Case Western Reserve University School of Graduate Studies
Model analysis of oxygen transport and metabolism in skeletal muscle: responses to a change in energy demand
Abstract
dc:description<p>The increase in skeletal muscle oxygen consumption (VO<sub>2</sub>) at the onset of contraction is an indicator of the ability to do work. The VO<sub>2</sub> response to contraction (i.e., VO<sub>2</sub> kinetics) is determined by oxygen delivery (convective and diffusive) to tissue, oxygen utilization in muscle myocytes, and intracellular PO<sub>2</sub> (iPO<sub>2</sub>). However, factors determining oxygen diffusion, including permeability-surface area (PS) and the blood-tissue O<sub>2</sub> gradient, are difficult to measure during the onset of contraction. Therefore, computational models of O<sub>2</sub> transport and metabolism in skeletal muscle can be used to elucidate underlying factors and predict the effects of alterations in oxygen transport and metabolism on VO<sub>2</sub> kinetics in skeletal muscle.</p><p>A computational model of O<sub>2</sub> transport and utilization in skeletal muscle, including changes in blood volume fractions at the onset of contraction, can be used to quantify changes in hemoglobin (Hb) and myoglobin (Mb) oxygenation in skeletal muscle at the onset of contraction. The model quantifies the increase in Mb deoxygenation where convective or diffusive oxygen delivery is limited, which increases the relative contribution of Mb to the total change in heme oxidation (measured by near-infrared spectroscopy) as compared to normal physiological conditions.</p><p>A computational model of O<sub>2</sub> transport and utilization, including anaerobic glycogenolysis, is used to investigate VO<sub>2</sub> and iPO<sub>2</sub> kinetics in response to submaximal and maximal contraction intensity in the canine gastrocnemius. The model is able to predict VO<sub>2</sub> kinetics for different blood flow (Q), contraction intensity, and arterial oxygen content in addition to quantifying the role of iPO<sub>2</sub> at higher contraction intensity. The model (A) predicts that PS is the major controller of oxygen diffusion and (B) quantifies the relationship between iPO<sub>2</sub> and contraction intensity, which depends on transport and metabolic properties of the muscle.</p><p>This model is also used to explore the effects of convective and diffusive limitations on VO<sub>2</sub> kinetics at the onset of contraction. The model (A) predicts a linear relationship between PS and Q and (B) quantifies the effects of convective, diffusive, and metabolic limitations on VO<sub>2</sub> kinetics in skeletal muscle.</p>
Degree
thesis:*- Name thesis:degree_name
- Doctor of Philosophy
- Level thesis:degree_level
- doctoral
- Discipline thesis:degree_discipline
- Biomedical Engineering
- Grantor dc:publisher
- Case Western Reserve University School of Graduate Studies
- Year dc:date
- 2013
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Spires, Jessica Rose
- Contributors dc:contributor
-
- Saidel, Gerald
Subjects
dc:subject × 16Rights
dc:rights- Statement dc:rights
-
- unrestricted
- This thesis or dissertation is protected by copyright: all rights reserved. It may not be copied or redistributed beyond the terms of applicable copyright laws.
- Language dc:language
- English
Identifiers
dc:identifier.*- Repository record dc:identifier
- http://rave.ohiolink.edu/etdc/view?acc_num=case1365177364
- OAI identifier oai:identifier
- oai:etd.ohiolink.edu:case1365177364