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Dunnett, Mark
(1996).
DOI: https://doi.org/10.21954/ou.ro.0000e0c7
Abstract
Thoroughbred horseracing involves high-intensity exercise characterized by the production and accumulation of hydrogen (H+) ions within the skeletal muscles. Without a system for maintaining acid-base balance the consequential accumulation of H+ ions within the working muscles would produce a rapid decline in intra-cellular pH with a concomitant impairment of the contractile process. Carnosine (ß-alanyl-L-histidine, pKa 6.83) occurs at high concentration in equine muscle where it functions as an effective H+ ion buffer at physiological pH.
High-performance liquid chromatography analytical methods were developed for carnosine and used to investigate its distribution and metabolism in equine fluids and tissues, with emphasis on type 1, IIA and IIB muscle fibres. Foals and yearlings had significantly lower plasma carnosine concentrations than older horses. Plasma carnosine concentration showed little change during normal feeding and high-intensity exercise, however, episodes of equine exertional rhabdomyolysis produced large increases. Carnosine concentrations in tissues, such as the heart, liver and intestine were 10 to 100-fold lower than in skeletal muscle. Carnosine displayed a heterogeneous distribution within skeletal muscle. Its concentration in type IIA and 1113fi bres was approximately 5-fold higher than in type I fibres.
Extensive, partly anaerobic training produced a 2-fold increase in the carnosine concentration in type IIA fibres, and an increase, although non-significant, in type I and IIB fibres. Thirty days of dietary ß-alanine and histidine supplementation produced an adaptive increase in ß-alanine and histidine bioavailability, and significant increases in the carnosine concentration in type IIA and IIB fibres.
A greater skeletal muscle carnosine concentration via training and/or ß-alanine and histidine supplementation would produce a corresponding increase in H+ ion buffering capacity, which may reduce the rate of metabolic acidosis during high-intensity exercise, and possibly delay the subsequent onset of localized muscle fatigue.