Journal
JOURNAL OF COMPARATIVE PHYSIOLOGY B-BIOCHEMICAL SYSTEMIC AND ENVIRONMENTAL PHYSIOLOGY
Volume 170, Issue 1, Pages 51-58Publisher
SPRINGER VERLAG
DOI: 10.1007/s003600050007
Keywords
protein catabolism; N-tau-methylhistidine; muscle protein; flight; pigeon
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In order to study protein degradation during flight in homing, a high-performance liquid chromatography technique was developed for the quantitative analysis of N-tau-methylhistidine. Secondly, it was necessary to confirm that the excretion of N-tau-methylhistidine correlates with myofilament breakdown in homing pigeons. In these experiments, ten birds were subcutaneously injected with N-tau-[C-14]methylhistidine and the excreta were quantitatively collected for 1 week. Of the 94.5% radioactivity recovered, 87.1% was associated with N-tau-[C-14]methylhistidine and 6.1% with N-acetyl-N-tau-[C-14]methylhistidine. This rapid excretion of unmetabolized N-tau-[C-14]methylhistidine validates the assumption that the amount of N-tau-methylhistidine excreted is a measure of myofilament catabolism in homing pigeons. The influence of endurance flight on protein breakdown was determined after flights from release sites 368-646 km away. Immediately after return, plasma urea and uric acid levels were increased, whereas plasma concentration of N-tau-methylhistidine remained unchanged compared to unflown control birds. Flown pigeons excreted significantly more urea and N-tau-methylhistidine within 24 h and significantly more urea and uric acid within 96 h after flight than unflown controls. Our findings support the hypothesis that in homing pigeons protein catabolism is increased during endurance flight. Elevated N-tau-methylhistidine excretion probably results from repair processes in damaged muscle fibers, including breakdown of myofilaments.
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