75 EXERCISE-INDUCED ALTERATION OF ERYTHROCYTE GLYCOLYSIS ASSOCIATED WITH HYOGENIC HYPERURICEMIA

Abstract

Myogenic hyperuricemia is caused by increased production of uric acid secondary to enhanced release of inosine and hypoxanthine from exercising muscles into blood. This novel mechanism is evident in glycogenosis types VII (muscle phosphofructokinase deficiency), III (debranching enzyme deficiency), and V. In this study, we examined the effect of muscular exercise on the glycolysis of circulating erythrocytes in glycogenosis types VII and III. The concentration of erythrocyte 2,3-bisphosphoglycerate, which had decreased because of genetic partial deficiency of erythrocyte phosphofructokinase, was further decreased after prolonged bed rest in patients with type VII. Ergometric exercise rapidly increased fructose-1,6-P2, dihydroxyacetone-P plus glyceraldehyde-3-P, and 2,3-bisphosphoglycerate in circulating erythrocytes. Similar changes were observed after exercise in patients with type III. The exercise-induced metabolic alteration of erythrocytes was reproduced in vitro by incubating normal erythrocytes in the presence of inosine. We conclude that physical activity affects glycolysis in erythrocytes in glycogenosis types VII and III, and that myogenic factors including inosine are responsible for this change.