Daily exercise facilitates phase delays of circadian melatonin rhythm in very dim light

2004 ◽  
Vol 286 (6) ◽  
pp. R1077-R1084 ◽  
Author(s):  
Laura K. Barger ◽  
Kenneth P. Wright ◽  
Rod J. Hughes ◽  
Charles A. Czeisler
Keyword(s):  
Exercise Intervention ◽  
Light Exposure ◽  
Phase Relationship ◽  
Shift Workers ◽  
Circadian Phase ◽  
Daily Exercise ◽  
Timing System ◽  
Before And After ◽  
Circadian Timing System ◽  
Dim Light

Shift workers and transmeridian travelers are exposed to abnormal work-rest cycles, inducing a change in the phase relationship between the sleep-wake cycle and the endogenous circadian timing system. Misalignment of circadian phase is associated with sleep disruption and deterioration of alertness and cognitive performance. Exercise has been investigated as a behavioral countermeasure to facilitate circadian adaptation. In contrast to previous studies where results might have been confounded by ambient light exposure, this investigation was conducted under strictly controlled very dim light (standing ∼0.65 lux; angle of gaze) conditions to minimize the phase-resetting effects of light. Eighteen young, fit males completed a 15-day randomized clinical trial in which circadian phase was measured in a constant routine before and after exposure to a week of nightly bouts of exercise or a nonexercise control condition after a 9-h delay in the sleep-wake schedule. Plasma samples collected every 30–60 min were analyzed for melatonin to determine circadian phase. Subjects who completed three 45-min bouts of cycle ergometry each night showed a significantly greater shift in the dim light melatonin onset (DLMO25%), dim light melatonin offset, and midpoint of the melatonin profile compared with nonexercising controls (Student t-test; P < 0.05). The magnitude of phase delay induced by the exercise intervention was significantly dependent on the relative timing of the exercise after the preintervention DLMO25% ( r = −0.73, P < 0.05) such that the closer to the DLMO25%, the greater the phase shift. These data suggest that exercise may help to facilitate circadian adaptation to schedules requiring a delay in the sleep-wake cycle.

Daytime naps in darkness phase shift the human circadian rhythms of melatonin and thyrotropin secretion

2000 ◽  
Vol 278 (2) ◽  
pp. R373-R382 ◽  
Author(s):  
Orfeu M. Buxton ◽  
Mireille L'Hermite-Balériaux ◽  
Fred W. Turek ◽  
Eve van Cauter
Keyword(s):  
Circadian Rhythms ◽  
Phase Shift ◽  
Light Exposure ◽  
Caloric Intake ◽  
Stimulus Exposure ◽  
Blood Samples ◽  
Circadian Misalignment ◽  
Circadian Phase ◽  
Before And After ◽  
Dim Light

To systematically determine the effects of daytime exposure to sleep in darkness on human circadian phase, four groups of subjects participated in 4-day studies involving either no nap (control), a morning nap (0900–1500), an afternoon nap (1400–2000), or an evening nap (1900–0100) in darkness. Except during the scheduled sleep/dark periods, subjects remained awake under constant conditions, i.e., constant dim light exposure (36 lx), recumbence, and caloric intake. Blood samples were collected at 20-min intervals for 64 h to determine the onsets of nocturnal melatonin and thyrotropin secretion as markers of circadian phase before and after stimulus exposure. Sleep was polygraphically recorded. Exposure to sleep and darkness in the morning resulted in phase delays, whereas exposure in the evening resulted in phase advances relative to controls. Afternoon naps did not change circadian phase. These findings indicate that human circadian phase is dependent on the timing of darkness and/or sleep exposure and that strategies to treat circadian misalignment should consider not only the timing and intensity of light, but also the timing of darkness and/or sleep.

scholarly journals Photoperiodic Requirements for Induction and Maintenance of Rhythm Bifurcation and Extraordinary Entrainment in Male Mice

