Muscle blood flow and vasodilation are blunted at the onset of exercise following an acute bout of ischemia-reperfusion

Abstract

Ischemia-reperfusion (I/R) injury can attenuate endothelial function and impair nitric oxide bioavailability. We tested the hypothesis that I/R also blunts the rapid and steady-state hyperemic and vasodilatory responses to handgrip exercise. Ten subjects (8M/2F; 24 ± 4 yr) 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 forearm 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 DFBF (from baseline) and DFVC 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 DFBF and DFVC 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 × time interactions P = 0.34 and 0.21, respectively). Plasma [nitrite] under resting conditions and during steady-state rhythmic exercise was attenuated following I/R (P < 0.05 for both), but not following time control (P = 0.54 and 0.93). These data indicate that I/R blunts hyperemia and vasodilation at the onset of muscle contractions but does not attenuate these responses during steady-state exercise.