This study examined the effects of 6 weeks of moderate- (MD) and high-intensity endurance training (HD) and resistance training (RD) on the vasorelaxation responsiveness of the aorta, iliac, and femoral vessels in type 1 diabetic (D) rats. Vasorelaxation to acetylcholine was modeled as a mono-exponential function. A potential mediator of vasorelaxation, endothelial nitric oxide synthase (e-NOS) was determined by Western blots. Vessel lumen-to-wall ratios were calculated from H&E stains. The vasorelaxation time-constant (τ) (s) was smaller in control (C) (7.2 ± 3.7) compared to D (9.1 ± 4.4) and it was smaller in HD (5.4 ± 1.5) compared to C, D, RD (8.3 ± 3.7) and MD (8.7 ± 3.8) (p<0.05). The rate of vasorelaxation (% · s(-1)) was larger in HD (2.7 ± 1.2) compared to C (2.0 ± 1.2), D (2.0 ± 1.5), RD (2.0 ± 1.0), and MD (2.0 ± 1.2) (p<0.05). τ vasorelaxation was smaller in the femoral (6.9 ± 3.7) and iliac (6.9 ± 4.7) than the aorta (9.0 ± 5.0) (p<0.05). The rate of vasorelaxation was progressively larger from the femoral (3.1 ± 1.4) to the iliac (2.0 ± 0.9) and to the aorta (1.3 ± 0.5) (p<0.05). e-NOS content (% of positive control) was greater in HD (104 ± 90) compared to C (71 ± 64), D (85 ± 65), RD (69 ± 43), and MD (76 ± 44) (p<0.05). e-NOS normalized to lumen-to-wall ratio (% · mm(-1)) was larger in the femoral (11.7 ± 11.1) compared to the aorta (3.2 ± 1.9) (p<0.05). Although vasorelaxation responses were vessel-specific, high-intensity endurance training was the most effective exercise modality in restoring the diabetes-related loss of vascular responsiveness. Changes in the vasoresponsiveness seem to be endothelium-dependent as evidenced by the greater e-NOS content in HD and the greater normalized e-NOS content in the smaller vessels.