Aerobic Exercise and Redox Modulation in the Adipose Microvasculature
thesisposted on 19.10.2016, 00:00 authored by Austin T. Robinson
Purpose: Cardiovascular disease (CVD) is the number one cause of death in the U.S. Obesity is an epidemic that increases the risk of CVD. Regular exercise lowers the risk of CVD, and is important for weight management. Paradoxically, acute exercise increases the risk of CV events in sedentary individuals, but not in regular exercisers. One of the key mechanisms is an acute increase in blood pressure. The purpose of this study included to investigate if regular aerobic exercise protects obese individuals from acute exercise-induced vascular dysfunction; and to further elucidate the mechanisms through which high pressure may cause vascular dysfunction. In addition we sought to determine the mechanisms through which arteries from the regular exercisers are protected against high pressure. Methods: Obese adults were assigned to an aerobic training intervention or to a control group. Brachial artery flow-mediated dilation (FMD) was assessed before and after acute leg press exercise; before and after the regular exercise intervention. Ex vivo adipose resistance artery FMD was also assessed. In an additional study, mice were subjected to two weeks of voluntary wheel running or control. Hind limb adipose resistance arteries were dissected from mice for measures of FMD or protein expression. Lastly endothelial cells were subjected to laminar shear stress (or static condition) to mimic exercise in cells. Results: Brachial FMD was reduced post-acute leg press exercise in the aerobic exercise and control groups before the aerobic exercise intervention, but was preserved in the aerobic exercise group following the aerobic exercise intervention. Post-acute leg press resistance artery FMD was impaired in the control group; but was preserved in the aerobic exercise group. The mechanism of preserved dilation after exercise was different than at rest (hydrogen peroxide in place of nitric oxide). Resistance arteries from exercised mice maintained FMD after being exposed to high pressure, but not arteries from control mice. In addition arteries from exercised animals and endothelial cells subjected to laminar shear stress expressed less pro-oxidant enzymes and more anti-oxidant enzymes. Conclusion: Aerobic exercise prevents acute exercise-induced vascular dysfunction in obese individuals and improves the redox environment in the adipose microvasculature.