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Nitric oxide and vasodilating prostaglandins contribute to the augmented skeletal muscle hyperemia during hypoxic exercise in humans

dc.contributor.authorCrecelius, Anne Renee, author
dc.contributor.authorDinenno, Frank A., advisor
dc.contributor.authorEarley, Scott, committee member
dc.contributor.authorHamilton, Karyn L., committee member
dc.date.accessioned2007-01-03T07:43:02Z
dc.date.available2007-01-03T07:43:02Z
dc.date.issued2009
dc.descriptionDepartment Head: Richard Gay Israel.
dc.description.abstractExercise hyperemia in hypoxia is augmented relative to the same level of exercise in normoxia. At mild exercise intensities, the augmented response is not explained by β-adrenoceptor mediated dilation. We hypothesized that elevated synthesis of nitric oxide (NO) and vasodilating prostaglandins (PGs) contribute to the augmented hyperemic response during hypoxic exercise. To test this hypothesis, in 10 healthy adults, we measured forearm blood flow (FBF; Doppler ultrasound) and calculated the vascular conductance (FVC) responses to rhythmic forearm handgrip exercise (20% maximal voluntary contraction) in normoxia and during systemic isocapnic hypoxia (85% arterial oxygen saturation; pulse oximetry) before and after local intra-brachial combined blockade of nitric oxide synthase (NOS; via NG-monomethyl-ʟ-arginine: ʟ -NMMA) and cyclooxygenase (COX; via ketorolac) inhibition. All trials were performed during local blockade of α- and β-adrenoceptors to eliminate the sympathoadrenal effects on the forearm vasculature and isolate local vasodilation. A deep venous catheter was also placed in the experimental arm. Blood samples were taken from both the arterial and venous catheters and analyzed to assess oxygen extraction and oxygen consumption of the exercising tissue. In control (saline) conditions, FBF after 5 minutes of exercise in hypoxia was greater than in normoxia (345 ± 21 ml min-1 vs 297 ± 18 ml min-1; P<0.05). After NO/PG block, exercise hyperemia was significantly reduced in hypoxia (312 ± 19 ml min-1; P<0.05), but not in normoxia (289 ± 15 ml min-1; P=NS). The observed reduction in FBF during hypoxic exercise after NO/PG block resulted in a significant decrease in oxygen delivery (62 ± 5 ml min-1 vs 56 ± 4 ml min-1; P<0.05). A compensatory increase in extraction was measured (59 ± 3% vs 64 ± 3%; P<0.05) which maintained oxygen consumption (36 ± 3 ml min-1 vs 36 ± 2 ml min-1; P<0.05). We conclude that under the experimental conditions employed, NO and PGs have little role in normoxic exercise hyperemia whereas they significantly contribute to hypoxic exercise hyperemia at this intensity of exercise. The augmented response to hypoxia as compared to normoxia is reduced ~50% with combined NO/PG block. Additionally, during hypoxic exercise after combined NO/PG block, despite a decrease in oxygen delivery driven by attenuated blood flow, muscle oxygen extraction increases to maintain oxygen consumption. The factors contributing to the remaining augmentation of hypoxic exercise hyperemia (~50%) are yet to be determined.
dc.format.mediummasters theses
dc.identifier2009_spring_Crecelius.pdf
dc.identifierETDF2009100001HAES
dc.identifier.urihttp://hdl.handle.net/10217/20067
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relationCatalog record number (MMS ID): 991012183989703361
dc.relationRB145.C743 2009
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.titleNitric oxide and vasodilating prostaglandins contribute to the augmented skeletal muscle hyperemia during hypoxic exercise in humans
dc.typeText
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineHealth and Exercise Science
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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