| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1990: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1989: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1988: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
The purpose of this study was to investigate the mechanism of a prolonged exercise-induced hyperuricemia in an animal model. Adult male rats were administered allopurinol 2h before an exercise, and forced for a running exercise until exhaustion on motor-driven treadmill. Purine metabolites in Plantaris muscle, soleus muscle and plasma were assayed by high performance liquid chromatography.
1. In plasma hypoxanthine and xanthine significantly increased compared with controls after an exhaustive exercise, and xantine showed a significant higher tendency at 3h.
2. In plantaris muscle, ATP was decreased at 5 min, but not significant compared with controls. Inosine and hypoxanthine reached peak at 5 min, and they decreased remaining a higher tendency at 1h and a significant higher tendency at 2h, respectively.
3. In soleus muscle, ATP was significantly decreased compared with controls at 0 min. Inosine and hypoxanthine reached peak at 0 min, and they decreased remaining a higher tendency at 1h.
4. In kidney, total adenine nucleotides (ATP+ADP+AMP) was significantly decreased compared with controls at 5 min, and returned to control level remaining a significantly lower tendency at 5h.
In conclusion, these date suggest that production of hypoxanthine from inosine in skeletal muscle continues subsequently after an exhaustive exercise, as result of continuous release of hypoxanthine to blood. Based on these, it is concluded that a persistent production and release of hypoxanthine is responsible for the prolonged exercise-induced hyperuricemia. In addition, these data suggest that adenine nucleotides degradation in slow muscle at an exhaustive exercise also participate in prolonged exercise-induced hyperuricemia.
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