Myogenic hyperuricemia, as a result of the purine nucleotide cycle running when ATP reservoirs in muscle cells are low (ADP > ATP), is a common pathophysiologic feature of glycogenoses such as GSD-III, GSD-V and GSD-VII, as they are metabolic myopathies which impair the ability of ATP (energy) production within muscle cells. In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest. Excess AMP (adenosine monophosphate) is converted into uric acid. 
:AMP → IMP → Inosine → Hypoxanthine → Xanthine → Uric acid
Hyperammonemia is also seen post-exercise in McArdle disease (GSD-V) and phosphoglucomutase deficiency (PGM1-CDG, formerly GSD-XIV), due to the purine nucleotide cycle running when the ATP reservoir is low due to the glycolytic block.O + H → IMP + NH </blockquote>