• E M Balog, N R Enzmann, and E M Gallant.
• Department of Veterinary PathoBiology, University of Minnesota, St. Paul, Minnesota 55455, USA. balog004@.tc.umn.edu
• Muscle Nerve. 2000 Feb 1;23(2):223-30.

AbstractAlthough the defects in cellular Ca(2+) homeostasis associated with malignant hyperthermia (MH) have been extensively studied, the functional consequences of the MH mutation are not clear. We used continuous and intermittent high-frequency stimulation to determine whether this mutation might alter the fatigue resistance of muscle from MH susceptible (MHS) pigs. Force decline with 10 s continuous stimulation (150 Hz) was significantly less in MHS muscle (58.4 +/- 1.0%) than in normal muscle (50.5 +/- 3.0%). With intermittent stimulation, there was no significant difference in tension decline between muscle types. Post-stimulation twitch and tetanus responses were similar in MHS and normal muscles except: 1) twitch potentiation was significantly greater in normal muscle after continuous stimulation, and 2) recovery of tetanic tension was slowed in MHS muscle. Although the MH defect does not cause major functional abnormalities, subtle differences in MHS muscle response to fatiguing stimulation are apparent. Therefore, it is unlikely the work capacity of MH patients would be limited by any MH associated defect within the muscle.Copyright 2000 John Wiley & Sons, Inc.

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