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.
Original language | English |
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Number of pages | 4 |
Journal | Journal of Sports Medicine & Doping Studies |
Volume | 3 |
Issue number | 2 |
DOIs | |
Publication status | Published - 31 Aug 2013 |
Keywords
- Exercise intolernace
- ADP
- AMP
- AMPD
- ATP