Two theories, myogenic and metabolic, have been proposed for reactive hyperemia. Since the metabolic theory implies that the changes in flow rate during reactive hyperemia must be explained in terms of changes in concentration of a vasodilator metabolite produced during anoxia, the rate of rise to peak reactive hyperemic flow should discriminate between these two possible mechanisms. Accordingly, changes in human cutaneous blood flow were monitored during postocclusive reactive hyperemia. The absolute values of both the rate of rise from zero blood flow to peak reactive hyperemic flow and the rate of recovery from peak reactive hyperemic flow to resting levels decrease with increasing durations of arterial occlusion. The time-dependent decrease in both rates is compatible with viscoelastic characteristics of the wall of resistance vessels and is not consistent with changes in concentration of a hypothesized vasodilator metabolite produced during occlusion.