Research Interests:

Obesity is increasing at an alarming rate in the United States and is a major risk factor for a variety of cardiovascular diseases. Obese humans have an impaired ability to increase muscle blood flow in response to exercise, and the mechanisms underlying this abnormal increase in blood flow (functional hyperemia) are unclear. An impaired functional hyperemia could potentially prevent the obese patient from adequate exercise, a therapy known to improve glucose, lipids and weight control. Therefore, a better understanding of the mechanisms underlying improved functional hyperemia by chronic exercise training in obesity is important. Our published studies suggest that hyperglycemia and/or hyperlipidemia impair functional vasodilation through attenuated arachidonic acid mediated vasodilation. We have demonstrated that chronic exercise training improves acute functional vasodilatory responses in an animal model of obesity, the obses Zucker rat. The mechanisms responsible for the improvement in vascular responses following an exercise training period are not known. Our current research is based on determining mechanisms by which functional hyperemia is impaired in obesity, and the mechanisms by which chronic exercise treatment improves vascular function. We use combinations of in vivo and in vitro microcirculatory and biochemical techniques to determine the mechanisms for the altered vascular responses in obesity.

Additional work in the laboratory involves the development and use of mathematical models of physiology processes to understand the integration of physiological processes. Information about this can be found on our web site at http://physiology.umc.edu/themodelingworkshop