The reviewer deduces that the initial flow increase in functional hyperemia is elicited by central neural systems, since it is reported that the central cholinergic pathway increases CBF immediately after the onset of somatosensory stimuli. The flow increase occurs concurrently with neuronal activation, but is much faster than the increase of neuronal metabolism. The novel hypothesis is proposed that functional hyperemia is biphasic: an initial flow increase under central neural control and a delayed increase is under traditional metabolic control. The metabolic phase may supply more blood than is needed, and may last even after discontinuation of the stimulation (overcompensation). These two phases of hyperemia are suggested to be well mixed, presumably in glial processes, which coordinate blood redistribution in the surrounding microvascular network. Many stimuli from the environment might be managed simply by the neurogenic control of functional hyperemia, without the metabolic change.