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The involvement of the lactacid and alactacid mechanisms in oxygen debt was examined in 2 dogs prior to and after a 6-week training program by using tryptophan and quinolinic acid to block the removal of lactate by the liver. The results show that the lactacid mechanism is involved at work loads resulting in sufficient elevation of blood lactate during the recovery period. It was further shown that training produced a significant decrease in both oxygen debt and blood lactate. Mechanisms responsible for the findings are discussed.
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