Journal: Journal of Applied Physiology
. (E-publication ahead of print August 3, 2006). Article in Press as of October 25, 2006 PMID: 16888049 Authors and affiliation: Jennifer L. McCord and John R. Halliwill. Department of Human Physiology, University of Oregon, Eugene, Oregon, United States. [E-mail: firstname.lastname@example.org
In sedentary individuals, H1-receptors mediate the early portion of postexercise skeletal muscle hyperemia while H2- receptors mediate the later portion. It is not known if postexercise hyperemia also presents in endurance trained individuals. We hypothesized that the postexercise skeletal muscle hyperemia would also exist in endurance trained individuals and that combined blockade of H1- and H2-receptors would abolish the long-lasting postexercise hyperemia in trained and sedentary individuals.
We studied 28 sedentary and endurance trained men and women before and through 90 minutes after a 60 minute bout of cycling at 60% VO2peak on control and combined H1- and H2-receptor antagonist days (fexofenadine and ranitidine). We measured arterial pressure (brachial auscultation) and femoral blood flow (Doppler ultrasound). On the control day, femoral vascular conductance (calculated as flow/pressure) was elevated in all groups sixty minutes after exercise (sedentary men: Delta 86 ± 35; trained men: Delta 65 ± 18; sedentary women: Delta 61 ± 19; trained women: Delta 59 ± 23%: all P < 0.05 vs preexercise). In contrast, on the histamine antagonist day, femoral vascular conductance was not elevated in any of the groups after exercise (sedentary men: Delta 21 ± 17; trained men: Delta 9 ± 5; sedentary women: 19 ± 4; trained women: Delta 11 ± 11%; all P > 0.16 vs preexercise; all P < 0.05 vs control day).
These data suggest postexercise skeletal muscle hyperemia exists in endurance trained men and women. Furthermore, histaminergic mechanisms produce the long-lasting hyperemia in sedentary and endurance trained individuals.