Ischemic exercise hyperemia in the human forearm: Reproducibility and roles of adenosine and nitric oxide

The roles of local metabolites in reactive and exercise hyperemia remain incompletely understood. Amaximum metabolic stimulus caused by ischemic exercise (IE) could potentially fully activate all vasodilator pathways and limit potential redundancy amongst vasoactive substances. We tested the hypotheses that IE elicits areproducible hyperemic response in the forearm and that adenosine (ADO) and nitric oxide (NO) contribute to this response. In separate protocols, forearm blood flow (FBF) was measured with venous occlusion plethysmography following IE trials consisting of 5 min of ischemia and rhythmic forearm handgrip exercise (performed during last 2 min of ischemia). In protocol 1 (n = 8), FBF was measured after three trials of IE. In protocol 2 (n = 9), subjects performed IE during control (saline), aminophylline (APH; adenosine receptor antagonist), and combined APH/NG-monomethyl-L-arginine (L-NMMA; NOS inhibition) infusions. In protocol 1, coefficients of variation for total (area under the curve) DFBF and DFVC (forearm vascular conductance) following IE were 10.4 ± 1.0% and 14.9 ± 1.0%, respectively. In protocol 2, peak DFBF was similar for saline and APH trials. Peak DFBF for the APH+L-NMMA trial was greater than that of the APH trial (P = 0.03), and peak DFVC was marginally non-significant (P = 0.053). Total DFBF (54.8 ± 3.9, 55.2 ± 5.4, and 60.4 ± 4.8 ml 100 ml^-1; P = 0.43) and DFVC (51.4 ± 3.5, 52.1 ± 5.5, and 56.5 ± 5.0 ml 100 ml ^-1 100 mmHg^-1; P = 0.52) were similar for saline, APH, and APH+_L-NMMA, respectively. Our data suggest that (1) the hyperemic response to IE is reproducible and (2) inhibition of ADO alone or combined ADO and NO does not blunt the hyperemic response following IE.