Histamine blockade reduces femoral blood flow with no apparent change in vascular permeability after muscle damaging exercise (LB523)

Abstract

Blood flow to previously exercised muscle remains elevated for up to two hrs after exercise and is mediated by activation of histamine receptors. Activation of histamine receptors could lead to increased vascular permeability, an initial stage of inflammation, associated with muscle damage. Therefore, the purpose of this experiment was to determine if histamine receptors contribute to the increased permeability in a model of exercise‐induced muscle damage. Muscle damage was induced in seven volunteers (2F, 5M) by 45‐min of downhill running (‐10% grade) at a heart rate of ~150 BPM. Volunteers were randomly assigned to histamine blockade (540 mg fexofenadine; an H1 blocker and 300 mg ranitidine; an H2 blocker) or control (no drug). Prior to and for 120 min following exercise, femoral blood flow was measured using Doppler ultrasound, while vascular permeability was measured as a change in thigh and calf circumference during four min of supravenous pressure occlusion. The rise in femoral blood flow after exercise was 52 ± 12% (Mean ± SE) lower with histamine blockade vs control (p<0.05). Additionally, thigh and calf vascular permeability tended to be higher with histamine blockade (109 ± 92%; 42 ± 21%) vs control (73 ± 58%; 34 ± 20 %)(p>0.05). Thus, it appears that post‐exercise histamine receptor activation may not contribute to the initial stages of an inflammatory response for muscle damaging exercise.Grant Funding Source: NIH grant HL115027