Is there a histaminergic postexercise hyperemia in endurance exercise‐trained men and women?

In sedentary individuals, postexercise hypotension results from a histamine receptor‐mediated skeletal muscle hyperemia. We hypothesized that the skeletal muscle hyperemia would also exist in endurance trained individuals and would be abolished by histamine receptor antagonists. We studied 12 endurance trained (VO 2peak 51.7 ±7.9 ml kg −1 min −1 ) men and women (20–27 yr) before and through 90 min after a 60 min bout of cycling at 60% VO 2peak on a control and a combined H 1 ‐ and H 2 ‐receptor antagonist day (540 mg fexofenadine plus 300 mg ranitidine). We measured arterial blood pressure (auscultation) and femoral blood flow (Doppler ultrasound). Femoral vascular conductance was calculated as flow/pressure. Prior to exercise, the histamine antagonists had no effect on femoral vascular conductance or mean arterial pressure ( P > 0.6). After exercise on the control day, femoral vascular conductance was elevated (Δ61.2 ± 13.9 %; P < 0.05 vs. preexercise) while mean arterial pressure was reduced (Δ‐ 4.7 ± 1.1 mmHg; P < 0.05 vs. preexercise). In contrast, after exercise on the histamine antagonists day, femoral vascular conductance was not elevated (Δ10.6 ± 6.7 %; P = 0.14 vs. preexercise; P < 0.05 vs. control day) and mean arterial pressure was not reduced (Δ‐1.2 ± 1.2 mmHg; P = 0.13 vs. preexercise; P < 0.05 vs. control day). These data suggest that not only is there a postexercise skeletal muscle hyperemia present in endurance exercise‐trained men and women but that this long‐lasting hyperemia is produced by a histaminergic mechanism. Furthermore, the postexercise skeletal muscle hyperemia contributes to the postexercise hypotension in this population. Supported by AHA grant: 555623Z