Muscle Blood Flow and Vasodilation are Blunted at the Onset of Exercise Following an Acute Bout of Ischemia-Reperfusion.

Abstract

Ischemia-reperfusion injury (I/R) can inhibit endothelial function and impair nitric oxide bioavailability. We tested the hypothesis that I/R also blunts the rapid and steady-state hyperemic and vasodilatory response to handgrip exercise. Ten subjects (8M/2F; 24±4yr) performed handgrip exercises before and after I/R (20 min of ischemia/20 min of reperfusion) and time control (40 min supine rest) trials. Forearm blood flow (FBF) and vascular conductance (FVC) were assessed with Doppler ultrasound during single forearm contractions and 3 min of rhythmic handgrip exercise. Venous blood samples were drawn at rest and during exercise to assess plasma [nitrite]. Peak ΔFBF (from baseline) and ΔFVC following single contractions were attenuated following I/R (134±48 vs. 103±42 ml·min-1; 160±55 vs. 118±48 ml·min-1·100 mmHg-1, P<0.05 for both) but not following time control (115±63 vs. 124±57 ml·min-1; 150±80 vs. 148±64 ml·min-1·100 mmHg-1, P=0.16 and P=0.95, respectively). Steady-state ΔFBF and ΔFVC during rhythmic exercise were unchanged in both I/R (192 ± 52 vs. 190±53 ml·min-1; 208±56 vs. 193±60 ml·min-1·100 mmHg-1) and time control (188±54 vs. 196±48 ml·min-1; 206±60 vs. 207±49 ml·min-1·100 mmHg-1) trials (group x time interactions P=0.34 and 0.21, respectively). Plasma [nitrite] under resting conditions and during steady-steady state rhythmic exercise was attenuated following I/R (P<0.05 for both) but not time control (P=0.54 and 0.93). These data indicate I/R blunts hyperemia and vasodilation at the onset of muscle contractions but does not attenuate these responses during steady-state exercise.