2019 ◽  
Vol 1 (3) ◽  
pp. 290-305 ◽  
Author(s):  
Jonathan Sun ◽  
Deborah A. M. Joye ◽  
Andrew H. Farkas ◽  
Michael R. Gorman
Keyword(s):  
Male Mice ◽  
Shift Workers ◽  
Circadian Timing ◽  
Non Invasive ◽  
Circadian Control ◽  
Timing System ◽  
Circadian Timing System ◽  
Activity Cycles ◽  
Rest Activity

Exposure of mice to a 24 h light:dark:light:dark (LDLD) cycle with dimly illuminated nights induces the circadian timing system to program two intervals of activity and two intervals of rest per 24 h cycle and subsequently allows entrainment to a variety of extraordinary light regimens including 30 h LDLD cycles. Little is known about critical lighting requirements to induce and maintain this non-standard entrainment pattern, termed “bifurcation,” and to enhance the range of apparent entrainment. The current study determined the necessary duration of the photophase for animals to bifurcate and assessed whether requirements for maintenance differed from those for induction. An objective index of bifurcated entrainment varied with length of the photophase over 4–10 h durations, with highest values at 8 h. To assess photic requirements for the maintenance of bifurcation, mice from each group were subsequently exposed to the LDLD cycle with 4 h photophases. While insufficient to induce bifurcation, this photoperiod maintained bifurcation in mice transferred from inductive LDLD cycles. Entrainment to 30 h LDLD cycles also varied with photoperiod duration. These studies characterize non-invasive tools that reveal latent flexibility in the circadian control of rest/activity cycles with important translational potential for addressing needs of human shift-workers.

scholarly journals Circadian Potency Spectrum with Extended Exposure to Polychromatic White LED Light under Workplace Conditions

2020 ◽  
Vol 35 (4) ◽  
pp. 405-415 ◽  
Author(s):  
Martin Moore-Ede ◽  
Anneke Heitmann ◽  
Rainer Guttkuhn
Keyword(s):  
Spectral Sensitivity ◽  
White Light ◽  
Light Exposure ◽  
Human Subjects ◽  
Light Sources ◽  
Led Light ◽  
Light Spectra ◽  
Timing System ◽  
Circadian Timing System ◽  
Spectral Sensitivity Curve

Electric light has enabled humans to conquer the night, but light exposure at night can disrupt the circadian timing system and is associated with a diverse range of health disorders. To provide adequate lighting for visual tasks without disrupting the human circadian timing system, a precise definition of circadian spectral sensitivity is required. Prior attempts to define the circadian spectral sensitivity curve have used short (≤90-min) monochromatic light exposures in dark-adapted human subjects or in vitro dark-adapted isolated retina or melanopsin. Several lines of evidence suggest that these dark-adapted circadian spectral sensitivity curves, in addition to 430- to 499-nm (blue) wavelength sensitivity, may include transient 400- to 429-nm (violet) and 500- to 560-nm (green) components mediated by cone- and rod-originated extrinsic inputs to intrinsically photosensitive retinal ganglion cells (ipRGCs), which decay over the first 2 h of extended light exposure. To test the hypothesis that the human circadian spectral sensitivity in light-adapted conditions may have a narrower, predominantly blue, sensitivity, we used 12-h continuous exposures of light-adapted healthy human subjects to 6 polychromatic white light-emitting diode (LED) light sources with diverse spectral power distributions at recommended workplace levels of illumination (540 lux) to determine their effect on the area under curve of the overnight (2000–0800 h) salivary melatonin. We derived a narrow steady-state human Circadian Potency spectral sensitivity curve with a peak at 477 nm and a full-width half-maximum of 438 to 493 nm. This light-adapted Circadian Potency spectral sensitivity permits the development of spectrally engineered LED light sources to minimize circadian disruption and address the health risks of light exposure at night in our 24/7 society, by alternating between daytime circadian stimulatory white light spectra and nocturnal circadian protective white light spectra.

scholarly journals Circadian tau differences and rhythm associations in delayed sleep–wake phase disorder and sighted non-24-hour sleep–wake rhythm disorder

