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  • Title: Purine nucleotides and AMP deamination during maximal and endurance swimming exercise in heart and skeletal muscle of rats.
    Author: Weicker H, Hageloch W, Luo J, Müller D, Werle E, Sehling KM.
    Journal: Int J Sports Med; 1990 May; 11 Suppl 2():S68-77. PubMed ID: 2361782.
    Abstract:
    The purine nucleotides, phosphocreatine (PCr), ammonia, and lactic acid were investigated in skeletal muscles of rats with prominent type I, type IIa, type IIb fibers, and the heart after exhaustive and endurance swimming tests. ATP, ADP, AMP, IMP, and PCr were determined by HPLC with UV detection in controls after maximal and endurance training for 6 weeks with or without a respective final test and also after final exhaustive or endurance test without preceding training. The swimming time in these tests was longer with than without training. A pronounced ATP decrease and a large increase in IMP, up to 4.9 mumol/g wet weight, were found in type IIb fibers after the maximal final test without preceding training. Compared with skeletal muscle, the IMP concentration in the heart was significantly lower after all exercise bouts, even though after maximal exercise AMP augmentation was highest, ATP reduction was greatest, and energy charge was lowest. The difference between the heart and skeletal muscle in the production of IMP indicates that despite AMP and ADP accumulation, myoadenylate deaminase (MAD) activity in the heart is considerably lower than in skeletal muscle, especially in type IIb fibers. The smaller amount of MAD per tissue, and also the different MAD isozyme pattern of the heart as reported in the literature, may be attributed to lower activation. The difference between MAD activation of the soleus muscle and of the iliacus muscle, both consisting predominantly of type I fibers, suggests that MAD activity may be influenced by biochemical demand and oxygen supply, varying with the anatomical localization. Even though ammonia and lactic acid were highly correlated, it is questionable whether the H+ ion increase due to the lactate accumulation itself triggers MAD activation, as has been found for AMP and ADP in skeletal muscle.
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