Aerobic training-induced changes in vascular reactivity have been evaluated in vessels of a variety of sizes and tissue origins. In trained animals large coronary arteries have increased responses to adenosine (Ad) and decreased responses to norepinephrine (NE) and nitroprusside (Np). Smaller coronary arterioles have increased responses to bradykinin (Bk) but not Ad; intermediate size vessels have enhanced responses to both Ad and Bk. A similar size dependence has been found in the vascular bed of the rat spinotrapezius muscle. The terminal feed arteries of trained animals demonstrate increased dilation in response to Np and increased constriction in response to epinephrine (Epi) and NE. Smaller arterioles demonstrate increasedβ-dilation at low doses of Epi and decreased constriction at higher doses. Intermediate size vessels demonstrate adaptive responses that appear to be a combination of those in larger and smaller vessels. These vascular alterations are evident despite the fact that blood flow does not increase in this muscle during treadmill running and the oxidative capacity of this tissue is not enhanced by treadmill training. Recently, training-induced vascular adaptations have also been observed in the rat intestine; these adaptations include decreased responses to NE and acetylcholine and increased responses to Np. Experimental evidence suggests that vascular smooth muscle adaptations to training are highly dependent on the size and tissue location of the vessel and occur in tissues other than those activated during the training bout. Potential mediators of these adaptations are discussed.