Changes in corticospinal drive to spinal motoneurones following visuo-motor skill learning in humans

We have previously demonstrated an increase in the excitability of the leg motor cortical area in relation to acquisition of a visuo-motor task in healthy humans. It remains unknown whether the interaction between corticospinal drive and spinal motoneurones is also modulated following motor skill learning. Here we investigated the effect of visuo-motor skill training involving the ankle muscles on the coupling between electroencephalographic (EEG) activity recorded from the motor cortex (Cz) and electromyographic (EMG) activity recorded from the left tibialis anterior (TA) muscle in 11 volunteers. Coupling in the time (cumulant density function) and frequency domains (coherence) between EEG–EMG and EMG–EMG activity were calculated during tonic isometric dorsiflexion before and after 32 min of training a visuo-motor tracking task involving the ankle muscles or performing alternating dorsi- and plantarflexion movements without visual feedback. A significant increase in EEG–EMG coherence around 15–35 Hz was observed following the visuo-motor skill session in nine subjects and in only one subject after the control task. Changes in coherence were specific to the trained muscle as coherence for the untrained contralateral TA muscle was unchanged. EEG and EMG power were unchanged following the training. Our results suggest that visuo-motor skill training is associated with changes in the corticospinal drive to spinal motorneurones. Possibly these changes reflect sensorimotor integration processes between cortex and muscle as part of the motor learning process.     

Decline in voluntary activation contributes to reduced maximal performance of fatigued human lower limb muscles

In upper limb muscles, altered corticospinal excitability and reduction in neural drive are observed in parallel with peripheral fatigue during prolonged and/or repeated contractions. However, the fatigue-induced adaptations of central and peripheral elements and their relative contribution to lower limb muscle performance are yet to be fully explored. In the present study, corticospinal excitability and peripheral contractility of ankle flexor muscles were quantified before, during and after repeated brief unilateral maximal dorsiflexions to fatigue in eleven healthy volunteers. Transcranial magnetic stimulation of the motor cortex area related to lower limb muscles was performed, and the evoked twitch and EMG responses in tibialis anterior (TA) and soleus (SOL) were measured. The motor evoked potentials (MEPs) in fatigued TA during post-exercise maximal dorsiflexions were smaller (?20?±?6?%, p?=?0.026) and remained depressed for at least 5?min. Post-exercise MEPs in fatigued SOL and silent periods in TA and SOL were not different compared to pre-exercise. These changes were accompanied by lower voluntary torque (?8?±?3?%, p?=?0.013), estimated resting twitch (?36?±?5?%, p?=?0.003) and voluntary activation (?17?±?9?%, p?=?0.021) versus pre-exercise. During last versus first maximal contraction in the fatiguing protocol lower voluntary torque (?40?±?4?%, p?=?0.003), higher MEP amplitudes (>+49?%, p?<?0.021) and longer silent periods (>+24?%, p?<?0.004) were recorded in both muscles. Decreased corticospinal excitability contributes significantly to the reduced maximal performance of fatigued lower limb muscles. During prolonged intermittent maximal dorsiflexions the performance of ankle muscles declines despite enhanced corticospinal excitability presumably due to deficient descending drive and/or spinal motoneuron responsiveness to the cortical drive.     

Cortical involvement in anticipatory postural reactions in man

All movements are accompanied by postural reactions which ensure that the balance of the body is maintained. It has not been resolved that to what extent the primary motor cortex and corticospinal tract are involved in the control of these reactions. Here, we investigated the contribution of the corticospinal tract to the activation of the soleus (SOL) muscle in standing human subjects (n = 10) in relation to voluntary heel raise, anticipatory postural activation of the soleus muscle when the subject pulled a handle and to reflex activation of the soleus muscle when the subject was suddenly pulled forward by an external perturbation. SOL motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) increased significantly in relation to rest −75 ms prior to the onset of EMG in the heel-raise and handle-pull tasks. The short-latency facilitation of the soleus H-reflex evoked by TMS increased similarly, suggesting that the increased MEP size prior to movement was caused at least partly by increased excitability of corticospinal tract cells with monosynaptic projections to SOL motoneurones. Changes in spinal motoneuronal excitability could be ruled out since there was no significant increase of the SOL H-reflex until immediately prior to EMG onset for any of the tasks. Tibialis anterior MEPs were unaltered prior to the onset of SOL EMG activity in the handle-pull task, suggesting that the MEP facilitation was specific for the SOL muscle. No significant increase of the MEPs was observed prior to EMG onset for the external perturbation. These data suggest that the primary motor cortex is involved in activating the SOL muscle as part of an anticipatory postural reaction.     