SLEEP ◽  
2020 ◽  
Author(s):  
Gorica Micic ◽  
Nicole Lovato ◽  
Sally A Ferguson ◽  
Helen J Burgess ◽  
Leon Lack
Keyword(s):  
Circadian Rhythm ◽  
Core Body Temperature ◽  
Sleep Onset ◽  
Phase Relationship ◽  
Biological Rhythms ◽  
Circadian Phase ◽  
Behavioral Rhythm ◽  
Rhythm Disorder ◽  
Dim Light ◽  
Delayed Sleep

Abstract Study Objectives We investigated biological and behavioral rhythm period lengths (i.e. taus) of delayed sleep–wake phase disorder (DSWPD) and non-24-hour sleep–wake rhythm disorder (N24SWD). Based on circadian phase timing (temperature and dim light melatonin onset), DSWPD participants were dichotomized into a circadian-delayed and a circadian non-delayed group to investigate etiological differences. Methods Participants with DSWPD (n = 26, 17 m, age: 21.85 ± 4.97 years), full-sighted N24SWD (n = 4, 3 m, age: 25.75 ± 4.99 years) and 18 controls (10 m, age: 23.72 ± 5.10 years) participated in an 80-h modified constant routine. An ultradian protocol of 1-h “days” in dim light, controlled conditions alternated 20-min sleep/dark periods with 40-min enforced wakefulness/light. Subjective sleepiness ratings were recorded prior to every sleep/dark opportunity and median reaction time (vigilance) was measured hourly. Obtained sleep (sleep propensity) was derived from 20-min sleep/dark opportunities to quantify hourly objective sleepiness. Hourly core body temperature was recorded, and salivary melatonin assayed to measure endogenous circadian rhythms. Rhythm data were curved using the two-component cosine model. Results Patients with DSWPD and N24SWD had significantly longer melatonin and temperature taus compared to controls. Circadian non-delayed DSWPD had normally timed temperature and melatonin rhythms but were typically sleeping at relatively late circadian phases compared to those with circadian-delayed DSWPD. Conclusions People with DSWPD and N24SWD exhibit significantly longer biological circadian rhythm period lengths compared to controls. Approximately half of those diagnosed with DSWPD do not have abnormally delayed circadian rhythm timings suggesting abnormal phase relationship between biological rhythms and behavioral sleep period or potentially conditioned sleep-onset insomnia.

scholarly journals Nutrition in the spotlight: metabolic effects of environmental light

2016 ◽  
Vol 75 (4) ◽  
pp. 451-463 ◽  
Author(s):  
Ruth I. Versteeg ◽  
Dirk J. Stenvers ◽  
Andries Kalsbeek ◽  
Peter H. Bisschop ◽  
Mireille J. Serlie ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Food Intake ◽  
Feeding Behaviour ◽  
Light Exposure ◽  
Human Subjects ◽  
Metabolic Effects ◽  
Artificial Light ◽  
Circadian Timing ◽  
Timing System ◽  
Circadian Timing System

Use of artificial light resulted in relative independence from the natural light–dark (LD) cycle, allowing human subjects to shift the timing of food intake and work to convenient times. However, the increase in artificial light exposure parallels the increase in obesity prevalence. Light is the dominant Zeitgeber for the central circadian clock, which resides within the hypothalamic suprachiasmatic nucleus, and coordinates daily rhythm in feeding behaviour and metabolism. Eating during inappropriate light conditions may result in metabolic disease via changes in the biological clock. In this review, we describe the physiological role of light in the circadian timing system and explore the interaction between the circadian timing system and metabolism. Furthermore, we discuss the acute and chronic effects of artificial light exposure on food intake and energy metabolism in animals and human subjects. We propose that living in synchrony with the natural daily LD cycle promotes metabolic health and increased exposure to artificial light at inappropriate times of day has adverse effects on metabolism, feeding behaviour and body weight regulation. Reducing the negative side effects of the extensive use of artificial light in human subjects might be useful in the prevention of metabolic disease.

scholarly journals Clock Gene Expression in Adult Primate Suprachiasmatic Nuclei and Adrenal: Is the Adrenal a Peripheral Clock Responsive to Melatonin?

