To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated 4-5 skeletal muscle fibres in the anaesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibres. Diameter was measured before, during and after two minutes of skeletal muscle contraction stimulated over a range of stimulus frequencies (4, 20, and 40Hz; 15 contractions per minute (CPM), 250ms train duration) and a range of contraction frequencies (6, 15 and 60CPM; 20Hz stimulus frequency, 250ms train duration). Muscle fibres were stimulated in the absence and presence of an inhibitor of ADO receptors (10^-6M xanthine amine congener, XAC), a K_ATP channel inhibitor (10^-5M glibenclamide), an inhibitor of a source of potassium (K⁺) by inhibition of voltage dependent K⁺ channels (3x10^-4M 3,4-diaminopyridine, DAP) and an inhibitor of nitric oxide synthase (10^-6M nitro-L-arginine methyl ester, L-NAME plus 10^-7M SNAP (a nitric oxide donor)). L-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60CPM. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40Hz.Glibenclamide inhibited all dilations at all stimulus and contraction frequencies and DAP did not inhibit dilations at any stimulus while attenuating dilation at a contraction frequency of 60CPM only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency, therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia.