This review summarizes the genetic mutations, pathology, and symptoms associated with skeletal muscle AMPD deficiency, which can lead to faster fatigue during exercise.
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AMPD deficiency may warrant consideration in unexplained fatigue; leaves open need for prevalence studies and interventions.
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.
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Lawrence D. Hayes (2013) studied this question.
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