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Ingestion of sodium citrate (Na-Cit), an alkalizing agent, increases extracellular pH via liver oxidation by decreasing [H+] and increasing bicarbonate concentration (HCO3-). Studies have confirmed that increasing extracellular pH promotes the efflux of La- and H+ from active muscles. This is due to an increase in activity of the pH sensitive monocarboxylate transporter as the gradient of intracellular versus extracellular H+ increases. Therefore, artificially inducing alkalosis prior to anaerobic exercise may reduce intracellular acidosis and increase the time to fatigue - defined as a decrease in force production with an increased perception of effort. The investigators will test the null hypothesis that sodium citrate ingestion (chronic and acute) will not have an effect on exercise performance compared to placebo.
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Anaerobic glycolysis quickly provides adenosine triphosphate (ATP) for muscular contraction during high intensity, short duration exercise. The fast rate of glycolysis during anaerobic exercise results in pyruvate formation exceeding pyruvate oxidation resulting in a build up of lactic acid. Lactic acid dissociates quickly to lactate (La-) and hydrogen ion (H+) which causes a decrease in muscle and blood pH. The increase in H+ causes impaired release of calcium from the sarcoplasmic reticulum and calcium ion binding which inhibits the coupling of actin and myosin.
Ingestion of sodium citrate (Na-Cit), an alkalizing agent, increases extracellular pH via liver oxidation by decreasing [H+] and increasing bicarbonate concentration (HCO3-). Studies have confirmed that increasing extracellular pH promotes the efflux of La- and H+ from active muscles. This is due to an increase in activity of the pH sensitive monocarboxylate transporter as the gradient of intracellular versus extracellular H+ increases. Therefore, artificially inducing alkalosis prior to anaerobic exercise may reduce intracellular acidosis and increase the time to fatigue - defined as a decrease in force production with an increased perception of effort. Furthermore, Cit- enters the cell through the Plasma Membrane Citrate Transporter and in the cell Cit- is involved in a number of processes: i) intermediary in the Krebs Cycle, ii) transports acetyl-Co-enzyme A (CoA)from the mitochondria to the cytosol for fatty-acid synthesis, iii) negative allosteric effector of phosphofructokinase, iv) anionic effect on membrane potential can cause a reduction in the contraction threshold.
Researchers have studied sodium bicarbonate and Na-Cit as potential alkalizing agents. Na-Cit has been studied in few sports over a broad array of doses, times, and distances with inconclusive results. McNaughton et al. researched the optimal doses and durations for Na-Cit to be potentially beneficial to performance. They concluded that 0.3-0.5g/kg, 90-120 minutes prior to maximal effort are the optimal conditions for potential ergogenic effect. The only reported side effect was gastrointestinal (GI) discomfort in a 3 of the 8 subjects. However, it seems Na-Cit is handled better than the more commonly employed sodium bicarbonate.
The investigators will test the null hypothesis that sodium citrate ingestion (chronic and acute) will not have an effect on exercise performance compared to placebo.
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10 participants in 4 patient groups, including a placebo group
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