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1454-1461 ◽  
Author(s):  
F. J. Valenzuela ◽  
C. Torres-Farfan ◽  
H. G. Richter ◽  
N. Mendez ◽  
C. Campino ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Clock Gene ◽  
Clock Genes ◽  
Phase Relationship ◽  
Suprachiasmatic Nuclei ◽  
Rhythmic Expression ◽  
Peripheral Oscillators ◽  
Clock Gene Expression ◽  
Timing System ◽  
Circadian Timing System

The circadian production of glucocorticoids involves the concerted action of several factors that eventually allow an adequate adaptation to the environment. Circadian rhythms are controlled by the circadian timing system that comprises peripheral oscillators and a central rhythm generator located in the suprachiasmatic nucleus (SCN) of the hypothalamus, driven by the self-regulatory interaction of a set of proteins encoded by genes named clock genes. Here we describe the phase relationship between the SCN and adrenal gland for the expression of selected core clock transcripts (Per-2, Bmal-1) in the adult capuchin monkey, a New World, diurnal nonhuman primate. In the SCN we found a higher expression of Bmal-1 during the h of darkness (2000–0200 h) and Per-2 during daytime h (1400 h). The adrenal gland expressed clock genes in oscillatory fashion, with higher values for Bmal-1 during the day (1400–2000 h), whereas Per-2 was higher at nighttime (about 0200 h), resulting in a 9- to 12-h antiphase pattern. In the adrenal gland, the oscillation of clock genes was accompanied by rhythmic expression of a functional output, the steroidogenic enzyme 3β-hydroxysteroid dehydrogenase. Furthermore, we show that adrenal explants maintained oscillatory expression of Per-2 and Bmal-1 for at least 36 h in culture. The acrophase of both transcripts, but not its overall expression along the incubation, was blunted by 100 nm melatonin. Altogether, these results demonstrate oscillation of clock genes in the SCN and adrenal gland of a diurnal primate and support an oscillation of clock genes in the adrenal gland that may be modulated by the neurohormone melatonin.

scholarly journals Epigenetic Regulation of Circadian Clocks and Its Involvement in Drug Addiction

Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1263
Author(s):  
Lamis Saad ◽  
Jean Zwiller ◽  
Andries Kalsbeek ◽  
Patrick Anglard
Keyword(s):  
Circadian Clock ◽  
Drug Addiction ◽  
Epigenetic Regulation ◽  
Molecular Mechanisms ◽  
Feedback System ◽  
Circadian Clocks ◽  
Shift Workers ◽  
Timing System ◽  
Small Regulatory Rnas ◽  
Circadian Timing System

Based on studies describing an increased prevalence of addictive behaviours in several rare sleep disorders and shift workers, a relationship between circadian rhythms and addiction has been hinted for more than a decade. Although circadian rhythm alterations and molecular mechanisms associated with neuropsychiatric conditions are an area of active investigation, success is limited so far, and further investigations are required. Thus, even though compelling evidence connects the circadian clock to addictive behaviour and vice-versa, yet the functional mechanism behind this interaction remains largely unknown. At the molecular level, multiple mechanisms have been proposed to link the circadian timing system to addiction. The molecular mechanism of the circadian clock consists of a transcriptional/translational feedback system, with several regulatory loops, that are also intricately regulated at the epigenetic level. Interestingly, the epigenetic landscape shows profound changes in the addictive brain, with significant alterations in histone modification, DNA methylation, and small regulatory RNAs. The combination of these two observations raises the possibility that epigenetic regulation is a common plot linking the circadian clocks with addiction, though very little evidence has been reported to date. This review provides an elaborate overview of the circadian system and its involvement in addiction, and we hypothesise a possible connection at the epigenetic level that could further link them. Therefore, we think this review may further improve our understanding of the etiology or/and pathology of psychiatric disorders related to drug addiction.

scholarly journals The Effect of Cognitive Behaviour Therapy on Sleep and Circadian Rhythm in Young College Students

