scholarly journals Corticospinal contributions to lower limb muscle activity during cycling in humans

2012 ◽  
Vol 107 (1) ◽  
pp. 306-314 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Ben W. Hoffman ◽  
Andrew G. Cresswell ◽  
Timothy J. Carroll

The purpose of the current study was to investigate corticospinal contributions to locomotor drive to leg muscles involved in cycling. We studied 1) if activation of inhibitory interneurons in the cortex via subthreshold transcranial magnetic stimulation (TMS) caused a suppression of EMG and 2) how the responses to stimulation of the motor cortex via TMS and cervicomedullary stimulation (CMS) were modulated across the locomotor cycle. TMS at intensities subthreshold for activation of the corticospinal tract elicited suppression of EMG for approximately one-half of the subjects and muscles during cycling, and in matched static contractions in vastus lateralis. There was also significant modulation in the size of motor-evoked potentials (MEPs) elicited by TMS across the locomotor cycle ( P < 0.001) that was strongly related to variation in background EMG in all muscles ( r > 0.86; P < 0.05). When MEP and CMEP amplitudes were normalized to background EMG, they were relatively larger prior to the main EMG burst and smaller when background EMG was maximum. Since the pattern of modulation of normalized MEP and CMEP responses was similar, the data suggest that phase-dependent modulation of corticospinal responses during cycling in humans is driven mainly by spinal mechanisms. However, there were subtle differences in the degree to which normalized MEP and CMEP responses were facilitated prior to EMG burst, which might reflect small increases in cortical excitability prior to maximum muscle activation. The data demonstrate that the motor cortex contributes actively to locomotor drive, and that spinal factors dominate phase-dependent modulation of corticospinal excitability during cycling in humans.

2012 ◽  
Vol 113 (3) ◽  
pp. 401-409 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Andrew G. Cresswell ◽  
Timothy J. Carroll

The excitability of the motor cortex increases as fatigue develops during sustained single-joint contractions, but there are no previous reports on how corticospinal excitability is affected by sustained locomotor exercise. Here we addressed this issue by measuring spinal and cortical excitability changes during sustained cycling exercise. Vastus lateralis (VL) and rectus femoris (RF) muscle responses to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs) and electrical stimulation of the descending tracts (cervicomedullary evoked potentials, CMEPs) were recorded every 3 min from nine subjects during 30 min of cycling at 75% of maximum workload (Wmax), and every minute during subsequent exercise at 105% of Wmax until subjective task failure. Responses were also measured during nonfatiguing control bouts at 80% and 110% of Wmax prior to sustained exercise. There were no significant changes in MEPs or CMEPs ( P > 0.05) during the sustained cycling exercise. These results suggest that, in contrast to sustained single-joint contractions, sustained cycling exercise does not increase the excitability of motor cortical neurons. The contrasting corticospinal responses to the two modes of exercise may be due to differences in their associated systemic physiological consequences.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Martje G. Pauly ◽  
Annika Steinmeier ◽  
Christina Bolte ◽  
Feline Hamami ◽  
Elinor Tzvi ◽  
...  

AbstractNon-invasive brain stimulation techniques including repetitive transcranial magnetic stimulation (rTMS), continuous theta-burst stimulation (cTBS), paired associative stimulation (PAS), and transcranial direct current stimulation (tDCS) have been applied over the cerebellum to induce plasticity and gain insights into the interaction of the cerebellum with neo-cortical structures including the motor cortex. We compared the effects of 1 Hz rTMS, cTBS, PAS and tDCS given over the cerebellum on motor cortical excitability and interactions between the cerebellum and dorsal premotor cortex / primary motor cortex in two within subject designs in healthy controls. In experiment 1, rTMS, cTBS, PAS, and tDCS were applied over the cerebellum in 20 healthy subjects. In experiment 2, rTMS and PAS were compared to sham conditions in another group of 20 healthy subjects. In experiment 1, PAS reduced cortical excitability determined by motor evoked potentials (MEP) amplitudes, whereas rTMS increased motor thresholds and facilitated dorsal premotor-motor and cerebellum-motor cortex interactions. TDCS and cTBS had no significant effects. In experiment 2, MEP amplitudes increased after rTMS and motor thresholds following PAS. Analysis of all participants who received rTMS and PAS showed that MEP amplitudes were reduced after PAS and increased following rTMS. rTMS also caused facilitation of dorsal premotor-motor cortex and cerebellum-motor cortex interactions. In summary, cerebellar 1 Hz rTMS and PAS can effectively induce plasticity in cerebello-(premotor)-motor pathways provided larger samples are studied.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ivan Pozdniakov ◽  
Alicia Nunez Vorobiova ◽  
Giulia Galli ◽  
Simone Rossi ◽  
Matteo Feurra

