This thesis is an investigation of the role of skeletal muscle stimulation parameters in the dilatory response to muscle contraction. A protocol using a single muscle contraction was used to establish the effect of stimulus frequency and train duration on arteriolar dilation. We have shown that significant arteriolar dilation occurs within 1sec in response to a single contraction over a wide range of stimulus frequencies and train durations representing muscle contraction from a twitch to an unfused tetanic contraction to a fused tetanic contraction. The pattern of dilation is complex, either monophasic or biphasic and is established by both stimulus frequency and train duration. The biphasic dilation is characterized by an initial peak at approx 4sec and a secondary peak at approx 20sec. A linear relationship between the magnitude of dilation and stimulus frequency or train duration was not observed. Dilation was more dependent on submaximal stimulus frequencies (<=30Hz). Across the range of stimulus frequencies, there were significant increases in dilation from 100 to 250 to 500ms but there were no further significant increases at 1000ms. To determine the effect of a series of contractions over time on arteriolar dilation, we observed the arteriolar response after 1, 2, 3, or 4 contractions (250ms train duration) at 4sec intervals. The dilatory processes were similar for the first two contractions and full-expressed within two contractions by processes independent of stimulus frequency. The plateau in dilation after the third and fourth contractions indicates that dilation is not constant per contraction and implies that rapid changes in either the nature and/or concentration of dilators released or changes in vascular reactivity have occurred. The dilations produced by a single contraction of 250ms result from at least four dilatory processes. The initial dilatory peak at 4sec involves K+ induced dilation via KIR channels and the N +K+ATPase and the secondary dilation at 20sec involves activation of muscarinic receptors, Ado receptors, KATP channels and the Na+K+ATPase. The involvement of multiple dilatory processes in response to a very short period of contractile activity demonstrates the complexity of the initiation of vasodilation in response to muscle contraction.