Sleep is typically initiated on the declining portion of the circadian rhythm of core body temperature (CBT) when its rate of change, and body heat loss, is maximal. Distal vasodilatation plays a primary role in the circadian regulation of body heat loss and is strongly associated with sleepiness and sleep induction. In contrast, sleep (i.e. non-REM sleep and slow-wave activity, SWA) has no or only a minor thermoregulatory function. Two lines of evidence support this statement. First, detailed analyses of thermoregulatory changes before and after lights off show clearly that they start before stage 2 sleep begins. Second, accumulation of sleep pressure with increasing time awake, increases subjective sleepiness and SWA during the succeeding recovery night, but does not influence the thermoregulatory system. Taken together, the circadian modulation of sleepiness and sleep induction is clearly associated with thermoregulatory changes, but the thermoregulatory system seems to be independent of the sleepiness/sleep regulatory system. A simplified model is presented which attempts to explain the relationship between these two systems. It is based on the main hypothesis that all thermoregulatory effects which lead to an increase in the core/shell ratio (e.g. a reduced shell by increased distal skin temperature) lead to increased sleepiness and, as a consequence, to increased sleep propensity. However, the sleepiness/sleep regulatory system feeds back onto the thermoregulatory system only indirectly via sleep-related behaviors (e.g. relaxation, lying down).