On the potential role of the corticospinal tract in the control and progressive adaptation of the soleus h-reflex during backward walking

When untrained subjects walk backward on a treadmill, an unexpectedly large amplitude soleus H-reflex occurs in the midswing phase of backward walking. We hypothesized that activity in the corticospinal tract (CST) during midswing depolarizes the soleus alpha-motoneurons subliminally and thus brings them closer to threshold. To test this hypothesis, transcranial magnetic stimulation (TMS) was applied to the leg area of the motor cortex (MCx) during backward walking. Motor-evoked potentials (MEPs) were recorded from the soleus and tibialis anterior (TA) muscles in untrained subjects at different phases of the backward walking cycle. We reasoned that if soleus MEPs could be elicited in midswing, while the soleus is inactive, this would be strong evidence for increased postsynaptic excitability of the alpha-motoneurons. In the event, we found that in untrained subjects, despite the presence of an unexpectedly large H-reflex in midswing, no soleus MEPs were observed at that time. The soleus MEPs were in phase with the soleus electromyographic (EMG) activity during backward walking. Soleus MEPs increased more rapidly as a function of the EMG activity during voluntary activity than during backward walking. Furthermore, a conditioning stimulus to the motor cortex facilitated the soleus H-reflex at rest and during voluntary plantarflexion but not in the midswing phase of backward walking. With daily training at walking backward, the time at which the H-reflex began to increase was progressively delayed until it coincided with the onset of soleus EMG activity, and its amplitude was considerably reduced compared with its value on the first experimental day. By contrast, no changes were observed in the timing or amplitude of soleus MEPs with training. Taken together, these observations make it unlikely that the motor cortex via the CST is involved in control of the H-reflex during the backward step cycle of untrained subjects nor in its progressive adaptation with training. Our observations raise the possibility that the large amplitude of H-reflex in untrained subjects and its adaptation with training are mainly due to control of presynaptic inhibition of Ia-afferents by other descending tracts.     

Rhythmic arm cycling modulates Hoffmann reflex excitability differentially in the ankle flexor and extensor muscles

Rhythmic arm movement significantly suppresses H-reflex amplitude in the soleus (SOL) muscle. This is evidence of neural linkages between the arms and legs which can be exploited during locomotion and have been ascribed to the descending effects of CPGs for arm cycling. However, the generalizability of the effects of arm movement on reflex excitability within the lower leg musculature has not been confirmed, as findings have been limited solely to the ankle extensor group. Here we tested the hypothesis that rhythmic arm movement similarly modulates H-reflex amplitude in both the ankle flexors and extensors by observing responses in the SOL and tibialis anterior (TA) muscles. SOL and TA H-reflex recruitment curves were recorded bilaterally during control and 1 Hz arm cycling conditions. Our results showed significant suppression in H-reflex amplitude (H_max) in the SOL muscle in both the dominant and non-dominant legs during arm movement. However, results also revealed an unpredicted bidirectional (i.e. either suppression or facilitation) modulation of TA reflex amplitude that was not present in the SOL muscle. These findings suggest a differential regulation of ankle flexor and extensor H-reflex responses during rhythmic arm movement. This may be the result of differences in CPG output to the flexors and extensors during rhythmic movement, as well as increased involvement of cortical drive to the flexors relative to the extensors during rhythmic movement. These findings may be pertinent to future investigation of rehabilitative therapies that involve facilitative modulation of ankle flexor motor responses.     

