H1 and H2 receptors mediate postexercise hyperemia in sedentary and endurance exercise-trained men and women.
Level 3 - non-randomized controlled study
Controlled crossover laboratory study in humans (randomization not specified in abstract)
PubMed 16888049 · doi:10.1152/japplphysiol.00441.2006
What was done
The authors studied 28 sedentary and endurance-trained men and women before and through 90 minutes after a 60-minute bout of cycling at 60% peak oxygen uptake under two conditions: a control day and a combined H1- and H2-receptor antagonist day (oral fexofenadine and ranitidine). Femoral blood flow was measured by Doppler ultrasound and arterial pressure by brachial auscultation to calculate femoral vascular conductance (flow/pressure).
What was found
On the control day, femoral vascular conductance was significantly elevated 60 minutes post-exercise across all groups relative to pre-exercise values: sedentary men (Δ86 ± 35%), trained men (Δ65 ± 18%), sedentary women (Δ61 ± 19%), and trained women (Δ59 ± 23%) (all P < 0.05). On the combined histamine antagonist day, post-exercise elevation in femoral vascular conductance was abolished: sedentary men (Δ21 ± 17%), trained men (Δ9 ± 5%), sedentary women (Δ19 ± 4%), and trained women (Δ11 ± 11%) (all P > 0.16 vs. pre-exercise; all P < 0.05 vs. control day).
Why it matters
This study demonstrates that sustained post-exercise skeletal muscle hyperemia occurs in endurance-trained individuals similarly to sedentary adults and is mediated by histaminergic H1 and H2 receptor pathways regardless of sex or training status.
Limits
The total sample size is small (n = 28 across four distinct subgroups), yielding small sub-cohorts. The abstract does not specify whether testing order was randomized or blinded, and it evaluates only a single moderate exercise intensity (60% peak VO2) and modality (cycling).
Cited by
- supports Exercise causes the release of histamine, which functions to dilate blood vessels for increased blood flow.