Maximal Voluntary Activation of the Elbow Flexors Is under Predicted by Transcranial Magnetic Stimulation Compared to Motor Point Stimulation Prior to and Following Muscle Fatigue.

Transcranial magnetic (TMS) and motor point stimulation have been used to determine voluntary activation (VA). However, very few studies have directly compared the two stimulation techniques for assessing VA of the elbow flexors. The purpose of this study was to compare TMS and motor point stimulation for assessing VA in non-fatigued and fatigued elbow flexors. Participants performed a fatigue protocol that included twelve, 15 s isometric elbow flexor contractions. Participants completed a set of isometric elbow flexion contractions at 100, 75, 50, and 25% of maximum voluntary contraction (MVC) prior to and following fatigue contractions 3, 6, 9, and 12 and 5 and 10 min post-fatigue. Force and EMG of the bicep and triceps brachii were measured for each contraction. Force responses to TMS and motor point stimulation and EMG responses to TMS (motor evoked potentials, MEPs) and Erb's point stimulation (maximal M-waves, Mmax) were also recorded. VA was estimated using the equation: VA% = (1-SITforce/PTforce) × 100. The resting twitch was measured directly for motor point stimulation and estimated for both motor point stimulation and TMS by extrapolation of the linear regression between the superimposed twitch force and voluntary force. MVC force, potentiated twitch force and VA significantly (p < 0.05) decreased throughout the elbow flexor fatigue protocol and partially recovered 10 min post fatigue. VA was significantly (p < 0.05) underestimated when using TMS compared to motor point stimulation in non-fatigued and fatigued elbow flexors. Motor point stimulation compared to TMS superimposed twitch forces were significantly (p < 0.05) higher at 50% MVC but similar at 75 and 100% MVC. The linear relationship between TMS superimposed twitch force and voluntary force significantly (p < 0.05) decreased with fatigue. There was no change in triceps/biceps electromyography, biceps/triceps MEP amplitudes, or bicep MEP amplitudes throughout the fatigue protocol at 100% MVC. In conclusion, motor point stimulation as opposed to TMS led to a higher estimation of VA in non-fatigued and fatigued elbow flexors. The decreased linear relationship between TMS superimposed twitch force and voluntary force led to an underestimation of the estimated resting twitch force and thus, a reduced VA.

Differences in corticospinal excitability to the biceps brachii between arm cycling and tonic contraction are not evident at the immediate onset of movement.

This is the first study to examine changes in corticospinal excitability to the biceps brachii during the onset of arm cycling from a resting position to a point when steady-state arm cycling was obtained. Supraspinal and spinal excitability were assessed using motor-evoked potentials (MEPs) elicited via transcranial magnetic stimulation and cervicomedullary evoked potentials (CMEPs) elicited via transmastoid electrical stimulation, respectively. Evoked responses were recorded from the biceps brachii during elbow flexion (6 o'clock relative to a clock face) for both arm cycling and an intensity-matched tonic contraction at three separate periods: (1) immediately at the onset of motor output and after completion of the (2) 4th revolution and (3) 9th revolution. There was no difference during initiation between tasks for MEP (P = 0.79) or CMEP amplitudes (P = 0.57). However, MEP amplitudes were significantly larger during arm cycling than an intensity-matched tonic contraction after the completion of the 4th (Cycling 76.48 ± 17.35 % of M max, Tonic 63.45 ± 18.45 % of M max, P < 0.05) and 9th revolutions (Cycling 72.37 ± 15.96 % of M max, Tonic 58.1 ± 24.23 % of M max, P < 0.05). There were no differences between conditions in CMEP amplitudes at the 4th (Cycling 49.6 ± 25.4 % of M max, Tonic 41.6 ± 11.2 % of M max, P = 0.31) or the 9th revolution (Cycling 47.2 ± 17.0 % of M max, Tonic 40.8 ± 13.6 % of M max, P = 0.29). These results demonstrate that corticospinal excitability is not different between arm cycling and a tonic contraction at motor output onset, but supraspinal excitability is enhanced during steady-state arm cycling. This suggests a similarity in the way the corticospinal tract initiates motor outputs in humans, regardless of the differences that present themselves in the later, steady-state stages.

Cadence-dependent changes in corticospinal excitability of the biceps brachii during arm cycling.

This is the first study to report the influence of different cadences on the modulation of supraspinal and spinal excitability during arm cycling. Supraspinal and spinal excitability were assessed using transcranial magnetic stimulation of the motor cortex and transmastoid electrical stimulation of the corticospinal tract, respectively. Transcranial magnetic stimulation-induced motor evoked potentials and transmastoid electrical stimulation-induced cervicomedullary evoked potentials (CMEPs) were recorded from the biceps brachii at two separate positions corresponding to elbow flexion and extension (6 and 12 o'clock relative to a clock face, respectively) while arm cycling at 30, 60 and 90 rpm. Motor evoked potential amplitudes increased significantly as cadence increased during both elbow flexion (P < 0.001) and extension (P = 0.027). CMEP amplitudes also increased with cadence during elbow flexion (P < 0.01); however, the opposite occurred during elbow extension (i.e., decreased CMEP amplitude; P = 0.01). The data indicate an overall increase in the excitability of corticospinal neurons which ultimately project to biceps brachii throughout arm cycling as cadence increased. Conversely, changes in spinal excitability as cadence increased were phase dependent (i.e., increased during elbow flexion and decreased during elbow extension). Phase- and cadence-dependent changes in spinal excitability are suggested to be mediated via changes in the balance of excitatory and inhibitory synaptic input to the motor pool, as opposed to changes in the intrinsic properties of spinal motoneurons.

Chronic resistance training enhances the spinal excitability of the biceps brachii in the non-dominant arm at moderate contraction intensities.

The purpose of the study was to assess corticospinal excitability of the biceps brachii in the non-dominant arm of chronic resistance-trained (RT) and non-RT individuals. Seven chronic-RT and six non-RT male participants performed 4 sets of 5s pseudo-randomized contractions of the non-dominant elbow flexors at 25, 50, 75, 90, and 100% of maximum voluntary contraction (MVC). During each contraction, transcranial magnetic stimulation, transmastoid electrical stimulation, and Erb's point electrical stimulation were administered to assess the amplitudes of motor evoked potentials (MEPs), cervicomedullary evoked potentials (CMEPs), and maximal muscle compound potentials (Mmax), respectively, in the biceps brachii. MEP and CMEP amplitudes were normalized to Mmax. Training did not affect (p>0.14) MEP amplitudes across any contraction intensity. CMEP amplitudes were significantly (p<0.05) higher in the chronic-RT group at 50% and 75% of MVC by 38% and 27%, respectively, and there was a trend for higher amplitudes at 25%, 90%, and 100% MVC by 25% (p=0.055), 36% (p=0.077), and 35% (p=0.078), respectively, compared to the non-RT group. Corticospinal excitability of the non-dominant biceps brachii was increased in chronic-RT individuals mainly due to changes in spinal excitability.