In humans, acute aerobic exercise elicits a sustained post-exercise vasodilation within previously active skeletal muscle. This response is dependent on activation of histamine H1 and H2 receptors, but the source of intramuscular histamine remains unclear. We tested the hypothesis that interstitial histamine in skeletal muscle would be increased with exercise and would be dependent on de novo formation via the inducible enzyme histidine decarboxylase and/or mast cell degranulation. Subjects performed 1 h of unilateral dynamic knee-extension exercise or sham (seated rest). We measured the interstitial histamine concentration and local blood flow (ethanol washout) via skeletal muscle microdialysis of the vastus lateralis. In some probes, we infused either α-fluoromethylhistidine hydrochloride (α-FMH), a potent inhibitor of histidine decarboxylase, or histamine H1/H2 receptor blockers. We also measured interstitial tryptase concentrations, a biomarker of mast cell degranulation. Compared with pre-exercise, histamine was increased after exercise by Δ4.2 ± 1.8 ng ml-1 (P < 0.05), but not when α-FMH was administered (Δ-0.3 ± 1.3 ng ml-1, P = 0.9). Likewise, local blood flow after exercise was reduced to pre-exercise levels by both α-FMH and H1/H2 blockade. In addition, tryptase was elevated during exercise by Δ6.8 ± 1.1 ng ml-1 (P < 0.05). Taken together, these data suggest that interstitial histamine in skeletal muscle increases with exercise and results from both de novo formation and mast cell degranulation. This suggests that exercise produces an anaphylactoid signal which affects recovery, and may influence skeletal muscle blood flow during exercise.
- post-exercise hypotension
- regional blood flow
- extracellular fluid
- Copyright © 2016, Journal of Applied Physiology