Abstract:
:In normal skeletal muscle, prolonged stimulation results in some cellular adenosine triphosphate (ATP) being converted to adenosine monophosphate (AMP) and then deaminated to inosine monophosphate (IMP). Here, we investigate whether the build-up of IMP contributes to muscle fatigue and also determine what happens if AMP is instead hydrolyzed to adenosine. Rat skeletal muscle fibers were mechanically skinned, allowing rapid manipulation of the cytoplasmic conditions, while still retaining the normal excitation-contraction coupling mechanism. Inosine monophosphate (3 mM) had no noticeable effect on either depolarization-induced or caffeine-induced Ca(2+) release from the sarcoplasmic reticulum. In contrast, 3 mM adenosine substantially inhibited depolarization-induced force responses and completely abolished caffeine activation of Ca(2+) release in a reversible fashion, with noticeable inhibition occurring even at 0.4 mM adenosine. These results indicate that IMP does not appreciably inhibit excitation-contraction coupling in normal muscle, and further suggest that the build up of adenosine may be at least partly responsible for the early onset of fatigue occurring in subjects with myoadenylate deaminase deficiency.
journal_name
Muscle Nervejournal_title
Muscle & nerveauthors
Blazev R,Lamb GDdoi
10.1002/(sici)1097-4598(199912)22:12<1674::aid-mussubject
Has Abstractpub_date
1999-12-01 00:00:00pages
1674-83issue
12eissn
0148-639Xissn
1097-4598pii
10.1002/(SICI)1097-4598(199912)22:12<1674::AID-MUSjournal_volume
22pub_type
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