• blood redistribution;
  • core body temperature;
  • distal and proximal skin temperatures;
  • sleep inertia;
  • vasoconstriction;
  • vasodilatation


We assume that alertness should be highest at the end of a sleep episode: it is not. There is always sleep inertia upon awakening, which can last minutes to hours, and whose underlying physiological mechanisms are largely unknown. Previously, we had found a functional relationship between the degree of distal vasodilatation (as measured by the distal-proximal skin temperature gradient (DPG) and sleepiness (as measured by subjective ratings), promoting rapid sleep onset. This led us to hypothesize that the dissipation of sleep inertia (sleepiness) would be associated with reverse thermoregulatory mechanisms, i.e. distal vasoconstriction. In two sets of experiments with either a nocturnal sleep episode (study 1) or an afternoon nap (study 2) we could show that vasodilatation of hands and feet increased after lights off and that this was reversed after lights on. The time course of the DPG was significantly and positively correlated with subjective sleepiness (KSS), reflecting similar temporal relationships in both studies 1 and 2. The extremities cooled at a rate very closely parallel to the decay of sleepiness [time constants for the exponential decline calculated for study 2: DPG, 0.286 ± 0.048 h versus KSS, 0.332 ± 0.050 h; NS], indicating redistribution of heat from the shell to the core during dissipation of sleepiness. There was no statistical evidence that the time course of sleep inertia and its thermophysiological correlates depend on sleep structure prior to awakening. The symmetry between the thermoregulatory processes initiating sleepiness and those dissipating it is striking. In order to directly test our hypothesis, further studies with thermophysiological interventions (e.g. cooling the extremities) are needed.