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To determine whether the increased wake within a bedrest episode in healthy older people is due to an increased number and/or increased duration of awakenings by evaluating the rates of transition between sleep and wake bouts within a bedrest episode.

Circadian rhythms are endogenous rhythms with a cycle length of approximately 24 h. Rhythmic production of specific proteins within pacemaker structures is the basis for these physiological and behavioral rhythms. Prior work on mathematical modeling of molecular circadian oscillators has focused on the fruit fly, Drosophila melanogaster. Recently, great advances have been made in our understanding of the molecular basis of circadian rhythms in mammals. Mathematical models of the mammalian circadian oscillator are needed to piece together diverse data, predict experimental results, and help us understand the clock as a whole. Our objectives are to develop mathematical models of the mammalian circadian oscillator, generate and test predictions from these models, gather information on the parameters needed for model development, integrate the molecular model with an existing model of the influence of light and rhythmicity on human performance, and make models available in BioSpice so that they can be easily used by the general community. Two new mammalian models have been developed, and experimental data are summarized. These studies have the potential to lead to new strategies for resetting the circadian clock. Manipulations of the circadian clock can be used to optimize performance by promoting alertness and physiological synchronization.

1Ocular exposure to early morning room light can significantly advance the timing of the human circadian pacemaker. The resetting response to such light has a non‐linear relationship to illuminance. The dose‐response relationship of the human circadian pacemaker to late evening light of dim to moderate intensity has not been well established.2Twenty‐three healthy young male and female volunteers took part in a 9 day protocol in which a single experimental light exposure6.5 h in duration was given in the early biological night. The effects of the light exposure on the endogenous circadian phase of the melatonin rhythm and the acute effects of the light exposure on plasma melatonin concentration were calculated.3We demonstrate that humans are highly responsive to the phase‐delaying effects of light during the early biological night and that both the phase resetting response to light and the acute suppressive effects of light on plasma melatonin follow a logistic dose‐response curve, as do many circadian responses to light in mammals.4Contrary to expectations, we found that half of the maximal phase‐delaying response achieved in response to a single episode of evening bright light (≈9000 lux (lx)) can be obtained with just over 1 % of this light (dim room light of ≈100 lx). The same held true for the acute suppressive effects of light on plasma melatonin concentrations. This indicates that even small changes in ordinary light exposure during the late evening hours can significantly affect both plasma melatonin concentrations and the entrained phase of the human circadian pacemaker.

In 1990, Kronauer proposed a mathematical model of the effects of light on the human circadian pacemaker. Although this model predicted many general features of the response of the human circadian pacemaker to light exposure, additional data now available enable us to refine the original model. We first refined the original model by incorporating the results of a dose response curve to light into the model's predicted relationship between light intensity and the strength of the drive onto the pacemaker. Data from three bright light phase resetting experiments were then used to refine the amplitude recovery characteristics of the model. Finally, the model was tested and further refined using data from an extensive phase resetting experiment in which a 3-cycle bright light stimulus was presented against a background of dim light. In order to describe the results of the four resetting experiments, the following major refinements to the original model were necessary: (i) the relationship between light intensity (I) and drive onto the pacemaker was reduced fromI1.3toI0.23for light levels between 150 and 10000 lux; (ii) the van der Pol oscillator from the original model was replaced with a higher-order limit cycle oscillator so that amplitude recovery is slower near the singularity and faster near the limit cycle; (iii) a direct effect of light on circadian period (τx) was incorporated into the model such that asIincreases, τxdecreases, which is in accordance with “Aschoff's rule”.

A suprathreshold luminance flash (1°, 200 msec) on a large uniform yellow field facilitates detection of a coincident (1°, 200 msec) red or green equiluminant flash and approximately linearizes the psychometric function for detecting the chromatic flash. The facilitation is produced by the suprathreshold contour created by the luminance flash. We tested whether the contour facilitates detection by reducing spatiotemporal uncertainty in detecting the chromatic flash. Uncertainty increases false alarms, and this effect can be factored out by correcting yes–no psychometric functions for guessing. Uncertainty also alters the shape of the receiver operating characteristic. Measurements of yes–no psychometric functions and receiver operating characteristics do not support the uncertainty reduction hypothesis.

The description of the random-dot model for photographic granularity by independent and identical grain-location statistics allows the average transmittance and transmittance autocorrelation function to be determined in a few straightforward steps. Here, the analysis is applied to the case of uniform exposures and arbitrarily shaped opaque grains, although the formalism allows nonopaque phase-retarding grains and the result of image exposures to be described. The results are interpreted in terms of the granularity Wiener spectrum, giving simple bounds on the low-frequency noise level, an inverse-third-power form for high frequencies, and bounds on a spectrum width that increase monotonically with decreasing average transmittance.

The description of the random-dot model for photographic granularity by independent and identical grain-location statistics allows the average transmittance and transmittance autocorrelation function to be determined in a few straightforward steps. Here, the analysis is applied to the case of uniform exposures and arbitrarily shaped opaque grains, although the formalism allows nonopaque phase-retarding grains and the result of image exposures to be described. The results are interpreted in terms of the granularity Wiener spectrum, giving simple bounds on the low-frequency noise level, an inverse-third-power form for high frequencies, and bounds on a spectrum width that increase monotonically with decreasing average transmittance.

There are circadian (∼24 h) rhythms for a wide range of human physiological and psychological functions including mood and performance efficiency1. These rhythms are self-sustaining in conditions of temporal isolation, indicating that internal oscillators (or biological clocks) control them2. Recent research has proposed an endogenous two-oscillator model of the human circadian system, with one oscillator indicated by the core body temperature rhythm and a second oscillator responsible for the daily cycle of sleep and wakefulness3,4. The present study was designed to produce a desynchronization in period between the two oscillators, to assess directly the behaviour of the rhythms of different performance tasks. The results, reported here, indicate that a simple manual dexterity task is almost entirely under the control of the temperature rhythm oscillator, whereas a more complex cognitive task demonstrates a periodicity which appears to be influenced by those oscillators controlling temperature and the sleep/wake cycle.

Light resets the circadian clock through a non–image-forming receptor system—or so it was thought; now, cone photoreceptors are shown to also participate.

The cumulative effects of chronic sleep loss may be overcome at certain times of day, but the residual effects of sleep deprivation profoundly degrade performance and may thereby compromise safety.