THE POSSIBLE MECHANISMS OF CONTRACTING AND PAYING THE OXYGEN DEBT AND THE RÔLE OF LACTIC ACID IN MUSCULAR CONTRACTION

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Abstract
A series of exps. were performed on the same subject in which the exercise (running) lasted 10 min. The results show that the removal of lactic acid from the blood during recovery is, disregarding the first period, an exponential function of time; i.e., its speed of disappearance is proportional to the concn. of the lactic acid at each moment. Evidence is given for the validity of the assumption that the concn. of lactic acid in the blood is proportional to the amt. of lactic acid in the body at any time. No extra lactic acid appears in the blood up to a rate of work corresponding to about 2/3 of the max. metabolic rate, after which the lactic acid increases very rapidly, with an increment of 7 gm. per increment of 1 liter of O2 debt as calculated after A. V. Hill. Hence the lactic acid mechanism can not play any important part in muscular contraction except in very strenuous exercise. For lower rates of work the O2 debt is independent of any lactic acid formation or removal, and is therefore described in this paper as "alactacid." The alactacid O2 debt is approximately a linear function of the O2 intake in exercise. It is supposed to be related to the oxidation of substances furnishing the energy for the resynthesis of phosphagen split down during muscular contraction. The max. amt. of O2 debt by this mechanism was in this subject about 2.5 liters. The lactacid O2 debt apparently comes into play only when the work is carried on in anaerobic condition. The max. absolute amt. is about 5 liters. It may be increased by increasing the capacity of the body to accumulate lactic acid, as for example, after ingestion of alkali. The disappearance of lactic acid from the blood at the beginning of recovery after strenuous exercise shows a lag which does not seem to be fully explained either by a lag in the diffusion of lactic acid from muscles to the blood or by a slower oxidation of lactic acid, or by a delayed lactic acid production. In a trained subject this lag has a duration of 6 or 8 min. In non-athletic and untrained subjects, incapable of good performances, the tog may last 2 or 3 times as long.