It has been generally recognized that in a living body various biochemical changes were induced as a consequence of hard physical exercise. In the previous paper (1), the authors reported on the metabolism of glucuronic acid in the case of fatigue by physical exercise. This report was summarized as follows: the toxic (amine-like) substance in a living body increased due to physical exercise, and resulted in fatigue. The glucuronic acid content of urine, serum, liver and kidney, and the hepatic glycogen content of a living body decreased. The activity of o-aminophenylglucuronide synthesis of rat's liver was inhibited after hard physical exercise. However, these phenomena were significantly blocked by the administration of glucuronolactone. The arrest of an isolated frog heart due to the accumulation of toxic substance was checked, both prophylactically and therapeutically, by the administration of glucuronolactone. Dutton et al. (2-8) have recently proved that glucuronic acid exerted its effect after it was converted into uridine-diphospho-glucuronic acid. It is therefore apparent that exogenous glucuronic acid cannot exert its effect unless it is changed into uridine-diphospho-glucuronic acid through the Xylulose pathway, or different pathway not yet known. Though the authors have no description of the mechanism of these pathway at present, it is a fact that glucuronolactone can inhibit the toxic substance which stopped the beating of a frog's heart. As well known, uridine-diphospho-glucuronic acid is converted from various kinds of carbohydrate, namely glucose, galactose, glycogen and sodium pyruvate. The authors therefore proceeded to ascertain the effects of these carbohydrates and glucuronolactone upon the swimming-record, o-aminophenylglucuronide synthesis, glucuronic acid content, ascorbic acid content, blood sugar content, hepatic glycogen content, and β-D-glucuronide glucuronohydolase activity in albino rats made to swim hard.