Modulation of transmission in the corticospinal and group Ia afferent pathways to soleus motoneurons during bicycling

Transmission in the corticospinal and Ia pathways to soleus motoneurons was investigated in healthy human subjects during bicycling. Soleus H reflexes and motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) were modulated similarly during the crank cycle being large during downstroke [concomitant with soleus background electromyographic (EMG) activity] and small during upstroke. Tibialis anterior MEPs were in contrast large during upstroke and small during downstroke. The soleus H reflexes and MEPs were also recorded during tonic plantarflexion at a similar ankle joint position, corresponding ankle angle, and matched background EMG activity as during the different phases of bicycling. Relative to their size during tonic plantarflexion, the MEPs were found to be facilitated in the early part of downstroke during bicycling, whereas the H reflexes were depressed in the late part of downstroke. The intensity of TMS was decreased below MEP threshold and used to condition the soleus H reflex. At short intervals (conditioning-test intervals of -3 to -1 ms), TMS produced a facilitation of the H reflex that is in all likelihood caused by activation of the fast monosynaptic corticospinal pathway. This facilitation was significantly larger in the early part of downstroke during bicycling than during tonic plantarflexion. This suggests that the increased MEP during downstroke was caused by changes in transmission in the fast monosynaptic corticospinal pathway. To investigate whether the depression of H reflexes in the late part of downstroke was caused by increased presynaptic inhibition of Ia afferents, the soleus H reflex was conditioned by stimulation of the femoral nerve. At a short interval (conditioning-test interval: -7 to -5 ms), the femoral nerve stimulation produced a facilitation of the H reflex that is mediated by the heteronymous monosynaptic Ia pathway from the femoral nerve to soleus motoneurons. Within the initial 0.5 ms after its onset, the size of this facilitation depends on the level of presynaptic inhibition of the Ia afferents, which mediate the facilitation. The size of the facilitation was strongly depressed in the late part of downstroke, compared with the early part of downstroke, suggesting that increased presynaptic inhibition was indeed responsible for the depression of the H reflex. These findings suggest that there is a selectively increased transmission in the fast monosynaptic corticospinal pathway to soleus motoneurons in early downstroke during bicycling. It would seem likely that one cause of this is increased excitability of the involved cortical neurons. The increased presynaptic inhibition of Ia afferents in late downstroke may be of importance for depression of stretch reflex activity before and during upstroke.     

Different resting state brain activity and functional connectivity in patients who respond and not respond to bifrontal tDCS for tinnitus suppression

Training a muscle group in one limb yields strength gains bilaterally—the so-called cross-education effect. However, to date there has been little study of the targeted application of this phenomenon in a manner relevant to clinical rehabilitation. For example, it may be applicable post-stroke, where hemiparesis leads to ankle flexor weakness. The purpose of this study was to examine the effects of high-intensity unilateral dorsiflexion resistance training on agonist (tibialis anterior, TA) and antagonist (plantarflexor soleus, SOL) muscular strength and H-reflex excitability in the trained and untrained limbs. Ankle flexor and extensor torque, as well as SOL and TA H-reflexes evoked during low-level contraction, were measured before and after 5 weeks of dorsiflexion training (n = 19). As a result of the intervention, dorsiflexor maximal voluntary isometric contraction force (MVIC) significantly increased (P < 0.05) in both the trained and untrained limbs by 14.7 and 8.4%, respectively. No changes in plantarflexor MVIC force were observed in either limb. Significant changes in H-reflex excitability threshold were also detected: H_@thresh significantly increased in the trained TA and SOL; and H_@max decreased in both SOL muscles. These findings reveal that muscular crossed effects can be obtained in the ankle dorsiflexor muscles and provide novel information on agonist and antagonist spinal adaptations that accompany unilateral training. It is possible that the ability to strengthen the ankle dorsiflexors bilaterally could be applied in post-stroke rehabilitation, where ankle flexor weakness could be counteracted via dorsiflexor training in the less-affected limb.     

