Background Motor fatigue is a common complaint in patients with chronic neurological disorders such as post-polio syndrome and multiple sclerosis. Fatigue occurs via central and peripheral mechanisms. Central fatigue is caused by decreased output from the motor cortex to spinal motor neurons. Transcranial magnetic stimulation (TMS) is a non-invasive technique used to study the intracortical networks that may produce fatigue. Motor evoked potential (MEP) amplitude is a measure of the motor cortex output and functional state of the pre-motor inhibitory and facilitatory circuits. During sub-fatiguing exercise, there is facilitation (MEP amplitude increases). Central mechanisms underlying this phenomenon are not known. A possibility is that intracortical networks mediate post-exercise MEP facilitation.
Objectives Our aim was to examine intracortical inhibition (ICI) and facilitation (ICF) during sub-fatiguing exercise, using paired-pulse TMS.
Methods Thirteen healthy adults ages 25-80 were recruited for this experiment. Subjects performed 6 sets of sub-fatiguing isometric exercise of the abductor digiti minimi muscle for 30 seconds at 50% maximal voluntary contraction. Muscle force was measured via a force transducer with continuous visual feedback. After each exercise set, the contralateral motor cortex was stimulated with 5 pulses of paired-pulse TMS at a rate of 0.2 Hz. MEPs were recorded by surface electromyography. TMS conditioning and test stimulus intensities were 75% and 120% of the resting motor thresholds respectively. Interstimulus intervals of 3 and 10 ms were used to measure ICI and ICF ratios.
Results The mean resting unconditioned MEP amplitude was 0.73 ± 0.69 mV. Resting ICI and ICF ratios were 0.4 ± 0.25 and 2.3 ± 1.4 respectively. After exercise, MEPs increased to 2.30 ± 1.08 mV (p < .0001). ICF ratios significantly decreased by 48% to 1.1 ± 0.4 (p = .003). ICI ratios were unchanged (0.4 ± 0.3 to 0.28 ± 0.1).
Conclusions While MEP amplitudes tripled during sub-fatiguing exercise, the ICF ratio decreased. This suggests that facilitation maximizes intracortical facilitatory networks such that there is a decreased reserve for further facilitation. ICI ratios were unchanged during exercise, suggesting that reduced activity in inhibitory networks is not affected in the same manner. Our findings suggest that healthy adults may draw upon a reserve of facilitatory intracortical networks during exercise to increase the output of the motor cortex. We hypothesize that patients with central fatigue may have a reduced ability to recruit this reserve. Investigation of other intracortical mechanisms such as long interval ICI and short interval ICF may supplement these findings.
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