Temporal dynamics of late-night photic stimulation of the human circadian timing system (original) (raw)
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Light of domestic intensity produces phase shifts of the circadian oscillator in humans
Neuroscience Letters, 1998
Twelve subjects have been studied in a chamber that isolated them from external noise and lighting. After several control days, one group (n = 6) was subjected to 18 × 27-h 'days' and the other to 11 × 30-h 'days'. Sleep was in the dark, and awake times were spent in normal domestic lighting (150-500 lux). Rectal temperature and wrist actimetry were measured throughout, and the phase of the circadian oscillator was inferred from that of the temperature data, purified to remove direct effects of activity. During the experimental 'days' the rhythms showed a mean period of 24.4 h. A detailed examination of the phase shifts from one day to the next showed that small advances and delays were superimposed upon this drift. Moreover, the mean size and direction of these shifts depended upon the time of exposure to lighting relative to the temperature minimum, as would be predicted from a phase-response curve.
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 1997
Fifty-six resetting trials were conducted across the subjective day in 43 young men using a three-cycle bright-light (∼10,000 lx) stimulus against a background of very dim light (10–15 lx). The phase-response curve (PRC) to these trials was assessed for the presence of a “dead zone” of photic insensitivity and was compared with another three-cycle PRC that had used a background of ∼150 lx. To assess possible transients after the light stimulus, the trials were divided into 43 steady-state trials, which occurred after several baseline days, and 13 consecutive trials, which occurred immediately after a previous resetting trial. We found that 1) bright light induces phase shifts throughout subjective day with no apparent dead zone; 2) there is no evidence of transients in constant routine assessments of the fitted temperature minimum 1–2 days after completion of the resetting stimulus; and 3) the timing of background room light modulates the resetting response to bright light. These da...
Circadian phase resetting by a single short-duration light exposure
JCI insight, 2017
BACKGROUND. In humans, a single light exposure of 12 minutes and multiple-millisecond light exposures can shift the phase of the circadian pacemaker. We investigated the response of the human circadian pacemaker to a single 15-second or 2-minute light pulse administered during the biological night. METHODS. Twenty-six healthy individuals participated in a 9-day inpatient protocol that included assessment of dim light melatonin onset time (DLMO time) before and after exposure to a single 15-second (n = 8) or 2-minute (n = 12) pulse of bright light (9,500 lux; 4,100 K fluorescent) or control background dim light (<3 lux; n = 6). Phase shifts were calculated as the difference in clock time between the two phase estimates. RESULTS. Both 15-second and 2-minute exposures induced phase delay shifts [median (± SD)] of -34.8 ± 47.2 minutes and -45.4 ± 28.4 minutes, respectively, that were significantly (P = 0.04) greater than the control condition (advance shift: +22.3 ± 51.3 minutes) but...
The Journal of Physiology, 2000
The light:dark cycle is the pre-eminent synchronizer of mammalian circadian pacemakers (Roenneberg & Foster, 1997; Czeisler & Wright, 1999). The response of mammalian pacemakers varies with both the timing and intensity of the photic stimuli. Both human and non-human mammals have been shown to share the same characteristic responses to variation in the timing of light exposure. Retinal light exposure in the early subjective night will delay the timing of the clock while light exposure in the late subjective night and early subjective morning will advance the timing of the clock (Czeisler et al. 1989; Johnson, 1990). Experimental light exposure at either time will induce a suppression of pineal melatonin production (Honma et al. 1992; Brainard et al. 1997). In non-human mammals, the intensity dependence of both phase shifting of the circadian pacemaker and acute suppression of melatonin have been well characterized (Brainard et al. 1983; Nelson & Takahashi, 1991b; Bauer, 1992; Sharma et al. 1999). In humans, it has been reported recently that three consecutive days of morning room-light exposure (•180 lx) can significantly phase advance the human circadian pacemaker (Boivin et al. 1996). The magnitude of the resetting response increased with the illuminance in a non-linear manner. This non-linearity was consistent with a cube-root compression of illuminance, one that had been reported previously for visual perception (Stevens, 1961). Though there were limited data below 180 lx, it was recognized that this postulated cube-root relationship could not account for responses observed to
Phase-dependent shift of free-running human circadian rhythms in response to a single bright pulse
Experientia, 1987
Responsiveness of free-running human circadian rhythms to a single pulse of bright light was examined in a temporal isolation unit. Bright light (5000 Ix) of either 3 or 6 h duration, applied during the early subjective day, produced phase-advance shifts in both the sleep-wake cycle and the rhythm of rectal temperature; the light pulse had essentially no effect on the phase of the circadian rhythms, when it was introduced during the late subjective day or the early subjective night. The results indicate that bright light can reset the human circadian pacemaker.
Circadian Responses to Fragmented Light: Research Synopsis in Humans
2019
Light is the chief signal used by the human circadian pacemaker to maintain precise biological timekeeping. Though it has been historically assumed that light resets the pacemaker’s rhythm in a dose-dependent fashion, a number of studies report enhanced circadian photosensitivity to the initial moments of light exposure, such that there are quickly diminishing returns on phase-shifting the longer the light is shown. In the current review, we summarize findings from a family of experiments conducted over two decades in the research wing of the Brigham and Women’s Hospital that examined the human pacemaker’s responses to standardized changes in light patterns generated from an overhead fluorescent ballast. Across several hundred days of laboratory recording, the research group observed phase-shifts in the body temperature and melatonin rhythms that scaled with illuminance. However, as suspected, phase resetting was optimized when exposure occurred as a series of minute-long episodes s...
Sleep, 2011
To evaluate the effect of increasing the intensity and/or duration of exposure on light-induced changes in the timing of the circadian clock of humans. Multifactorial randomized controlled trial, between and within subject design General Clinical Research Center (GCRC) of an academic medical center 56 healthy young subjects (20-40 years of age) Research subjects were admitted for 2 independent stays of 4 nights/3 days for treatment with bright or dim-light (randomized order) at a time known to induce phase delays in circadian timing. The intensity and duration of the bright light were determined by random assignment to one of 9 treatment conditions (duration of 1, 2, or 3 hours at 2000, 4000, or 8000 lux). Treatment-induced changes in the dim light melatonin onset (DLMO) and dim light melatonin offset (DLMOff) were measured from blood samples collected every 20-30 min throughout baseline and post-treatment nights. Comparison by multi-factor analysis of variance (ANOVA) of light-indu...
Combination of Light and Melatonin Time Cues for Phase Advancing the Human Cirdadian Clock
Phase Advancing with Bright Light and Melatonin-Burke et al The mammalian master circadian clock is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. 1,2 The SCN provides environmental and biological timing information to the rest of the body so that physiology and behavior are coordinated for optimal functioning relative to the time of day. The SCN receives input about environmental time through photic pathways via rod, cone, and melanopsin photoreceptors in the retina. 5,6 The SCN also receives input about behavioral and physiological states through non-photic pathways (e.g., serotonergic input from the raphe nucleus). 7-10 Misalignment between environmental time and internal biological timing (e.g., shift work, jet lag, circadian sleep-wakefulness disorders) can result in adverse psychological, neurobehavioral, and physiological consequences. 11-16 Photic and non-photic stimuli have both been used to phase shift the human circadian clock; however, there is limited information about how combinations of phase-shifting stimuli influence the timing of the circadian clock in humans. Findings from research in non-humans suggest the combination of photic and non-photic stimuli interact to increase or attenuate the magnitude of circadian phase shifts 17-21 and contribute to