α-Adrenergic blockade unmasks a greater compensatory vasodilation in hypoperfused contracting muscle

We previously demonstrated that acute hypoperfusion in exercising human muscle causes an immediate increase in vascular resistance that is followed by a partial restoration (less than 100% recovery) of flow. In the current study we examined the contribution of α-adrenergic vasoconstriction in the initial changes in vascular resistance at the onset of hypoperfusion as well as in the recovery of flow over time. Nine healthy male subjects (29 ±2) performed rhythmic forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included; baseline, exercise prior to inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound), local (brachial artery), and systemic arterial pressure (MAP; Finometer) were measured. The trial was repeated during phentolamine infusion (α-adrenergic receptor blockade). Forearm vascular conductance (FVC; ml min-1 100 mmHg ^-1) and resistance (mmHg mlmin ^-1) was calculated from BF (mlmin ^-1) and local MAP (mmHg). Recovery of FBF and FVC (steady state inflation plus exercise value-nadir)/[steady state exercise (control) value - nadir] with phentolamine was enhanced compared with the respective control (no drug) trial (FBF = 97 ±5% vs. 81 ±6%, P<0.05; FVC = 126 ±9% vs. 91 ±5%, P<0.01). However, the absolute (0.05±0.01 vs. 0.06±0.01 mmHg ml min ^-1; P = 0.17) and relative (35±5% vs. 31 ±2%; P = 0.41) increase in vascular resistance at the onset of balloon inflation was not different between the α-adrenergic receptor inhibition and control (no drug) trials. Therefore, our data indicate that α-adrenergic mediated vasoconstriction restricts compensatory vasodilation during forearm exercise with hypoperfusion, but is not responsible for the initial increase in vascular resistance at the onset of hypoperfusion.