Output of Human Motoneuron Pools to Corticospinal Inputs During Voluntary Contractions

2006 ◽  
Vol 95 (6) ◽  
pp. 3512-3518 ◽  
Author(s):  
P. G. Martin ◽  
S. C. Gandevia ◽  
J. L. Taylor

This study investigated transmission of corticospinal output through motoneurons over a wide range of voluntary contraction strengths in humans. During voluntary contraction of biceps brachii, motor evoked potentials (MEPs) to transcranial magnetic stimulation of the motor cortex grow up to about 50% maximal force and then decrease. To determine whether the decrease reflects events at a cortical or spinal level, responses to stimulation of the cortex and corticospinal tract (cervicomedullary motor evoked potentials, CMEPs) as well as maximal M-waves (Mmax) were recorded during strong contractions at 50 to 100% maximum. In biceps and brachioradialis, MEPs and CMEPs (normalized to Mmax) evoked by strong stimuli decreased during strong elbow flexions. Responses were largest during contractions at 75% maximum and both potentials decreased by about 25% Mmax during maximal efforts ( P < 0.001). Reductions were smaller with weaker stimuli, but again similar for MEPs and CMEPs. Thus the reduction in MEPs during strong voluntary contractions can be accounted for by reduced responsiveness of the motoneuron pool to stimulation. During strong contractions of the first dorsal interosseous, a muscle that increases voluntary force largely by frequency modulation, MEPs declined more than in either elbow flexor muscle (35% Mmax, P < 0.001). This suggests that motoneuron firing rates are important determinants of evoked output from the motoneuron pool. However, motor cortical output does not appear to be limited at high contraction strengths.

2017 ◽  
Vol 118 (6) ◽  
pp. 3242-3251 ◽  
Author(s):  
Brandon Wayne Collins ◽  
Edward W. J. Cadigan ◽  
Lucas Stefanelli ◽  
Duane C. Button

The purpose of this study was to examine the effect of shoulder position on corticospinal excitability (CSE) of the biceps brachii during rest and a 10% maximal voluntary contraction (MVC). Participants ( n = 9) completed two experimental sessions with four conditions: 1) rest, 0° shoulder flexion; 2) 10% MVC, 0° shoulder flexion; 3) rest, 90° shoulder flexion; and 4) 10% MVC, 90° shoulder flexion. Transcranial magnetic, transmastoid electrical, and Erb’s point stimulation were used to induce motor-evoked potentials (MEPs), cervicomedullary MEPs (CMEPs), and maximal muscle compound potentials (Mmax), respectively, in the biceps brachii in each condition. At rest, MEP, CMEP, and Mmax amplitudes increased ( P < 0.01) by 509.7 ± 118.3%, 113.3 ± 28.3%, and 155.1 ± 47.9%, respectively, at 90° compared with 0°. At 10% MVC, MEP amplitudes did not differ ( P = 0.08), but CMEP and Mmax amplitudes increased ( P < 0.05) by 32.3 ± 10.5% and 127.9 ± 26.1%, respectively, at 90° compared with 0°. MEP/Mmax increased ( P < 0.01) by 224.0 ± 99.1% at rest and decreased ( P < 0.05) by 51.3 ± 6.7% at 10% MVC at 90° compared with 0°. CMEP/Mmax was not different ( P = 0.22) at rest but decreased ( P < 0.01) at 10% MVC by 33.6 ± 6.1% at 90° compared with 0°. EMG increased ( P < 0.001) by 8.3 ± 2.0% at rest and decreased ( P < 0.001) by 21.4 ± 4.4% at 10% MVC at 90° compared with 0°. In conclusion, CSE of the biceps brachii was dependent on shoulder position, and the pattern of change was altered within the state in which it was measured. The position-dependent changes in Mmax amplitude, EMG, and CSE itself all contribute to the overall change in CSE of the biceps brachii. NEW & NOTEWORTHY We demonstrate that when the shoulder is placed into two common positions for determining elbow flexor force and activation, corticospinal excitability (CSE) of the biceps brachii is both shoulder position and state dependent. At rest, when the shoulder is flexed from 0° to 90°, supraspinal factors predominantly alter CSE, whereas during a slight contraction, spinal factors predominantly alter CSE. Finally, the normalization techniques frequently used by researchers to investigate CSE may under- and overestimate CSE when shoulder position is changed.


2022 ◽  
Author(s):  
Nelly Seusing ◽  
Sebastian Strauss ◽  
Robert Fleischmann ◽  
Christina Nafz ◽  
Sergiu Groppa ◽  
...  

