In acute experiments on dogs under nembutal anesthesia, stimulation of different parts of the hypothalamus increased the muscle blood flow and O2 consumption and decreased vascular resistance. PO2 in m. gastrocnemius altered in both directions as a function of blood flow and O2 consumption changes. There was a good correlation between the initial level of PO2 and its shifts caused by hypothalamic stimulation. In most cases flow reactions were blocked with atropine. The stimulation of the hypothalamus seems to evoke cholinergic vasodilatation in skeletal muscles. The data suggest that initial level of muscle PO2 determines the redistribution of the increased blood flow between nutritional and non-nutritional vessels within the skeletal muscles and thus affects transcapillary exchange and O2 consumption during cholinergic vasodilatation.