Effect of H(1)- and H(2)-histamine receptor blockade on postexercise insulin sensitivity

Following a bout of dynamic exercise, humans experience sustained postexercise vasodilatation in the previously exercised skeletal muscle which is mediated by activation of histamine (H(1) and H(2)) receptors. Skeletal muscle glucose uptake is also enhanced following dynamic exercise. Our aim was to determine if blunting the vasodilatation during recovery from exercise would have an adverse effect on blood glucose regulation. Thus, we tested the hypothesis that insulin sensitivity following exercise would be reduced with H(1)- and H(2)-receptor blockade versus control (no blockade). We studied 20 healthy young subjects (12 exercise; eight nonexercise sham) on randomized control and H(1)- and H(2)-receptor blockade (fexofenadine and ranitidine) days. Following 60 min of upright cycling at 60% VO(2 peak) or nonexercise sham, subjects consumed an oral glucose tolerance beverage (1.0 g/kg). Blood glucose was determined from “arterialized” blood samples (heated hand vein). Postexercise whole-body insulin sensitivity (Matsuda insulin sensitivity index) was reduced 25% with H(1)- and H(2)-receptor blockade (P < 0.05), whereas insulin sensitivity was not affected by histamine receptor blockade in the sham trials. These results indicate that insulin sensitivity following exercise is blunted by H(1)- and H(2)-receptor blockade and suggest that postexercise H(1)- and H(2)-receptor–mediated skeletal muscle vasodilatation benefits glucose regulation in healthy humans.