Presentation Type
Poster
Keywords
circulatory physiology, flow-induced dilation, rat model
Department
Sports Medicine
Major
Sports Medicine, B.S
Abstract
During exercise, an increase in blood flow to working skeletal muscle is necessary in order to sustain activity for longer than a few seconds. This is accomplished by the dilation of arteries and arterioles feeding the muscle. Arterioles, located within contracting muscle, are exposed to dilatory metabolites released by the muscle; however, the mechanism by which feed arteries dilate is still unknown, since they are located external to the muscle. The purpose of this study was to determine if flow-induced dilation (resulting from shear stress on endothelial cells) contributes to exercise hyperemia in rat extensor digitorum longus and gastrocnemius muscle feed arteries (EDLFA and GFA). We hypothesized that the response range for flow-induced dilation in GFA and EDLFA is lower than the shear stress normally present in non-exercising rats. Feed arteries (13 EDLFA and 16 GFA) were isolated from male Sprague-Dawley rats and cannulated on two glass micropipettes for in vitro videomicroscopy. Flow was induced through the arteries and corresponding flow measurements were used to calculate intraluminal wall shear stress in the arteries. The in vitro shear stress response range was compared to calculated in vivo shear stress values from previously published studies. Our results show that in vitro GFA dilated maximally to flow at 16.5 dynes/cm2, whereas in vivo shear stress in GFA was 48 dynes/cm2 in non-exercising rats. Because the response to flow is maximized at shear stress lower than that observed in non-exercising rats, flow-induced dilation cannot contribute to exercise hyperemia. Additionally, EDLFA did not dilate significantly to increasing levels of flow. Overall, these data support our hypothesis that flow-induced dilation does not contribute to exercise hyperemia in either GFA or EDLFA.
Faculty Mentor
Jeffrey Jasperse
Funding Source or Research Program
Summer Undergraduate Research in Biology
Included in
Flow-Induced Dilation of Skeletal Muscle Feed Arteries: Relevance to Exercise Hyperemia
During exercise, an increase in blood flow to working skeletal muscle is necessary in order to sustain activity for longer than a few seconds. This is accomplished by the dilation of arteries and arterioles feeding the muscle. Arterioles, located within contracting muscle, are exposed to dilatory metabolites released by the muscle; however, the mechanism by which feed arteries dilate is still unknown, since they are located external to the muscle. The purpose of this study was to determine if flow-induced dilation (resulting from shear stress on endothelial cells) contributes to exercise hyperemia in rat extensor digitorum longus and gastrocnemius muscle feed arteries (EDLFA and GFA). We hypothesized that the response range for flow-induced dilation in GFA and EDLFA is lower than the shear stress normally present in non-exercising rats. Feed arteries (13 EDLFA and 16 GFA) were isolated from male Sprague-Dawley rats and cannulated on two glass micropipettes for in vitro videomicroscopy. Flow was induced through the arteries and corresponding flow measurements were used to calculate intraluminal wall shear stress in the arteries. The in vitro shear stress response range was compared to calculated in vivo shear stress values from previously published studies. Our results show that in vitro GFA dilated maximally to flow at 16.5 dynes/cm2, whereas in vivo shear stress in GFA was 48 dynes/cm2 in non-exercising rats. Because the response to flow is maximized at shear stress lower than that observed in non-exercising rats, flow-induced dilation cannot contribute to exercise hyperemia. Additionally, EDLFA did not dilate significantly to increasing levels of flow. Overall, these data support our hypothesis that flow-induced dilation does not contribute to exercise hyperemia in either GFA or EDLFA.