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Regulation of skeletal muscle metabolism : supply and demand

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Di Maria, Carla A.(Carla Alexandra) (2002) Regulation of skeletal muscle metabolism : supply and demand. PhD thesis, University of Tasmania.

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Abstract

Regulation of Skeletal Muscle Metabolism
— Supply and Demand
This thesis examines the regulation of skeletal muscle metabolism under
resting conditions. Previous studies have shown that vasoconstrictors stimulate [type
A] or inhibit [type B] metabolism of the constant flow perfused rat hindlimb. There is
evidence that this may be due to redistribution of blood flow between the two vascular
pathways in skeletal muscle, either increasing [type A] or decreasing [type B] the
extent of nutritive perfusion. It is not clear if enhanced nutritive perfusion and
therefore enhanced oxygen delivery is enough to account for the observed increase in
metabolism with type A vasoconstrictors. It has been proposed that a cellular
thermogenic mechanism is activated in addition to redistribution. The identity of this
mechanism is not clear. A number of possibilities are explored. The effects of varied oxygen delivery on hindlimb oxygen uptake were
examined. Flow was maintained at a constant level while arterial oxygen content was
varied. Three independent methods (1-MX metabolism, microdialysis and laser
doppler flowmetry) were utilized to rigorously monitor redistribution. A positive
relationship between oxygen delivery and hindlimb oxygen uptake was detected,
independent of redistribution. Cellular ATP levels were maintained, though PCr
stores were depleted at low oxygen delivery. Lactate efflux increased, but was not
considered great enough to fully compensate for diminished ATP production from
aerobic sources. In this regard, the perfused rat hindlimb may be considered as an
oxygen conforming tissue. Thus oxygen delivery is a key determinant of skeletal
muscle metabolic rate, and type A vasoconstrictors may effectively enhance oxygen
delivery by improving nutritive perfusion. Mechanisms accounting for increased oxygen consumption during enhanced
delivery were explored. The roles of sodium cycling and accompanying Na+/K+-
ATPase pump activity were assessed. Comparisons were made between type A
vasoconstrictors and the sodium channel labilizer veratridine in both skeletal and
cardiac muscle. In perfused skeletal muscle both vasoconstrictor- and veratridinemediated
metabolism were blocked by the sodium pump inhibitor ouabain, however
vasoconstrictor-mediated metabolism was resistant to sodium channel inhibition with
tetrodotoxin (TTX). The same TTX-resistant vasoconstrictor-thermogenic effect was
absent from perfused arrested rat heart, possibly due to differences in vascular
anatomy. Intracellular recording techniques failed to detect any change in skeletal
fiber membrane potential during type A vasoconstrictor infusion, but did detect
changes with veratridine. In summary the data supports the notion that metabolic
demand (sodium load with veratridine) can stimulate hindlimb metabolism. However,
there was no evidence for type A vasoconstrictor mediated changes in muscle sodium
cycling, Na+/K+-ATPase activity, or membrane depolarization.
Oxygen consumption of resting skeletal muscle is largely controlled by
oxygen delivery, whether this is by changes in bulk flow or flow redistribution.
Cellular thermogenic mechanisms may well be activated in response to increased
oxygen delivery, though sodium cycling/pumping is no longer a candidate.

Item Type: Thesis (PhD)
Keywords: Blood flow, Musculoskeletal system, Muscles
Copyright Holders: The Author
Copyright Information:

Copyright 2002 the Author - The University is continuing to endeavour to trace the copyright
owner(s) and in the meantime this item has been reproduced here in good faith. We
would be pleased to hear from the copyright owner(s).

Additional Information:

Thesis (Ph.D.)--University of Tasmania, 2002. Includes bibliographical references

Date Deposited: 09 Dec 2014 00:06
Last Modified: 20 Jul 2016 00:10
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