Abstract

An acute bout of aerobic exercise is followed by a sustained postexercise vasodilation which is mediated by H1‐ and H2‐histamine receptors. We tested the hypothesis that this histamine‐receptor activation upregulates proangiogenic factors in previously exercised skeletal muscle. To this end, four healthy men performed unilateral dynamic knee extension for 1h at 60% of peak power. Two subjects received combined oral H1/H2‐receptor antagonism (540mg fexofenadine and 300mg ranitidine) 1h prior to exercise (Blockade); two did not (Control). Skeletal muscle biopsies were performed before exercise, immediately postexercise, and 3h postexercise. Relative mRNA abundance for vascular endothelial growth factor (VEGFa) and monocyte chemotactic protein‐1 (MCP‐1) were assessed by quantitative real‐time PCR. Before exercise, VEGFa and MCP‐1 expression were similar between Control and Blockade. Immediately after exercise, VEGFa increased 3.1‐fold for Control, but only 1.8‐fold for Blockade. Likewise, MCP‐1 increased 3.9‐fold for Control, but only 1.4‐fold for Blockade. At 3h postexercise, VEGFa increased 8.2‐fold for Control, but only 3.0‐fold for Blockade. At 3h, MCP‐1 increased 99.5‐fold for Control, but only 25.8‐fold for Blockade. These data suggest that histamine‐receptor activation contributes markedly to the generation of proangiongenic factors following an acute bout of exercise.

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