Previous studies have demonstrated that skeletal muscle perfusion is impaired in obese Zucker rats (OZR) under control conditions and with elevated metabolic demand versus responses in lean Zucker rats (LZR). To further our understanding of processes contributing to impaired perfusion, we determined if hyperemic responses following periods of occlusion were altered in skeletal muscle of OZR vs. LZR. In isolated hindlimbs, basal blood flow in OZR was less than in LZR, and total perfusion responses following 30, 90, and 180 seconds of occlusion were reduced. Treatment of animals with an antioxidant (PEG-SOD) had no effect on reactive hyperemia, although blockade of alpha-adrenoreceptors (₁>₂) improved responses to 30 and 90 seconds of occlusion; responses to 180 seconds of occlusion were unaltered. Pump-perfusion of a dilated distal hindlimb demonstrated that increased volume flow elicited a greater increase in perfusion pressure in OZR vs. LZR, suggesting structural contributions to an increased vascular resistance. Responses were comparable for in situ cremaster muscle, as reactive hyperemia following serial arteriolar occlusion was attenuated in OZR versus LZR, treatment with PEG-SOD was ineffective, and hyperemic responses were improved following inhibition of alpha-adrenoreceptors (₁>₂). Treatment of cremaster muscle with adenosine (10^-3 M) caused flow to increase to a level comparable to that following 180 seconds of occlusion in both strains, though this level was reduced in OZR vs. LZR. These results suggest that increased adrenergic tone may constrain reactive hyperemia in OZR with brief occlusion, although structural increases in vascular resistance can contribute to constrained perfusion following longer periods of occlusion.