Bicarbonate-induced alkalosis augments cellular acetyl group availability and isometric force during the rest-to-work transition in canine skeletal muscle.
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 re-synthesis 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 approximately 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.
Roberts
Paul A
PA
School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, UK. p.roberts@nottingham.ac.uk
Loxham
Susan J G
SJ
Poucher
Simon M
SM
Constantin-Teodosiu
Dumitru
D
Greenhaff
Paul L
PL
D000108:Acetylcarnitine / Q000032:analysis / Q000378:metabolism; D000471:Alkalosis / Q000139:chemically induced / Q000503:physiopathology; D000818:Animals; D002331:Carnitine / Q000032:analysis / Q000378:metabolism*; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D007262:Infusions, Intravenous; D007511:Ischemia / Q000188:drug therapy / Q000503:physiopathology*; D007537:Isometric Contraction / Q000187:drug effects*; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology*; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D012016:Reference Values; D015203:Reproducibility of Results; D012146:Rest; D012680:Sensitivity and Specificity; D017693:Sodium Bicarbonate / Q000008:administration & dosage*; D013314:Stress, Mechanical
D011768:Pyruvate Dehydrogenase Complex; D000108:Acetylcarnitine; D017693:Sodium Bicarbonate; D002331:Carnitine