Muscle function during fatigue in myoadenylate deaminase-deficient Dutch subjects

Myoadenylate deaminase (MAD) is an enzyme active in skeletal muscle, probab ly during exercise of moderate intensity but: certainly during vigorous exe rcise, when the deamination of AMP leads to increased levels of 1MP and amm onia. There is controversy about the clinical significance of MAD deficienc y. The main objective of the present study was to investigate the extent to which genetically confirmed MAD deficiency affects muscle function under c onditions of maximal short-term electrically induced activation. The left h and was immobilized and adductor pollicis muscle function was investigated. To exclude the influence of central factors, such as the patient's motivat ion, 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.) o f the values for unfatigued muscle in the control and MAD-deficient subject s respectively (P > 0.05; n = 7). Maximal isometric forces and shortening v elocities did not differ between groups in unfatigued, fatigued or recovere d muscle. None of the subjects experienced exercise-related muscle aches or cramps. In conclusion, MAD deficiency does not appear to affect adductor p ollicis muscle force, shortening velocity and relaxation, either during or after maximal short-term activation.