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Patients with type 2 diabetes mellitus (T2DM) exhibit diminished exercise capacity likely attributable to reduced skeletal muscle blood flow (i.e., exercise hyperemia). A potential underlying mechanism of the impaired hyperemic response to exercise could be inadequate blunting of sympathetic-mediated vasoconstriction (i.e., poor functional sympatholysis). Therefore, we studied the hyperemic and vasodilatory responses to hand grip exercise in patients with T2DM as well as vasoconstriction to selective α-agonist infusion. Forearm blood flow (FBF) and vascular conductance (FVC) were examined in patients with T2DM (n=30) as well as nondiabetic controls (n=15) with similar age (59±9 vs. 60±9yrs, P=0.69) and body mass index (31.4±5.2 vs. 29.5±4.6kg·m-2, P=0.48). Intra-arterial infusion of phenylephrine (α1-agonist) and dexmedetomidine (α2-agonist) were used to induce vasoconstriction: ((FVCwith drug-FVCpre-drug)/FVCpre-drugx100%). Subjects completed rest and dynamic hand grip exercise (20% of maximum) trials per α-agonist. Patients with T2DM had smaller increases (Δ from rest) in FBF (147±71 vs. 199±63ml·min-1) and FVC (126±58 vs. 176±50ml·min-1·100mmHg-1, P<0.01 for both) during exercise compared to controls, respectively. During exercise, patients with T2DM had greater α1- (-16.9±5.9 vs. -11.3±3.8%) and α2-mediated vasoconstriction (-23.5±7.1 vs. -19.0±6.5%, P<0.05 for both) versus controls. The magnitude of sympatholysis (Δ in %vasoconstriction between exercise and rest) for PE was lower (worse) in patients with T2DM versus controls (14.9±12.2 vs. 23.1±8.1%, P<0.05) whereas groups were similar during DEX trials (24.6±12.3 vs. 27.6±13.4%, P=0.47). Our data suggest patients with T2DM have attenuated hyperemic and vasodilatory responses to exercise which could be attributable to greater α1-mediated vasoconstriction in contracting skeletal muscle.

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