Rapid Report

Sympathetic vasoconstriction is blunted in the vascular beds of contracting skeletal muscles. We sought to determine whether this blunted vasoconstriction is specific for post‐junctional α 1 ‐ or α 2 ‐adrenergic receptors. We measured forearm blood flow (Doppler ultrasound) and calculated the vascular conductance (FVC) responses to brachial artery infusions of tyramine (which evokes endogenous noradrenaline release), phenylephrine (an α 1 agonist) and clonidine (an α 2 agonist) in 10 healthy men during rhythmic handgrip exercise (10‐15 % of maximum) and during a control non‐exercise vasodilator condition (intra‐arterial adenosine). Steady‐state FVC during exercise and adenosine was similar in all trials (range: 243‐272 and 234‐263 ml min −1 (100 mmHg) −1 , respectively; P > 0.5). During exercise the percentage reductions in FVC in response to tyramine (−24 ± 7 vs. −55 ± 6 %), phenylephrine (−12 ± 8 vs. −37 ± 8 %) and clonidine (−17 ± 6 vs. −49 ± 4 %) were significantly less compared with adenosine (all P < 0.05). The magnitude of the blunted vasoconstrictor responses was similar for both receptor subtypes. These findings are in contrast to those from studies in animals demonstrating that α 2 ‐adrenergic receptor‐mediated vasoconstrictor responses are much more sensitive to contraction‐induced inhibition than α 1 ‐mediated responses. We conclude that vasoconstrictor responses mediated via both post‐junctional α 1 ‐ and α 2 ‐adrenergic receptors are blunted in contracting human skeletal muscles.