Motor skill training induces changes in the excitability of the leg cortical area in healthy humans

Training-induced changes in cortical excitability may play an important role in rehabilitation of gait ability in patients with neurological disorders. In this study, we investigated the effect of a 32-min period of motor skill, non-skill and passive training involving the ankle muscles on leg motor cortical excitability in healthy humans. Transcranial magnetic stimulation (TMS) at a range of intensities was applied to obtain a recruitment curve of the motor evoked potentials (MEPs) in the tibialis anterior (TA) muscle before and after training. We also explored the effect of training on inhibitory and facilitatory cortical circuits by using a paired-pulse TMS technique at intervals of 2.5 ms (short-interval intracortical inhibition, SICI) and 8 ms (intracortical facilitation, ICF). During motor skill training, subjects were instructed to make a cursor follow a series of target lines on a computer screen by performing voluntary ankle dorsi- and plantarflexion movements. Non-skill and passive training consisted of repeated voluntary and assisted dorsi- and plantarflexion movements, respectively. Recruitment curves increased significantly after 32 min of motor skill training but not after non-skill and passive training, suggesting that only skill motor training increases motor cortical excitability. Motor skill training was not accompanied by any changes in the recruitment curves of TA MEPs evoked by transcranial electrical stimulation, suggesting that the increased MEPs to TMS was likely caused by changes in excitability at a cortical site. SICI was decreased after 32 min of motor skill training but no changes were observed in ICF. We conclude that similar plastic changes as have previously been reported for the hand motor following motor skill training may also be observed for the leg motor area. The observed plastic changes appeared to be related to the degree of difficulty in the motor task, and may be of relevance for rehabilitation of gait disorders.     

Changes in the excitability of soleus muscle short latency stretch reflexes during human hopping after 4 weeks of hopping training

Changes in the excitability of the human triceps surae muscle short latency stretch reflexes were investigated in six male subjects before and after 4 weeks of progressive two-legged hopping training. During the measurements the subjects performed 2-Hz hopping with: preferred contact time (PCT) and short contact time. The following reflex parameters were examined before and after the training period: the soleus muscle (SOL) Hoffmann-reflex (H-reflex) at rest and during hopping, the short latency electromyogram (EMG) components of the movement induced stretch reflex (MSR) in SOL and medial gastrocnemius muscle (MG), and the EMG amplitude of the SOL and MG tendon reflexes (T-reflexes) elicited at rest. The main results can be summarized as follows: the SOL T-reflex had increased by about 28% (P < 0.05) after training while the MG T-reflex was unchanged; the SOL MSR (always evident) and the MG MSR (when observable) did not change in amplitude with training, and before training the SOL H-reflex in both hopping situations was significantly depressed to about 40% of the reference value at standing rest (P < 0.05). After training the H-reflex during PCT hopping was no longer depressed. As the value of the measured mechanical parameters (the total work rate, joint angular velocity and the ankle joint work rate) was unchanged after training in both hopping situations, the reflex changes observed could not be ascribed to changes in the movement pattern. To explain the observed changes, hypotheses of changes in the excitability of the stretch reflex caused by the training were taken into consideration and discussed.     

Changes in reciprocal inhibition across the ankle joint with changes in external load and pedaling rate during bicycling

The purpose of this study was to investigate the role of reciprocal inhibition in the regulation of antagonistic ankle muscles during bicycling. A total of 20 subjects participated in the study. Reciprocal inhibition was induced by stimulation of the peroneal nerve (PN) at 1.2 times threshold for the M-response in the tibialis anterior muscle (TA) and recorded as a depression of the rectified soleus (SOL) EMG. Recordings were made during tonic plantar flexion and during bicycling on an ergometer bicycle. During tonic contraction, the amount of inhibition in the SOL EMG was linearly correlated to the amount of background EMG. This linear relation was used to calculate the expected amount of reciprocal inhibition at corresponding EMG levels during bicycling. During the early phase of down-stroke of bicycling at 60 revolutions per minute (RPM) and an external load of 1.0 kg, the amount of recorded reciprocal inhibition was significantly smaller than that calculated from the linear relation during tonic contraction. In nine subjects, the SOL H-reflex was used to evaluate the amount of inhibition. At a short conditioning test interval (2-3 ms), the PN stimulation depressed the SOL H-reflex when the subjects were at rest. This short latency inhibition was absent during downstroke, but appeared during upstroke just prior to and during TA activation. A positive linear relation was found between the level of SOL background EMG in early downstroke and the external load (0.5-2.5 kg) as well as the rate of pedaling (30-90 RPM at 1.0 kg external load). The amount of inhibition in the SOL EMG when expressed as a percentage of the background EMG activity decreased significantly with increasing load. During increased pedaling rate, a similar decrease was seen, but it did not reach a statistically significant level. The data illustrate that reciprocal inhibition of the soleus muscle is modulated during bicycling being small in downstroke when the SOL muscle is active and large in upstroke where the muscle is inactive and its antagonist becomes active. The depression of the inhibition in relation to increased load and pedaling rate likely reflects the need of reducing inhibition of the SOL motoneurons to ensure a sufficient activation of the muscle.     

