Abstract

Orally administered histamine H1‐ and H2‐receptor blockade blunts the sustained (90 min) hyperemia present in the previously exercised limbs of humans following dynamic exercise. Our aim was to determine if this postexercise hyperemic response could be prevented by local H1‐ and H2‐receptor blockade administered via skeletal muscle microdialysis. Thus, we tested the hypothesis that postexercise ethanol outflow/inflow ratios (an inverse surrogate of local blood flow) would be higher in sites that received H1‐ and H2‐receptor blockade versus control sites. Four microdialysis probes were inserted into the vastus lateralis muscle of five healthy subjects (21–26 yrs) immediately after 60 min of upright cycling at 60% VO2 peak. Microdialysis probes were perfused with a modified Ringer's solution containing 5 mM ethanol. Two of the sites received H1‐ and H2‐receptor antagonists (1 mM pyrilamine/3 mM cimetidine) and two sites served as controls. Consistent with our hypothesis, one hour after exercise, the outflow/inflow ratio was 0.48 ± 0.02 in blockade sites versus 0.41 ± 0.03 in control sites (P = 0.042). In addition, three subjects underwent a sham protocol (no exercise) in which blockade did not affect the ethanol outflow/inflow ratio (P ≥ 0.143). These results suggest that local H1‐ and H2‐receptors in skeletal muscle contribute to postexercise hyperemia.Supported by AHA grant 555623Z and the Evonuk Foundation

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