2021 ◽  
pp. 43-47
Author(s):  
Shweta Kanchan ◽  
Sunita Tiwari ◽  
Shweta Singh
Keyword(s):  
Cognitive Behaviour Therapy ◽  
Sleep Time ◽  
Behaviour Therapy ◽  
Circadian Phase ◽  
Dim Light Melatonin Onset ◽  
College Going ◽  
Cognitive Behaviour ◽  
Before And After ◽  
Sleep Parameters ◽  
Dim Light

The present study is to study the effect of cognitive behaviour therapy on various sleep parameters and circadian phase rhythmic in young college going adults. Fifty young college going adults were chosen from the MBBS and BDS students of King George's Medical University Lucknow, their polysomnography was conducted along with it salivary melatonin estimation was conducted to find the time of Dim light melatonin onset (DLMO), the subjects were administered cognitive behaviour therapy (CBT),after completing the sessions of cognitive behaviour therapy another Polysomnographic study and DLMO estimation was conducted, various sleep parameters were compared before and after the CBT. The study showed an improvement in the steep quality, a decrease in daytime sleepiness along with this total sleep time significantly increased, sleep efficiency also improved and there was a decrease in the REM sleep latency. The Dim light melatonin onset advanced for the subjects and the chronotype showed an inclination towards an earlier timings.

156 Evening Light-Induced Circadian Phase Shift in Preschool-Aged Children

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A63-A64
Author(s):  
Lauren Hartstein ◽  
Lameese Akacem ◽  
Cecilia Diniz Behn ◽  
Shelby Stowe ◽  
Kenneth Wright ◽  
...  
Keyword(s):  
Phase Shift ◽  
Light Exposure ◽  
Light Stimulus ◽  
Phase Delay ◽  
Healthy Children ◽  
Dependent Manner ◽  
Circadian Phase ◽  
Light Intensities ◽  
Dim Light ◽  
Dose Dependent

Abstract Introduction In adults, exposure to light at night delays the timing of the circadian clock in a dose-dependent manner with intensity. Although children’s melatonin levels are highly suppressed by evening bright light, the sensitivity of young children’s circadian timing to evening light is unknown. This research aimed to establish an illuminance response curve for phase delay in preschool children as a result of exposure to varying light intensities in the hour before bedtime. Methods Healthy children (n=36, 3.0 – 4.9 years, 39% males), participated in a 10-day protocol. For 7 days, children followed a strict parent-selected sleep schedule. On Days 8-10, an in-home dim-light assessment was performed. On Day 8, dim light melatonin onset (DLMO) was measured through saliva samples collected in 20-30-min intervals throughout the evening until 1-h past habitual bedtime. On Day 9, children were exposed to a white light stimulus (semi-randomly assigned from 5lx to 5000lx) for 1-h before their habitual bedtime, and saliva was collected before, during, and after the exposure. On Day 10, children provided saliva samples in the evening for 2.5-h past bedtime for a final DLMO assessment. Phase angle of entrainment (habitual bedtime – DLMObaseline) and circadian phase delay (DLMOfinal – DLMObaseline) were computed. Results Final DLMO (Day 10) shifted between -8 and 123 minutes (M = 56.1 +/- 33.6 min; negative value = phase advance, positive value = phase delay) compared with DLMO at baseline (Day 8). Raw phase shift did not demonstrate a dose-dependent relationship with light intensity. Rather, we observed a robust phase delay across all intensities. Conclusion These data suggest preschoolers’ circadian clocks are immensely sensitive to a large range of light intensities, which may be mechanistically influenced by less mature ophthalmologic features (e.g. clearer lenses, larger pupils). With young children’s ever-growing use of light-emitting devices and evening exposure to artificial lighting, as well as the prevalence of behavioral sleep problems, these findings may inform recommendations for parents on the effects of evening light exposure on sleep timing in early childhood. Support (if any) This research was supported with funds from the Eunice Kennedy Shriver National Institute of Child Health & Human Development (R01-HD087707).

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