Abstract ObjectiveThe role of ipsilateral descending motor pathways in voluntary movement of humans is still a matter of debate. Few studies have examined the task dependent modulation of ipsilateral motor evoked potentials (iMEPs). Here, we determined the location of upper limb biceps brachii (BB) representation within the ipsilateral primary motor cortex. MethodsMR-navigated transcranial magnetic stimulation mapping of the dominant hemisphere was undertaken with twenty healthy participants who made tonic unilateral, bilateral homologous or bilateral antagonistic elbow flexion-extension voluntary contractions. Map center of gravity (CoG) and area for each BB were obtained. ResultsThe map CoG of the ipsilateral BB was located more anterior-laterally than those of the contralateral BB within the primary motor cortex. However different tasks had no effect on either the iMEP CoG location or the size. ConclusionOur data suggests that ipsilateral and contralateral MEP might originate in distinct adjacent neural populations in the primary motor cortex, independent of task dependence.


2016 ◽  
Vol 115 (4) ◽  
pp. 2076-2082 ◽  
Author(s):  
James L. Nuzzo ◽  
Gabriel S. Trajano ◽  
Benjamin K. Barry ◽  
Simon C. Gandevia ◽  
Janet L. Taylor

Biceps brachii motor evoked potentials (MEPs) from cortical stimulation are influenced by arm posture. We used subcortical stimulation of corticospinal axons to determine whether this postural effect is spinal in origin. While seated at rest, 12 subjects assumed several static arm postures, which varied in upper-arm (shoulder flexed, shoulder abducted, arm hanging to side) and forearm orientation (pronated, neutral, supinated). Transcranial magnetic stimulation over the contralateral motor cortex elicited MEPs in resting biceps and triceps brachii, and electrical stimulation of corticospinal tract axons at the cervicomedullary junction elicited cervicomedullary motor evoked potentials (CMEPs). MEPs and CMEPs were normalized to the maximal compound muscle action potential (Mmax). Responses in biceps were influenced by upper-arm and forearm orientation. For upper-arm orientation, biceps CMEPs were 68% smaller ( P = 0.001), and biceps MEPs 31% smaller ( P = 0.012), with the arm hanging to the side compared with when the shoulder was flexed. For forearm orientation, both biceps CMEPs and MEPs were 34% smaller (both P < 0.046) in pronation compared with supination. Responses in triceps were influenced by upper-arm, but not forearm, orientation. Triceps CMEPs were 46% smaller ( P = 0.007) with the arm hanging to the side compared with when the shoulder was flexed. Triceps MEPs and biceps and triceps MEP/CMEP ratios were unaffected by arm posture. The novel finding is that arm posture-dependent changes in corticospinal excitability in humans are largely spinal in origin. An interplay of multiple reflex inputs to motoneurons likely explains the results.


2008 ◽  
Vol 105 (5) ◽  
pp. 1527-1532 ◽  
Author(s):  
T. Oya ◽  
B. W. Hoffman ◽  
A. G. Cresswell

This study investigated corticospinal-evoked responses in lower limb muscles during voluntary contractions at varying strengths. Similar investigations have been made on upper limb muscles, where evoked responses have been shown to increase up to ∼50% of maximal force and then decline. We elicited motor-evoked potentials (MEPs) and cervicomedullary motor-evoked potentials (CMEPs) in the soleus (Sol) and medial gastrocnemius (MG) muscles using magnetic stimulation over the motor cortex and cervicomedullary junction during voluntary plantar flexions with the torque ranging from 0 to 100% of a maximal voluntary contraction. Differences between the MEP and CMEP were also investigated to assess whether any changes were occurring at the cortical or spinal levels. In both Sol and MG, MEP and CMEP amplitudes [normalized to maximal M wave (Mmax)] showed an increase, followed by a plateau, over the greater part of the contraction range with responses increasing from ∼0.2 to ∼6% of Mmax for Sol and from ∼0.3 to ∼10% of Mmax for MG. Because both MEPs and CMEPs changed in a similar manner, the observed increase and lack of decrease at high force levels are likely related to underlying changes occurring at the spinal level. The evoked responses in the Sol and MG increase over a greater range of contraction strengths than for upper limb muscles, probably due to differences in the pattern of motor unit recruitment and rate coding for these muscles and the strength of the corticospinal input.


2008 ◽  
Vol 99 (2) ◽  
pp. 554-563 ◽  
Author(s):  
Morgan Lévénez ◽  
S. Jayne Garland ◽  
Malgorzata Klass ◽  
Jacques Duchateau

