circadian modulation. Fatigue ratings and the theta/ alpha power density of the waking EEG recorded at the same four time points during the constant routine protocol correlated significantly. Our data demonstrate the presence of a homeostatic component in the control of EEG power density in the 6.25- to 9.0-Hz range.

Adult↗

PubMed1994

Sleep in a sitting position: effect of triazolam on sleep stages and EEG power spectra.

The effect of triazolam (0.25 mg) and placebo was investigated in healthy, male subjects who slept in a sitting position. After the intake of placebo, sleep efficiency, rapid eye movement (REM) sleep and subjective sleep quality were lower than in the preceding sleep episode in bed, while stage 1 and REM sleep latency were higher. Triazolam did not prevent this impairment of sleep. However, in comparison with the placebo condition, the percentage of slow wave sleep was higher in the first third of the night, and in the morning sleep was rated as more quite. EEG power density in nonREM sleep was reduced in the frequency range of 1.25-10.0 Hz and enhanced in the range of sleep spindles (12.25-13.0 Hz). These changes were still present in the last third of the night. In REM sleep, triazolam reduced spectral activity in some frequency bins between 4.25 and 10.0 Hz. The sitting position itself affected the nonREM sleep spectra, since the placebo level in the 2.25-21.0-Hz range exceeded the baseline level. We conclude that a 0.25 mg dose of triazolam does not effectively counteract a posture-induced sleep disturbance, but induces changes in the EEG spectra which are typical for benzodiazepine receptor agonists.

Adult↗

PubMed1994

Heart rate dynamics during human sleep.

To investigate the dynamics of heart rate in the course of sleep and to relate cardiac activity to sleep intensity, the electrocardiogram was recorded concomitantly with the polysomnogram in healthy young males. Heart rate was assessed across consecutive non-REM sleep (NREMS)-REM sleep (REMS) cycles as well as within individual episodes of NREMS and REMS. Within a sleep cycle, heart rate was lower in the NREMS episode than in the subsequent REMS episode. A global declining trend was present over successive NREMS episodes and over successive REMS episodes. A rapid increase of heart rate at the NREMS-REMS transitions was followed by a slow decline that started within the REMS episodes. Heart rate variability was higher in REMS than in NREMS and showed an increasing trend over successive REMS episodes but not over successive NREMS episodes. EEG slow-wave activity (spectral power density in the 0.75-4.5 Hz band), an intensity measure of NREMS, declined across NREMS episodes and was not correlated with heart rate. The global trends and ultradian variations of heart rate may represent sleep state-dependent modulations and circadian variations of the autonomic nervous system, which are not fully reflected in the sleep EEG.

Adult↗

PubMed1992

Dynamics of EEG slow-wave activity and core body temperature in human sleep after exposure to bright light.

In seven subjects sleep was recorded after a single 3-hour (2100-0000 hours) exposure to either bright light (BL, approx. 2,500 lux) or dim light (DL, approx. 6 lux) in a crossover design. The latency to sleep onset was increased after BL. Whereas rectal temperature before onset and during the first 4 hours of sleep was higher after BL than after DL, the time course of electroencephalographic (EEG) slow-wave activity (SWA, EEG power density in the range of 0.75-4.5 Hz) in nonrapid eye movement sleep (NREMS) differed only slightly between the conditions. After BL, SWA tended to be lower than after DL in the first NREMS-REMS cycle and was higher in the fourth cycle at the time when the rectal temperature did not differ. The differences in SWA may have been due to a minor sleep-disturbing aftereffect of BL, which was followed by a rebound. The data are not in support of a close relationship between SWA and core body temperature.

Adult↗

PubMed1991

Effect of a single 3-hour exposure to bright light on core body temperature and sleep in humans.

Seven human subjects were exposed to bright light (BL, approx. 2500 lux) and dim light (DL, approx. 6 lux) during 3 h prior to nocturnal sleep, in a cross-over design. At the end of the BL exposure period core body temperature was significantly higher than at the end of the DL exposure period. The difference in core body temperature persisted during the first 4 h of sleep. The latency to sleep onset was increased after BL exposure. Rapid-eye movement sleep (REMS) and slow-wave sleep (SWS; stage 3 + 4 of non-REMS) were not significantly changed. Eight subjects were exposed to BL from 20.30 to 23.30 h while their eyes were covered or uncovered. During BL exposure with uncovered eyes, core body temperature decreased significantly less than during exposure with covered eyes. We conclude that bright light immediately affects core body temperature and that this effect is mediated via the eyes.

Adult↗

PubMed1991

Sleep extension in humans: sleep stages, EEG power spectra and body temperature.

In eight male subjects the electroencephalogram (EEG) and core body temperature (Tcore) were recorded during long sleep episodes from 0000 to 1,500 hr. EEGs were visually scored and subjected to spectral analysis by fast Fourier transform. Slow-wave sleep [SWS, i.e. stages 3 + 4 of non-rapid eye movement (NREM) sleep and slow wave activity (SWA, mean EEG power density in the range of 0.75-4.5 Hz)] in NREM sleep attained highest values in the first 3 hr of sleep and lowest values in the morning hours when rapid eye movement (REM) sleep was at its maximum. Wakefulness was significantly enhanced in the last 3 hr of the recording period. Occasional NREM episodes containing SWS were observed in the late morning and early afternoon. However, no significant increase in SWS or SWA in the last 3 hr of the sleep episode over any of the preceding 3-hr intervals was present and SWA in this interval was significantly below the values observed at the beginning of sleep. The duration of NREM episodes varied significantly over the sleep episode. Analysis of the dynamics of SWA within NREM episodes revealed that SWA gradually rose during the episode. Consequently, SWA averaged per episode was positively correlated with episode duration. Tcore dropped in the initial part of sleep, rose during the morning hours and reached values in the afternoon that were higher than at the beginning of sleep. Thus the time course of Tcore dissociated from the time course of SWA. This indicates that SWA in NREM sleep is not directly related to the variation in core body temperature.

Adult↗