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¹ Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240 USA

In normally active individuals, postexercise hypotension after a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. Histamine has been shown to be released during exercise and could contribute to postexercise vasodilatation via H₁ receptors in the peripheral vasculature. The purpose of this study was to determine the potential contribution of an H₁ receptor-mediated vasodilatation to postexercise hypotension. We studied 14 healthy normotensive men and women (ages 21.9 ± 2.1 years) before and through to 90 min after a 60 min bout of cycling at 60% on randomized control and H₁ receptor antagonist days (540 mg oral fexofenadine hydrochloride; Allegra). Arterial blood pressure (automated auscultation) and femoral blood flow (Doppler ultrasound) were measured in the supine position. Femoral vascular conductance was calculated as flow/pressure. Fexofenadine had no effect on pre-exercise femoral vascular conductance or mean arterial pressure (P > 0.5). At 30 min postexercise on the control day, femoral vascular conductance was increased ( +33.7 ± 7.8%; P < 0.05 versus pre-exercise) while mean arterial pressure was reduced ( –6.5 ± 1.6 mmHg; P < 0.05 versus pre-exercise). In contrast, at 30 min postexercise on the fexofenadine day, femoral vascular conductance was not elevated ( +10.7 ± 9.8%; P = 0.7 versus pre-exercise) and mean arterial pressure was not reduced ( –1.7 ± 1.2 mmHg; P = 0.2 versus pre-exercise). Thus, ingestion of an H₁ receptor antagonist markedly reduces vasodilatation after exercise and blunts postexercise hypotension. These data suggest H₁ receptor-mediated vasodilatation contributes to postexercise hypotension.

(Received 30 November 2004; accepted after revision 22 December 2004; first published online 23 December 2004)
Corresponding author J. R. Halliwill: 122 Esslinger Hall, 1240 University of Oregon, Eugene, OR 97403-1240, USA. Email: halliwil{at}uoregon.edu

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