Abstract
In the majority of the population, during high intensity exercise, Adenosine Monohosphate Deaminase (AMPD) Converts Adenosine Monophosphate (AMP) to Inosine Monophosphate (IMP), with the liberation of ammonia in the process. The AMPD reaction displaces the adenylate kinase equilibrium in the direction of ATP formation during exercise, providing additional energy and preventing a large increase in ADP. AMPD deficiency has been proposed to result in faster fatigue development and earlier inhibition of muscle contractions. This review considers a number of genetic mutations that lead to skeletal muscle AMPD deficiency, their pathology and likely symptoms of the disorder.
Highlights
Genetic Predictors of Adenosine Monophosphate Deaminase DeficiencyLawrence D Hayes, Fraser E Houston and Julien S Baker1* 1Institute of Clinical Exercise and Health Science, University of the West of Scotland, Scotland 2School of Human Sciences, London Metropolitan University, UK 3Center for Exercise Science, University of Florida, USA
Adenosine Triphosphate (ATP) hydrolysis exceeds the rate of Adenosine Diphosphate (ADP) rephosphorylation in the muscle cell, leading to excessive formation of the latter
There appeared to be no difference in Peak Power (PP) across genotypes, a premature decrease in power in the mutant c.34C>T allele (TT)+ individuals resulted in a difference in Mean Power (MP) across the genotypes (P=0.020)
Summary
Lawrence D Hayes, Fraser E Houston and Julien S Baker1* 1Institute of Clinical Exercise and Health Science, University of the West of Scotland, Scotland 2School of Human Sciences, London Metropolitan University, UK 3Center for Exercise Science, University of Florida, USA
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