Contrasting plasma free amino acid patterns in elite athletes: association with fatigue and infection

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Abstract

There is little information on the plasma free amino acid patterns of elite athletes against which fatigue and nutrition can be considered. Therefore the aim was to include analysis of this pattern in the medical screening of elite athletes during both especially intense and light training periods.

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Regulation of glutaminase activity and glutamine metabolism.

M Watford, Norman Curthoys (1994)

Glutamine is synthesized primarily in skeletal muscle, lungs, and adipose tissue. Plasma glutamine plays an important role as a carrier of nitrogen, carbon, and energy between organs and is used for hepatic urea synthesis, for renal ammoniagenesis, for gluconeogenesis in both liver and kidney, and as a major respiratory fuel for many cells. The catabolism of glutamine is initiated by either of two isoforms of the mitochondrial glutaminase. Liver-type glutaminase is expressed only in periportal hepatocytes of the postnatal liver, where it effectively couples ammonia production with urea synthesis. Kidney-type glutaminase is abundant in kidney, brain, intestine, fetal liver, lymphocytes, and transformed cells, where the resulting ammonia is released without further metabolism. The two isoenzymes have different structural and kinetic properties that contribute to their function and short-term regulation. Although there is a high degree of identity in amino acid sequences, the two glutaminases are the products of different but related genes. The two isoenzymes are also subject to long-term regulation. Hepatic glutaminase is increased during starvation, diabetes, and feeding a high-protein diet, whereas kidney-type glutaminase is increased only in kidney in response to metabolic acidosis. The adaptations in hepatic glutaminase are mediated by changes in the rate of transcription, whereas kidney-type glutaminase is regulated at a posttranscriptional level.

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Muscle and plasma amino acids following injury. Influence of intercurrent infection.

F Gump, D Elwyn, Y Carpentier … (1980)

The present study was undertaken to determine intracellular amino acid patterns in patients with multiple trauma, whether or not complicated by sepsis and during convalescence. A percutaneous muscle biopsy was performed three to four days following major accidental injury in ten patients and analyzed for muscle free amino acids. Venous blood was drawn at the time of the biopsy and analyzed for plasma free amino acids. Five patients developed sepsis and a repeat biopsy was performed on days 8 to 11. In five of the patients a biopsy was performed during the late convalescent period (anabolic phase). A marked depletion of nonessential amino acids in muscle occurred in both injury and sepsis due to a decrease (50%) in glutamine, which was equally marked in both states. The essential amino acids in muscle increased in injury. During sepsis, a further increase was observed with a return toward normal in the convalescent period. In injury, the most marked rise was in the branched-chain amino acids, phenylalanine, tryosine and methionine. With sepsis, a further rise in muscle branched-chain amino acids, phenylalanine and tryosine occurred, while plasma levels remain unchanged. During convalescence, muscle glutamine, arginine, histidine and plasma branched-chain amino acids were below normal, whereas muscle phenylalanine and methionine were elevated. The muscle free amino acid pattern observed after major trauma was essentially the same as earlier described following elective operation. This suggests a common response of intracellular amino acids irrespective of the degree of injury, and may indicate that the pump settings which regulate amino acid transport follow the "all or none" rule. The high intracellular levels of branched-chain amino acids in sepsis suggest that the energy deficit of this state is due to an impairment of substrate use rather than intracellular availability. The high concentrations of the aromatic amino acids and methionine may be due to altered liver function. During the late convalescent period (anabolic phase) the low levels of certain key amino acids suggests inadequate nutrition. The difficulties in nourishing the injured or septic patient are well recognized. The period following these catabolic states may be an important period for the application of an optimal, aggressive nutritional regimen.