Effect of Histamine‐receptor Antagonism on VO_2Peak Improvements to Exercise Training

Abstract

One of the physiological changes following moderate intensity aerobic exercise is a transient reduction in blood pressure, termed post‐exercise hypotension (PEH), which is exercise intensity and duration dependent. This short‐term reduction in blood pressure is dependent upon skeletal muscle histamine production and release, which causes increased conductance via local activation of histamine H1 and H2 receptors. PEH is abolished when antihistamines are consumed prior to exercise. Additionally, histamine‐receptor antagonism during a single bout of exercise modifies expression of the transcriptome related to inflammation, angiogenesis, and metabolism. Due to the large role histamine plays in post‐exercise recovery, the scope of histamine receptor activation in adaptations to aerobic exercise training needs to be determined. Therefore, the purpose of this study was to examine histamine’s role in promoting adaptation to exercise. It is hypothesized that blocking histamine’s actions will attenuate adaptations that occur from aerobic exercise training. 16 young, healthy, recreationally active individuals (5M, 11F) volunteered for this study. All volunteers completed 6 weeks of exercise training (3–4 times a week), for a total of 21 exercise sessions. Exercise training combined 18 sessions of continuous exercise (1 hour at 60% VO2peak) and 3 sessions of high intensity interval training (30 min between 30 and 90% VO2peak). Volunteers were randomly placed into a placebo or histamine antagonism (540 mg fexofenadine; a H1‐receptor antagonist, and 300 mg of ranitidine; a H2‐receptor antagonist) group, and consumed medication 1 hour prior to each exercise session. Data was collected 4 times throughout the study with pre and post exercise training measures, as well as after every 2 weeks of exercise training. Measurements of VO2peak and cycle ergometry work rate were obtained. Exercise training resulted in increased absolute VO2peak of all subjects (9.4±1.5%; P<0.01); however, no difference was seen between groups (10.9±1.8% control vs 7.9±2.4% blockade; P=0.35). Additionally, exercise training resulted in increased cycle ergometry work rate of all subjects (11.2±1.6%; P<0.01); however, there was a trend for blunted improvement with blockade (7.7±2.4%) vs control (14.6±2.8%; P=0.08). In conclusion, blocking histamine’s actions had no effect on VO2 adaptations to exercise training. Additional information about factors related to O2 delivery and consumption are needed to understand the relationship between histamine and cardiovascular adaptation to exercise training. Support or Funding Information Support provided by: The Eugene & Clarissa Evonuk Memorial Graduate Fellowship