Role of adenosine in exercise-induced human skeletal muscle vasodilatation

The role of adenosine in exercise-induced human skeletal muscle vasodilatat ion remains unknown. We therefore evaluated the effect of theophylline-indu ced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one-l egged, knee-extensor exercise at similar to 48% of peak power output, intra venous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (FaBF) by similar to 20%, i.e. from 3.6 +/- 0.5 to 2.9 +/- 0.5 L min(-1), a nd 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 oxy gen uptake and lactate release remained unaltered (P = n.s.). Bolus injecti ons 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 e xercise at similar to 62% of peak power output increased (P < 0.05) FaBF do se-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 adenos ine infusion during both rest and exercise. The present findings demonstrat e that endogenous adenosine controls at least similar to 20% of the hyperae mic response to submaximal exercise in skeletal muscle of humans. The resul ts 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.