In humans, circadian rhythms in a variety of physiological and behavioral variables including core body temperature, urine production, hormones subjective alertness, cognitive performance, short-term memory, sleep propensity and sleep structure have been described (reviewed in 
). Under normal conditions, these rhythms are synchronized to the 24-h solar day and to each other, and exhibit specific phase relationships with the light-dark/activity-rest cycle, and with each other. For instance, plasma melatonin crests in the middle of the habitual dark/sleep episode, approximately two hours before the nadir of the core body temperature rhythm and approximately 4–6 hours before the crest of the cortisol rhythm. Many of these rhythms persist during sustained wakefulness under constant environmental and behavioral conditions. According to current understanding of circadian organization in mammals, all these rhythms are driven by a central circadian pacemaker located in the suprachiasmatic nucleus (SCN) of the hypothalamus, which coordinates multiple circadian oscillators in the periphery 
. Single SCN neurons are competent circadian oscillators 
, and some of the genes involved in the generation of circadian rhythmicity have been identified 
The SCN receives light input from both classical photoreceptors (rods and cones), as well as from a more recently identified subset of intrinsically-photosensitive retinal ganglion cells 
. The phase (timing) of these endogenous circadian rhythms can be changed by an acute shift of the light-dark cycle 
. The largest phase advances (shifts to an earlier time) are observed when light is administered in the late subjective night/early subjective morning, shortly after the core body temperature nadir, which in a young man sleeping from 00:00–08:00 would be approximately 06:00 h. Although in some prior experiments phase shifts were assessed for multiple variables and found to be equivalent 
few experiments have investigated whether individual differences in phase shifts are similar for a multitude of variables.
Circadian phase resetting by light is in general not thought to be accompanied by a change in the amplitude of circadian rhythms, and the negative consequences of circadian desynchrony are typically discussed within the framework of circadian phase rather than amplitude. Circadian amplitude reduction has, however, been observed when light is carefully timed to drive the oscillator to its singularity 
but those findings and their interpretation remain controversial 
. Whether individual differences in amplitude reduction are similar across endocrine and behavioral variables is currently not known. Although phase-shifting of the human circadian system was once thought to require bright light, dose-response studies indicate that the pacemaker is sensitive to moderate light, i.e. intensities typically observed in artificially lit living rooms or offices 
, both in the phase advance 
and phase delay 
regions of the phase response curve to light. A similar sensitivity is observed for the acute suppression of melatonin by light 
and the acute alerting effect of light 
. Together, these studies indicate that the drive onto the pacemaker exerted by moderate light (~100–150 lux) appears to be nearly half of the drive exerted by much brighter light (~10,000 lux) 
. The effect of a light stimulus is, however, also dependent on the prior history of light exposure 
, and to what extent moderate intensity light can affect multiple circadian rhythms remains unclear.
There is evidence to suggest that in addition to ocular light exposure, nonphotic stimuli, such as an imposed rest-activity cycle, also affect the phase of human circadian rhythms of melatonin, body temperature and other variables 
. Furthermore, it is well established that the rest-activity cycle and associated light-dark cycle also contribute to the observed amplitude of many variables, such as core body temperature, alertness and many endocrine variables 
The recent insights into the sensitivity of the human circadian pacemaker to photic and non-photic stimuli, and the emerging complexity of circadian organization led us to re-analyze phase resetting and amplitude effects of the sleep-wake and light-dark cycles on multiple endocrine, physiologic and behavioral variables. In particular, we aimed to investigate to what extent altered timing of the sleep-wake cycle and associated room and bright light cycles could affect the phase and amplitude of multiple circadian rhythms, and how changes in those rhythms correlated within individuals and differed between individuals.