Author(s): De Ruiter CJ, Van EDE HAANngelen BG, Wevers RA, De Haan A
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Abstract Myoadenylate deaminase (MAD) is an enzyme active in skeletal muscle, probably during exercise of moderate intensity but certainly during vigorous exercise, when the deamination of AMP leads to increased levels of IMP and ammonia. There is controversy about the clinical significance of MAD deficiency. The main objective of the present study was to investigate the extent to which genetically confirmed MAD deficiency affects muscle function under conditions of maximal short-term electrically induced activation. The left hand was immobilized and adductor pollicis muscle function was investigated. To exclude the influence of central factors, such as the patient's motivation, the ulnar nerve was maximally electrically activated and force output was measured at the thumb. Sixty rapid shortening contractions resulted in a decrease of maximal power to 34.2+/-5.4\% and 33.3+/-6.3\% (means+/-S.D.) of the values for unfatigued muscle in the control and MAD-deficient subjects respectively (P>0.05; n=7). Maximal isometric forces and shortening velocities did not differ between groups in unfatigued, fatigued or recovered muscle. None of the subjects experienced exercise-related muscle aches or cramps. In conclusion, MAD deficiency does not appear to affect adductor pollicis muscle force, shortening velocity and relaxation, either during or after maximal short-term activation.
This article was published in Clin Sci (Lond)
and referenced in Journal of Sports Medicine & Doping Studies