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Bicarbonate-induced alkalosis augments cellular acetyl group availability and isometric force during the rest-to-work transition in canine skeletal muscle

Published online by Cambridge University Press:  25 June 2002

Paul A. Roberts*
Affiliation:
School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH
Susan J. G. Loxham
Affiliation:
Cardiovascular and Gastrointestinal Global Discovery Research Department, AstraZeneca Pharmaceuticals, Alderley Park SK10 4 TG, UK
Simon M. Poucher
Affiliation:
Cardiovascular and Gastrointestinal Global Discovery Research Department, AstraZeneca Pharmaceuticals, Alderley Park SK10 4 TG, UK
Dumitru Constantin-Teodosiu
Affiliation:
School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH
Paul L. Greenhaff
Affiliation:
School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH
*
*Corresponding author: p.roberts@nottingham.ac.uk
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Abstract

Increasing blood bicarbonate content has long been cited as a potential mechanism to improve contractile function. We investigated whether sodium bicarbonate-induced metabolic alkalosis could positively affect force development during the rest-to-work transition in ischaemic skeletal muscle. Secondly, assuming it could, we investigated whether bicarbonate could augment acetyl group availability through the same equilibrium reaction as sodium acetate pre-treatment and whether this underpins, at least in part, its ergogenic effect. Multiple biopsy samples were obtained from the canine gracilis muscle during 5 min of electrically evoked ischaemic contraction, which enabled the determination of the time course of acetyl group accumulation, substrate utilisation, pyruvate dehydrogenase complex activation and tension development in animals treated with saline (control; n = 6) or sodium bicarbonate (n = 5). Treatment with bicarbonate elevated acetylcarnitine content above the control level at rest (P<0.05), but at no time point during subsequent contraction. The pyruvate dehydrogenase complex was activated following 40 s of contraction in both groups, with no differences existing between treatments at any time point. The requirement for ATP resynthesis from non-oxygen-dependent routes was no different between groups at any time point during contraction. No difference in peak twitch force production existed between groups. However, at 3 min of stimulation, tension development was better maintained in the bicarbonate group (P<0.05), being ∼20% greater than control following 5 min of contraction (P<0.05). The results demonstrate, for the first time, that bicarbonate can augment acetyl group availability prior to contraction, independent of pyruvate dehydrogenase complex activation, but cannot influence the requirement for non-oxidative ATP re-synthesis during subsequent contraction. It would appear, therefore, that the bicarbonate-induced improvement in muscle tension development was probably mediated through the metabolic alkalosis and not via the increased availability of acetyl groups within the cell.

Type
Research Article
Copyright
Copyright © Experimental Physiology 2002

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Bicarbonate-induced alkalosis augments cellular acetyl group availability and isometric force during the rest-to-work transition in canine skeletal muscle
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Bicarbonate-induced alkalosis augments cellular acetyl group availability and isometric force during the rest-to-work transition in canine skeletal muscle
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