This study investigates the control mechanisms at the cortical and spinal levels of antagonist coactivation during a submaximal fatiguing contraction of the elbow flexors at 50% of maximal voluntary contraction (MVC). We recorded motor-evoked potentials in the biceps brachii and triceps brachii muscles in response to magnetic stimulation of the motor cortex (MEP) and corticospinal tract (cervicomedullary motor-evoked potentials—CMEPs), as well as the Hoffmann reflex (H-reflex) and maximal M-wave (Mmax) elicited by electrical stimulation of the brachial plexus, before, during, and after the fatigue task. The results showed that although the coactivation ratio did not change at task failure, the MVC torque produced by the elbow flexors declined by 48% ( P < 0.01) with no change in MVC torque for the elbow extensors. While the MEP and CMEP areas (normalized to Mmax) of the biceps brachii increased (∼50%) over the first 40% of the time to task failure and then plateaued, both responses in the triceps brachii increased (∼150–180%) gradually throughout the fatigue task. In contrast to the monotonic increase in the MEP and CMEP of the antagonist muscles, the H-reflex of the triceps brachii exhibited a biphasic modulation, increasing during the first part of the contraction before declining subsequently to 65% of its initial value. Collectively, these results suggest that the level of coactivation during a fatiguing contraction is mediated by supraspinal rather than spinal mechanisms and involves differential control of agonist and antagonist muscles.


2013 ◽  
Vol 38 (11) ◽  
pp. 1154-1161 ◽  
Author(s):  
Kevin E. Power ◽  
David B. Copithorne

Human studies have not assessed supraspinal or spinal motoneurone excitability in the quiescent state prior to a rhythmic and alternating cyclical motor output. The purpose of the current study was to determine whether supraspinal and (or) spinal motoneurone excitability was modulated in humans prior to arm cycling when compared with rest with no intention to move. We hypothesized that corticospinal excitability would be enhanced prior to arm cycling due, in part, to increased spinal motoneurone excitability. Supraspinal and spinal motoneurone excitability were assessed via transcranial magnetic stimulation (TMS) of the motor cortex and transmastoid stimulation of the corticospinal tract, respectively. Surface electromyography recordings of TMS motor evoked potentials (MEPs) and cervicomedullary MEPs (CMEPs) were made from the relaxed biceps brachii muscle prior to rhythmic arm cycling and at rest with no intention to move. The amplitude of the MEPs was greater (mean increase: +9.8% of maximal M wave; p = 0.006) and their onset latencies were shorter (mean decrease: –1.5 ms; p < 0.05) prior to cycling when compared with rest. The amplitudes of the CMEPs at any of 3 stimulation intensities were not different between conditions. We conclude that premovement enhancement of corticospinal excitability is greater prior to arm cycling than at rest because of increases in supraspinal but not spinal motoneurone excitability.


2018 ◽  
Vol 119 (2) ◽  
pp. 652-661 ◽  
Author(s):  
Siobhan C. Dongés ◽  
Jessica M. D’Amico ◽  
Jane E. Butler ◽  
Janet L. Taylor

Plasticity can be induced at human corticospinal-motoneuronal synapses by delivery of repeated, paired stimuli to corticospinal axons and motoneurons in a technique called paired corticospinal-motoneuronal stimulation (PCMS). To date, the mechanisms of the induced plasticity are unknown. To determine whether PCMS-induced plasticity is dependent on N-methyl-d-aspartate receptors (NMDARs), the effect of the noncompetitive NMDAR antagonist dextromethorphan on PCMS-induced facilitation was assessed in a 2-day, double-blind, placebo-controlled experiment. PCMS consisted of 100 pairs of stimuli, delivered at an interstimulus interval that produces facilitation at corticospinal-motoneuronal synapses that excite biceps brachii motoneurons. Transcranial magnetic stimulation elicited corticospinal volleys, which were timed to arrive at corticospinal-motoneuronal synapses just before antidromic potentials elicited in motoneurons with electrical brachial plexus stimulation. To measure changes in the corticospinal pathway at a spinal level, biceps responses to cervicomedullary stimulation (cervicomedullary motor evoked potentials, CMEPs) were measured before and for 30 min after PCMS. Individuals who displayed a ≥10% increase in CMEP size after PCMS on screening were eligible to take part in the 2-day experiment. After PCMS, there was a significant difference in CMEP area between placebo and dextromethorphan days ( P = 0.014). On the placebo day PCMS increased average CMEP areas to 127 ± 46% of baseline, whereas on the dextromethorphan day CMEP area was decreased to 86 ± 33% of baseline (mean ± SD; placebo: n = 11, dextromethorphan: n = 10). Therefore, dextromethorphan suppressed the facilitation of CMEPs after PCMS. This indicates that plasticity induced at synapses in the human spinal cord by PCMS may be dependent on NMDARs. NEW & NOTEWORTHY Paired corticospinal-motoneuronal stimulation can strengthen the synaptic connections between corticospinal axons and motoneurons at a spinal level in humans. The mechanism of the induced plasticity is unknown. In our 2-day, double-blind, placebo-controlled study we show that the N-methyl-d-aspartate receptor (NMDAR) antagonist dextromethorphan suppressed plasticity induced by paired corticospinal-motoneuronal stimulation, suggesting that an NMDAR-dependent mechanism is involved.


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