Adaptations associated with repeated aerobic exercise come in many forms and act synergistically to increase the amount of oxygen an individual can consume during exercise. Moderate intensity aerobic exercise causes increased histamine concentrations within the active skeletal muscle that is released from mast cell degranulation or de novo formation through the enzyme histidine decarboxylase (Steven A. Romero et al., 2016). Histamine activates H1 and H2 receptors on vascular endothelial cells and vascular smooth muscle cells of the working skeletal muscle to acutely cause vasodilation and promote increased blood flow. Exercise induced histamine release not only affects post-exercise hemodynamics, but also influences glucose delivery to skeletal muscle, mediates the normal inflammatory response to aerobic exercise, as well as mRNA expression following a single bout of exercise (S A Romero et al., 2016). Outside of the exercise-induced mRNA response, histamine release also mediates other signaling mechanisms that are indirectly involved with adaptation to exercise training such as angiogenesis and red blood cell maturation (Byron, 1877; Qin et al., 2013). Taken together, there is ample evidence that by repeatedly activating or antagonizing histamine receptors during exercise, physiological adaptations to repeated exercise stress could be modulated. The overall purpose of this dissertation was to determine the role of histamine receptor activation in adaptations to aerobic exercise training. We hypothesized histamine receptor antagonists would blunt positive physiologic adaptation, or gains in aerobic capacity, by effecting the ability to deliver and utilize oxygen during subsequent exercise. The results indicate that the ability to deliver oxygen through increased blood volume via hematopoiesis did not contribute to increased aerobic capacity and was not affected by histamine receptor blockade. However, the ability to deliver oxygen through increased angiogenesis (assessed via capillary density and corroborated by peak vasodilatory capacity) and utilize oxygen through increased SDH activity (corroborated by VO2peak) contribute to increased exercise capacity but that these adaptations occur either independent of the effects of histamine receptor activation or that adaptation is generated by redundant mechanisms in a highly resilient manner.
|Advisor:||Hallwill, John R.|
|Commitee:||Minson, Christopher T., Dreyer, Hans C., Sterner, Kirstin N.|
|School:||University of Oregon|
|Department:||Department of Human Physiology|
|School Location:||United States -- Oregon|
|Source:||DAI-B 82/4(E), Dissertation Abstracts International|
|Subjects:||Physiology, Health sciences, Public health|
|Keywords:||Cardiovascular, Exercise, Histamine|
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