Human sleep research is (mostly) carried out during the night. Yet sleep is embedded in the 24-hour day, and its timing, duration, and internal structure is strongly determined by the circadian pacemaker. Thus, in order to investigate mechanisms initiating sleepiness and sleep propensity, measurement needs to begin long before the sun sets. Our chronobiological approach to the physiology underlying sleep onset focuses on the role of melatonin and thermoregulation.In both night-active and diurnal species, the circadian peak of melatonin secretion occurs during the night (for review see: Arendt 1995). In contrast, all species, independent of temporal niche, sleep during the circadian trough of the core body temperature (CBT) rhythm. In rats, melatonin administration enhances norepinephrine-induced vasoconstriction of the tail (Viswanathan et al. 1990); in humans, melatonin induces vasodilation in fingers and toes (Kräuchi et al. 1998), suggesting that transduction of the nocturnal melatonin signal is linked to opposite physiological sequelae appropriate to behavioral niche. To further characterize the functional relationships preceding sleep onset, we have analyzed data from a series of experiments designed to phase-shift the circadian system with different putative zeitgebers, using identical methodology of a constant routine (CR) protocol to permit pooling of data.