AbstractTranscranial alternating current stimulation (tACS) is a non-invasive brain stimulation technique that allows interaction with endogenous cortical oscillatory rhythms by means of external sinusoidal potentials. The physiological mechanisms underlying tACS effects are still under debate. Whereas online (e.g., ongoing) tACS over the motor cortex induces robust state-, phase- and frequency-dependent effects on cortical excitability, the offline effects (i.e. after-effects) of tACS are less clear. Here, we explored online and offline effects of tACS in two single-blind, sham-controlled experiments. In both experiments we used neuronavigated transcranial magnetic stimulation (TMS) of the primary motor cortex (M1) as a probe to index changes of cortical excitability and delivered M1 tACS at 10 Hz (alpha), 20 Hz (beta) and sham (30 s of low-frequency transcranial random noise stimulation; tRNS). Corticospinal excitability was measured by single pulse TMS-induced motor evoked potentials (MEPs). tACS was delivered online in Experiment 1 and offline in Experiment 2. In Experiment 1, the increase of MEPs size was maximal with the 20 Hz stimulation, however in Experiment 2 neither the 10 Hz nor the 20 Hz stimulation induced tACS offline effects. These findings support the idea that tACS affects cortical excitability only during online application, at least when delivered on the scalp overlying M1, thereby contributing to the development of effective protocols that can be applied to clinical populations.


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.


2006 ◽  
Vol 100 (6) ◽  
pp. 1757-1764 ◽  
Author(s):  
J. M. Kalmar ◽  
E. Cafarelli

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude ( P = 0.055) and cortically evoked twitch ( P < 0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure ( r = 0.74, P < 0.05). Caffeine potentiated the MEP early in the fatigue protocol ( P < 0.05) and offset the 40% decline in placebo MEP ( P < 0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.


2019 ◽  
Vol 122 (4) ◽  
pp. 1397-1405 ◽  
Author(s):  
Hiroki Ohashi ◽  
Paul L. Gribble ◽  
David J. Ostry

Motor learning is associated with plasticity in both motor and somatosensory cortex. It is known from animal studies that tetanic stimulation to each of these areas individually induces long-term potentiation in its counterpart. In this context it is possible that changes in motor cortex contribute to somatosensory change and that changes in somatosensory cortex are involved in changes in motor areas of the brain. It is also possible that learning-related plasticity occurs in these areas independently. To better understand the relative contribution to human motor learning of motor cortical and somatosensory plasticity, we assessed the time course of changes in primary somatosensory and motor cortex excitability during motor skill learning. Learning was assessed using a force production task in which a target force profile varied from one trial to the next. The excitability of primary somatosensory cortex was measured using somatosensory evoked potentials in response to median nerve stimulation. The excitability of primary motor cortex was measured using motor evoked potentials elicited by single-pulse transcranial magnetic stimulation. These two measures were interleaved with blocks of motor learning trials. We found that the earliest changes in cortical excitability during learning occurred in somatosensory cortical responses, and these changes preceded changes in motor cortical excitability. Changes in somatosensory evoked potentials were correlated with behavioral measures of learning. Changes in motor evoked potentials were not. These findings indicate that plasticity in somatosensory cortex occurs as a part of the earliest stages of motor learning, before changes in motor cortex are observed. NEW & NOTEWORTHY We tracked somatosensory and motor cortical excitability during motor skill acquisition. Changes in both motor cortical and somatosensory excitability were observed during learning; however, the earliest changes were in somatosensory cortex, not motor cortex. Moreover, the earliest changes in somatosensory cortical excitability predict the extent of subsequent learning; those in motor cortex do not. This is consistent with the idea that plasticity in somatosensory cortex coincides with the earliest stages of human motor learning.


