<p>The studies composing this thesis were designed to address the question of changes in muscle excitability during fatigue and recovery: the indirectly-evoked muscle compound action potential (M-wave) was used as an index of excitability. Earlier studies from this laboratory indicated that the rate of fatigue in human skeletal muscle depends on the frequency of excitation. The present studies have extended these findings by using a wide range of stimulating frequencies (0-30 Hz) and by comparing the change in muscle excitability in fast-versus slow-twitch muscles; the effect of ischaemia was also studied as was recovery from fatigue. Ten subjects (out of a total of fifteen) each successfully completed five experiments, spaced at least one week apart, in which intermittent tetanic trains at different frequencies were used to fatigue the ishaemic ankle dorsiflexors. The effects of ischemia were studied by repeating one experiment under non-ischaemic conditions. Five out of the ten subjects also volunteered for the experiments comparing changes in muscle excitability in soleus, versus those in tibialis anterior, in response to intermittent fatiguing stimulation.</p> <p>It was found that maintenance of excitability was possible for one minute regardless of stiumulus frequency; thereafter stimulation at the highest frequencies induced the greatest change in the amplitude of the (M-wave). The amplitude decline was also dependent on the position of the M-wave within the train of potentials: thus, at 30 Hz stimulation, the first, fourth and seventh responses within the trained decreased by 50%, 80% and 95% respectively (p<.01). The decline in M-wave amplitude was always greater than the decline in the area of the compound action potential, indicating an increase in duration due to dispersion of single fiber action potentials. At 30 Hz stimulation the areas of the first, fourth and seventh responses decreased by 33%, 56% and 82% respectively.</p> <p>On the basis of animal studies, it was hypothesized that muscle excitability would be preferentially retained in the soleus muscle; however, no significant differences emerged in M-wave changes between soleus and tibialis anterior although the onset of decline was delayed in soleus. It is proposed that this delay was due to the early potentiating mechanisms observed in soleus but not in tibialis anterior. The presence of ischaemia significantly (p<.01) accelerated the decline in both amplitude and area of the tibialis anterior M-wave. Recovery of the M-wave was limited when the tetanic stimulation ceased but progressed rapidly after the circulation was restored. M-wave failure occurred at firing rates not normally associated with neuromuscular blockade, implying propagation failure along the sarcolemmal membrane.</p> / Doctor of Philosophy (PhD)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/6733 |
| Date | 06 1900 |
| Creators | Galea, Victoria |
| Contributors | McComas, Alan J., Medical Sciences |
| Source Sets | McMaster University |
| Detected Language | English |
| Type | thesis |
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