Role of adenosine in exercise-induced human skeletal muscle vasodilatation

Abstract

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ∼48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (FaBF) by ∼20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min−1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min−1 mmHg−1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) FaBF from 0.3 ± 0.03 L min−1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min−1. Continuous infusion of adenosine at rest and during one‐legged exercise at ∼62% of peak power output increased (P < 0.05) FaBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min−1, respectively. One‐legged exercise alone increased (P < 0.05) FaBF to 4.7 ± 1.7 L min−1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ∼20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.