<p>The purpose of this research was to determine the physiological mechanism(s) underlying the reduction in voluntary electromyographic (EMG) activity with maximal contractions during fatigue. The specific hypothesis was that this reduction in EMG activity results from reflex inhibition of homonymous motoneurons by afferents from the fatigued muscles. The experiments were conducted on the human ankle dorsiflexor and plantarflexor muscles, with the use of eschemia to accelerate the fatigue process. In the first part of the study it was shown that, within 3-4 minutes, repetitive indirect stimulation of the dorsiflexor muscles via the peroneal nerve, at either 15 Hz or 30 Hz, could abolish dorsiflexion torque elicited by single shocks and trains of stimuli. During the 15 Hz fatiguing frequency the relative loss of dorsiflexion torque was greater than the decline in the amplitude of the evoked muscle compound action potentials (M-waves). Tus 15 Hz was the rate of fatiguing stimulation used in the remainder of the study. In the second part of the study, fatiguing indirect stimulation at 15 Hz caused significant reduction in both the dorsiflexion torque and EMG activity associated with subsequent maximal voluntary contractions (MVCs) of 66.1 ± 16.4% and 50.3 ± 27% respectively. The relative preservation of M-wave amplitudes in the fatigued muscle (reduction of 13.1 ± 22.9%) indicated that most of the loss of EMG activity was not due to inexcitability of the neuromuscular junctions or muscle fibre membranes. Nor could the reduction in voluntary EMG activity have been due primarily to failure of subjects to exert maximal voluntary effort since supraspinal motor pathways had not been involved in the fatigue process. Furthermore, during the MVC, no additional force was evident with a supramaximal interpolated stimulus. Hence, reflex inhibition appeared to be the most likely mechanism. The third part of the study explored the possibility that the reduction in voluntary EMG activity during fatigue was due to a lower level of alpha motoneuron excitability; for these experiments recordings were made of the electrically-induced homonymous response (H-reflex) of the soleus muscle. It was shown that the H-reflex excitability was depressed by 44.4 ± 25.1% during fatigue of the right soleus muscle using 15 Hz stimulation under ischemic conditions; the H-reflex excitability in the nonfatigued left soleus did not change significantly. The maximum M-wave amplitudes demonstrated a mean decline of only 8.8 ± 11.9% indicating good peripheral excitability of the muscle fibre membranes. Control experiments performed under ischemic conditions alone (without induced fatigue) or with electrical stimulation alone (without ischemia and hence without fatigue) failed to demonstrate any significant changes in reflex excitability. Thus, in the absence of fatigue, the depression could not be accounted for on the basis of either ischemia or electrical stimulation; instead the findings were consistent with the presence of an inhibitory reflex from the fatigued muscle onto the homonymous alpha motoneurons. In the final part of the study it was demonstrated, by means of pressure-induced impulse blockade of large myelinated afferents in the sciatic nerve prior to fatigue, that the mean plantarflexor torque produced during MVCs decreased by 38.0 ± 18.6% from the postblock value compared to a decrease of 5.2 ± 7.0% in the ischemia control; the mean EMG activity decreased from postblock values by 43.4 ± 15.6% following fatigue and by only 6.6 ± 5.5% following ischemia alone. These results were very similar to those demonstrated without any blockade of large diameter afferents. This suggested that the afferents involved in the putative reflex inhibition of the alpha motoneuron pool with fatigue were likely to have been those with small diameters (Group III and IV). This research provided evidence suggestive that the reduction in voluntary EMG during fatigue, in both tibialis anterior and soleus muscles, resulted from reflex inhibition of the motoneuron pool.</p> / Doctor of Philosophy (PhD)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/6516 |
| Date | 05 1900 |
| Creators | Garland, Jayne S. |
| Contributors | McComas, Alan, Medical Sciences |
| Source Sets | McMaster University |
| Detected Language | English |
| Type | thesis |
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