NORMAL SPRINT PERFORMANCE DESPITE AMP DEAMINASE DEFICIENCY 365

Abstract

During heavy exercise AMP is deaminated to IMP by the enzyme AMP deaminase. Deficiency of AMP deaminase has been suggested as the cause of easy fatiguability and exertional myalgias in patients with this defect. Increasing evidence, however, imply that many individuals are asymptomatic despite AMP deaminase deficiency. The aim of this investigation was to compare the performance and the acute metabolic response during short term heavy exercise in asymptomatic subjects with AMP deaminase deficiency and in subjects with normal AMP deaminase levels. 15 women (including two with AMP deaminase deficiency) performed three 30-s cycle sprints (Wingate test) with 20 min rest between the sprints. Mean power/body weight (MP) and peak power/body weight(PP) were calculated for each of the three tests. Blood samples were collected before exercise and after each of the three cycle bouts and analyzed for lactate and ammonia. The MP (W/kg) was 7.0±0.5 vs 6.4 and 7.2 in bout I, 7.1±0.6 vs 6.8 and 7.7 in bout II and 7.2±0.7 vs 6.7 and 7.8 in bout III and the PP (W/kg) was 9.6±1.0 vs 9.3 and 9.1 in bout I, 9.8±1.0 vs 9.8 and 9.6 in bout II and 9.7±1.2 vs 9.6 and 9.8 in bout III for the subjects with normal AMP deaminase levels vs the subjects with AMP deaminase deficiency. The highest ammonia levels (μmol/l) were reached after the first bout and were 69±24 vs 21 and 11 after 3 min, 88±40 vs 18 and 10 after 6 min and 83±47 vs 17 and 9 after 9 min for the subjects with normal AMP deaminase levels vs the subjects with AMP deaminase deficiency. The corresponding lactate levels (mmol/l) were 7.0±2.4 vs 10 and 9.3 after 3 min, 8.4 ±2.1 and 9.9 and 9.1 after 6 min and 8.7±2.1 vs 10 and 9.2 after 9 min. Conclusion: lack of AMP deaminase seems not to affect sprint performance.