Abstract
The purpose of this study was to investigate cortical mechanisms upstream to the corticospinal motor neuron that may be associated with central fatigue and sense of effort during and after a fatigue task. We used two different isometric finger abduction protocols to examine the effects of muscle activation and fatigue the right first dorsal interosseous (FDI) of 12 participants. One protocol was intended to assess the effects of muscle activation with minimal fatigue (control) and the other was intended to elicit central fatigue (fatigue). We hypothesized that high frequency repetitive transcranial magnetic stimulation (rTMS) of the supplementary motor area (SMA) would hasten recovery from central fatigue and offset a fatigue-induced increase in sense of effort by facilitating the primary motor cortex (M1). Constant force-sensation contractions were used to assess sense of effort associated with muscle contraction. Paired-pulse TMS was used to assess intracortical inhibition (ICI) and facilitation (ICF) in the active M1 and interhemispheric inhibitory (IHI) was assessed to determine if compensation occurs via the resting M1. These measures were made during and after the muscle contraction protocols. Corticospinal excitability progressively declined with fatigue in the active hemisphere. ICF increased at task failure and ICI was also reduced at task failure with no changes in IHI found. Although fatigue is associated with progressive reductions in corticospinal excitability, compensatory changes in inhibition and facilitation may act within, but not between hemispheres of the M1. rTMS of the SMA following fatigue enhanced recovery of maximal voluntary force and higher levels of ICF were associated with lower sense of effort following stimulation. rTMS of the SMA may have reduced the amount of upstream drive required to maintain motor output, thus contributing to a lower sense of effort and increased rate of recovery of maximal force.
Highlights
Central fatigue is a progressive reduction in the ability of the central nervous system to maximally activate muscle
A fourth measure of corticospinal excitability at baseline was the stimulator output required to elicit motor evoked potential (MEP) that were 1mV in peak-to-peak amplitude (Table 2)
Unconditioned MEPs were elicited in the right first dorsal interosseous (FDI) (TS1mV) by applying single monophasic pulse from the Bistim2 stimulator to the left motor cortex
Summary
Central fatigue is a progressive reduction in the ability of the central nervous system to maximally activate muscle. Supraspinal fatigue is characterized by reduced output from the motor cortex to the spinal motor neuron pool and has been suggested to contribute to reduced activation of muscle (for review see [1,2]). Studies employing ischemia (for review see [4]) and caffeine [3,8] suggest that fatigue-associated changes in cortical and spinal motor neuron excitability can be dissociated from measures of supraspinal fatigue and appear to accompany, but not cause voluntary activation failure. To address the contribution of cortical components upstream to the corticospinal motor neuron pool, the present study compared changes in intracortical inhibition and facilitation and interhemispheric inhibition following a series of contractions of the first dorsal interosseous (FDI) that elicited voluntary activation failure (central fatigue) to changes elicited by a less rigorous series of contractions that elicited peripheral but not central fatigue. SMA activity is reduced following a fatiguing task [18,19] and maytherefore may be a source of reduced excitatory drive to the corticospinal motor neuron pool
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