2011 ◽  
Vol 105 (6) ◽  
pp. 2937-2942 ◽  
Author(s):  
Alana B. McCambridge ◽  
Lynley V. Bradnam ◽  
Cathy M. Stinear ◽  
Winston D. Byblow

Proximal upper limb muscles are represented bilaterally in primary motor cortex. Goal-directed upper limb movement requires precise control of proximal and distal agonist and antagonist muscles. Failure to suppress antagonist muscles can lead to abnormal movement patterns, such as those commonly experienced in the proximal upper limb after stroke. We examined whether noninvasive brain stimulation of primary motor cortex could be used to improve selective control of the ipsilateral proximal upper limb. Thirteen healthy participants performed isometric left elbow flexion by contracting biceps brachii (BB; agonist) and left forearm pronation (BB antagonist) before and after 20 min of cathodal transcranial direct current stimulation (c-tDCS) or sham tDCS of left M1. During the tasks, motor evoked potentials (MEPs) in left BB were acquired using single-pulse transcranial magnetic stimulation of right M1 150–270 ms before muscle contraction. As expected, left BB MEPs were facilitated before flexion and suppressed before pronation. After c-tDCS, left BB MEP amplitudes were reduced compared with sham stimulation, before pronation but not flexion, indicating that c-tDCS enhanced selective muscle activation of the ipsilateral BB in a task-specific manner. The potential for c-tDCS to improve BB antagonist control correlated with BB MEP amplitude for pronation relative to flexion, expressed as a selectivity ratio. This is the first demonstration that selective muscle activation in the proximal upper limb can be improved after c-tDCS of ipsilateral M1 and that the benefits of c-tDCS for selective muscle activation may be most effective in cases where activation strategies are already suboptimal. These findings may have relevance for the use of tDCS in rehabilitation after stroke.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Desmond Agboada ◽  
Mohsen Mosayebi Samani ◽  
Asif Jamil ◽  
Min-Fang Kuo ◽  
Michael A. Nitsche

AbstractSize and duration of the neuroplastic effects of tDCS depend on stimulation parameters, including stimulation duration and intensity of current. The impact of stimulation parameters on physiological effects is partially non-linear. To improve the utility of this intervention, it is critical to gather information about the impact of stimulation duration and intensity on neuroplasticity, while expanding the parameter space to improve efficacy. Anodal tDCS of 1–3 mA current intensity was applied for 15–30 minutes to study motor cortex plasticity. Sixteen healthy right-handed non-smoking volunteers participated in 10 sessions (intensity-duration pairs) of stimulation in a randomized cross-over design. Transcranial magnetic stimulation (TMS)-induced motor-evoked potentials (MEP) were recorded as outcome measures of tDCS effects until next evening after tDCS. All active stimulation conditions enhanced motor cortex excitability within the first 2 hours after stimulation. We observed no significant differences between the three stimulation intensities and durations on cortical excitability. A trend for larger cortical excitability enhancements was however observed for higher current intensities (1 vs 3 mA). These results add information about intensified tDCS protocols and suggest that the impact of anodal tDCS on neuroplasticity is relatively robust with respect to gradual alterations of stimulation intensity, and duration.


2001 ◽  
Vol 86 (3) ◽  
pp. 1195-1201 ◽  
Author(s):  
Martin Sommer ◽  
Joseph Classen ◽  
Leonardo G. Cohen ◽  
Mark Hallett

The primary motor cortex produces motor commands that include encoding the direction of movement. Excitability of the motor cortex in the reaction time (RT) task can be assessed using transcranial magnetic stimulation (TMS). To elucidate the timing of the increase in cortical excitability and of the determination of movement direction before movement onset, we asked six right-handed, healthy subjects to either abduct or extend their right thumb after a go-signal indicated the appropriate direction. Between the go-signal and movement onset, single TMS pulses were delivered to the contralateral motor cortex. We recorded the direction of the TMS-induced thumb movement and the amplitude of motor-evoked potentials (MEPs) from the abductor pollicis brevis and extensor pollicis brevis muscles. Facilitation of MEPs from the prime mover, as early as 200 ms before the end of the reaction time, preceded facilitation of MEPs from the nonprime mover, and both preceded measurable directional change. Compared with a control condition in which no voluntary movement was required, the direction of the TMS-induced thumb movement started to change in the direction of the intended movement as early as 90 ms before the end of the RT, and maximum changes were seen shortly before the end of reaction time. Movement acceleration also increased with maxima shortly before the end of the RT. We conclude that in concentric movements a change of the movement direction encoded in the primary motor cortex occurs in the 200 ms prior to movement onset, which is as early as increased excitability itself can be detected.


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