Facilitation of cortically evoked potentials with motor imagery during post-exercise depression of corticospinal excitability

This study examined whether muscle fatigue alters the facilitatory effect of motor imagery on corticospinal excitability. We aimed to determine if post-exercise depression of potentials evoked magnetically from the motor cortex is associated with alterations in internally generated movement plans. In experiment 1, motor-evoked potentials (MEPs) were recorded from two right hand and two right forearm muscles, at rest and during motor imagery of a maximal handgrip contraction, in eight neurologically normal subjects, before and after a 2-min maximal voluntary handgrip contraction. Resting MEP amplitude was facilitated by motor imagery in three of the four muscles, but consistently only in two. Motor imagery also reduced the trial-to-trial variability of resting MEPs. Following the exercise, resting MEP amplitude was depressed reliably in only one muscle engaged in the task, although two other muscles exhibited some depression. Motor imagery MEPs were smaller after exercise, but the degree of facilitation compared to the rest MEP was unchanged. In experiment 2, TMS intensity was increased after exercise-induced MEP depression so that the MEP amplitude matched the pre-exercise baseline. The amplitude of the MEP facilitated with motor imagery was not altered by MEP depression, nor was it increased when the TMS intensity was increased. These results suggest, at least with a simple motor task, that while post-exercise depression reduces corticospinal excitability, it does not appear to significantly affect the strength of the input to the motor cortex from those areas of the brain responsible for the storage and generation of internal representations of movement.     

Operant conditioning of reciprocal inhibition in rat soleus muscle

Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex (SSR), induces activity-dependent plasticity in the spinal cord and might be used to improve locomotion after spinal cord injury. To further assess the potential clinical significance of spinal reflex conditioning, this study asks whether another well-defined spinal reflex pathway, the disynaptic pathway underlying reciprocal inhibition (RI), can also be operantly conditioned. Sprague-Dawley rats were implanted with electromyographic (EMG) electrodes in right soleus (SOL) and tibialis anterior (TA) muscles and a stimulating cuff on the common peroneal (CP) nerve. When background EMG in both muscles remained in defined ranges, CP stimulation elicited the TA H-reflex and SOL RI. After collection of control data for 20 days, each rat was exposed for 50 days to up-conditioning (RIup mode) or down-conditioning (RIdown mode) in which food reward occurred if SOL RI evoked by CP stimulation was more (RIup mode) or less (RIdown mode) than a criterion. TA and SOL background EMG and TA M response remained stable. In every rat, RI conditioning was successful (i.e., change > or =20% in the correct direction). In the RIup rats, final SOL RI averaged 171+/- 28% (mean +/- SE) of control, and final TA H-reflex averaged 114 +/- 14%. In the RIdown rats, final SOL RI averaged 37 +/- 13% of control, and final TA H-reflex averaged 60 +/- 18%. Final SOL RI and TA H-reflex sizes were significantly correlated. Thus like the SSR and the H-reflex, RI can be operantly conditioned; and conditioning one reflex can affect another reflex as well.     

