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Permanent link (DOI): https://doi.org/10.7939/R3B601

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Satellite cell involvement in activity-induced skeletal muscle adaptations Open Access

Descriptions

Other title
Subject/Keyword
fast-to-slow transformation
nitric oxide
adaptation
chronic low-frequency stimulation
myosin heavy chain
satellite cell
exercise
skeletal muscle
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Martins, Karen
Supervisor and department
Putman, Charles (Physical Education and Recreation)
Examining committee member and department
Esser, Karyn (Physiology)
Syrotuik, Daniel (Physical Education and Recreation)
Dixon, Walter (Agricultural, Food and Nutritional Science)
Foxcroft, George (Agricultural, Food and Nutritional Science)
Department
Faculty of Physical Education and Recreation
Specialization

Date accepted
2009-09-28T20:06:28Z
Graduation date
2009-11
Degree
Doctor of Philosophy
Degree level
Doctoral
Abstract
Skeletal muscle is a heterogeneous, multinucleated, post-mitotic tissue that contains many functionally diverse fibre types that are capable of adjusting their phenotypic properties in response to altered contractile demands. This plasticity, or adaptability of skeletal muscle is largely dictated by variations in motoneuron firing patterns. For example, in response to increased tonic firing of slow motoneurons, which occurs during bouts of endurance training or chronic low-frequency stimulation (CLFS), skeletal muscle adapts by transforming from a faster to a slower phenotypic profile. CLFS is an animal model of endurance training that induces fast-to-slow fibre type transformations in the absence of fibre injury in the rat. The underlying signaling mechanisms regulating this fast-to-slow fibre type transformation, however, remain to be fully elucidated. It has been suggested that myogenic stem cells, termed satellite cells, may regulate and/or facilitate this transformational process. Therefore, the signaling mechanisms involved in CLFS-induced satellite cell activation as well as the role satellite cells may play in CLFS-induced skeletal muscle adaptation were investigated in rat. A pharmacological inhibitor of nitric oxide (NO) synthase, Nω-nitro-L-arginine methyl ester, was used to investigate CLFS-induced satellite cell activation in the absence of endogenous NO production. Results suggest that NO is required for early CLFS-induced satellite cell activation, but a yet-to-be defined pathway exists that is able to fully compensate in the absence of prolonged NO production. A novel method of satellite cell ablation (i.e. weekly focal γ-irradiation application) was used to investigate CLFS-induced skeletal muscle adaptation in the absence of a viable satellite cell population. Myosin heavy chain (MHC), an important structural and regulatory protein component of the contractile apparatus, was used as a cellular marker of the adaptive response to CLFS. Findings suggest that satellite cell activity may be required for early fast-to-slow MHC-based transformations to occur at the protein level without delay in the fast fibre population, and may also play an obligatory role in the final transformation from fast type IIA to slow type I fibres. Interestingly, additional results show that NO appears to be a key mediator of MHC isoform gene expression during CLFS-induced fast-to-slow fibre type transformations.
Language
English
DOI
doi:10.7939/R3B601
Rights
License granted by Karen Martins (martinuk@ualberta.ca) on 2009-09-28T19:39:02Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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