Abstract

Adenosine (ADO) is one of several endogenous substances known to mediate muscle vasodilation during exercise. The purpose of this study was to examine (1) the role of nitric oxide (NO) in ADO-mediated vasodilation; (2) the magnitude of muscle blood flow (MBF) responses to ADO infusion during exercise; and (3) the influence of ADO in regulating heterogeneous MBF distribution. In healthy, young participants (N=14), local MBF was measured using near-infared spectroscopy and indocyanine green (ICG) dye at two locations on the vastus lateralis (VL). Cardiac output was quantified using a dye-dilution technique with ICG dye. Participants were tested at rest and during 1-leg knee extension exercise (25W) under different conditions: control, ADO infusion (150mg·kg body mass -1 ·min -1 ) and ADO+NO blockade (L-NMMA; 1mg·kg body mass -1 ·min -1 ). At rest and exercise, we found that mean VLBF increased from control to ADO and decreased significantly from ADO to ADO+L-NMMA infusion; exercising BF values were always significantly higher than at rest. Additionally, with ADO infusion, a peak increase in oxy-hemoglobin concentration (O 2 Hb) was reached within 2 minutes of initiating infusion; however the magnitude differed between muscle regions, indirectly indicating ADO-induced metabolic heterogeneity. O 2 Hb subsequently decreased over time, reaching a stable level at 5 min. Also, we observed that when MBF is elevated through ADO infusion, usual exercise-mediated vasodilator signals are not subsequently down-regulated during contraction demonstrating a lack of autoregulation. We conclude that NO does playa role in mediating ADO-induced vasodilation and there is a lack of autoregulatory feedback when ADO is infused during exercise.