Yamanaka H, Kawagoe Y, Taniguchi A, Kaneko N, Kimata S, Hosoda S, Kamatani N, Kashiwazaki S
Institute of Rheumatology, Tokyo Women's Medical College, Japan.
Metabolism. 1992 Apr;41(4):364-9. doi: 10.1016/0026-0495(92)90069-m.
The exact conditions under which exercise causes purine nucleotide degradation are not well understood. We determined plasma hypoxanthine and uric acid levels serially in eight individuals during ergometer muscle exercise. When the load was increased gradually by 15 W/min, plasma hypoxanthine was elevated only after the status exceeded the anaerobic threshold (AT), as determined by analysis of expired gas. Nonstrenuous ergometer exercise, which kept the status continuously below the AT, induced neither blood lactic acid nor plasma hypoxanthine elevation. These results suggest that the AT is also the threshold for the acceleration of purine nucleotide degradation. Muscle exercise to a degree that does not exceed the AT does not cause major purine nucleotide degradation, and, therefore, is expected to be beneficial for patients with gout and/or hyperuricemia.
运动导致嘌呤核苷酸降解的确切条件尚未完全明确。我们在八名个体进行测力计肌肉运动期间连续测定了血浆次黄嘌呤和尿酸水平。当负荷以每分钟15瓦的速度逐渐增加时,血浆次黄嘌呤仅在运动状态超过无氧阈值(AT)后才升高,无氧阈值通过分析呼出气体来确定。保持运动状态持续低于无氧阈值的非剧烈测力计运动,既不会引起血乳酸升高,也不会导致血浆次黄嘌呤升高。这些结果表明,无氧阈值也是嘌呤核苷酸降解加速的阈值。不超过无氧阈值的肌肉运动不会导致主要的嘌呤核苷酸降解,因此,有望对痛风和/或高尿酸血症患者有益。