Effects of low-frequency whole-body vibration on motor-evoked potentials in healthy men

The aim of this study was to determine whether low-frequency whole-body vibration (WBV) modulates the excitability of the corticospinal and intracortical pathways related to tibialis anterior (TA) muscle activity, thus contributing to the observed changes in neuromuscular function during and after WBV exercise. Motor-evoked potentials (MEPs) elicited in response to transcranial magnetic stimulation (TMS) of the leg area of the motor cortex were recorded in TA and soleus (SOL) muscles of seven healthy male subjects whilst performing 330 s continuous static squat exercise. Each subject completed two conditions: control (no WBV) and WBV (30 Hz, 1.5 mm vibration applied from 111 to 220 s). Five single suprathreshold and five paired TMS were delivered during each squat period lasting 110 s (pre-, during and post-WBV). Two interstimulus intervals (ISIs) between the conditioning and the testing stimuli were employed in order to study the effects of WBV on short-interval intracortical inhibition (SICI, ISI = 3 ms) and intracortical facilitation (ICF, ISI = 13 ms). During vibration relative to squat exercise alone, single-pulse TMS provoked significantly higher TA MEP amplitude (56 ± 14%, P = 0.003) and total area (71 ± 19%, P = 0.04), and paired TMS with ISI = 13 ms provoked smaller MEP amplitude (−21 ± 4%, P = 0.01) but not in SOL. Paired-pulse TMS with ISI = 3 ms elicited significantly lower MEP amplitude (TA, −19 ± 4%, P = 0.009; and SOL, −13 ± 4%, P = 0.03) and total area (SOL, −17 ± 6%, P = 0.02) during vibration relative to squat exercise alone in both muscles. Tibialis anterior MEP facilitation in response to single-pulse TMS suggests that WBV increased corticospinal pathway excitability. Increased TA and SOL SICI and decreased TA ICF in response to paired-pulse TMS during WBV indicate vibration-induced alteration of the intracortical processes as well.     

Focal depression of cortical excitability induced by fatiguing muscle contraction: a transcranial magnetic stimulation study

Motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the motor cortex were recorded in separate sessions to assess changes in motor cortex excitability after a fatiguing isometric maximal voluntary contraction (MVC) of the right ankle dorsal flexor muscles. Five healthy male subjects, aged 37.4±4.2 years (mean±SE), were seated in a chair equipped with a load cell to measure dorsiflexion force. TMS or TES was delivered over the scalp vertex before and after a fatiguing MVC, which was maintained until force decreased by 50%. MEPs were recorded by surface electrodes placed over quadriceps, hamstrings, tibialis anterior (TA), and soleus muscles bilaterally. M-waves were elicited from the exercised TA by supramaximal electrical stimulation of the peroneal nerve. H-reflex and MVC recovery after fatiguing, sustained MVC were also studied independently in additional sessions. TMS-induced MEPs were significantly reduced for 20 min following MVC, but only in the exercised TA muscle. Comparing TMS and TES mean MEP amplitudes, we found that, over the first 5 min following the fatiguing MVC, they were decreased by about 55% for each. M-wave responses were unchanged. H-reflex amplitude and MVC force recovered within the 1st min following the fatiguing MVC. When neuromuscular fatigue was induced by tetanic motor point stimulation of the TA, TMS-induced MEP amplitudes remained unchanged. These findings suggest that the observed decrease in MEP amplitude represents a focal reduction of cortical excitability following a fatiguing motor task and may be caused by intracortical and/or subcortical inhibitory mechanisms.     

Rapid changes in corticospinal excitability during force field adaptation of human walking

Force field adaptation of locomotor muscle activity is one way of studying the ability of the motor control networks in the brain and spinal cord to adapt in a flexible way to changes in the environment. Here, we investigate whether the corticospinal tract is involved in this adaptation. We measured changes in motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in the tibialis anterior (TA) muscle before, during, and after subjects adapted to a force field applied to the ankle joint during treadmill walking. When the force field assisted dorsiflexion during the swing phase of the step cycle, subjects adapted by decreasing TA EMG activity. In contrast, when the force field resisted dorsiflexion, they increased TA EMG activity. After the force field was removed, normal EMG activity gradually returned over the next 5 min of walking. TA MEPs elicited in the early swing phase of the step cycle were smaller during adaptation to the assistive force field and larger during adaptation to the resistive force field. When elicited 5 min after the force field was removed, MEPs returned to their original values. The changes in TA MEPs were larger than what could be explained by changes in background TA EMG activity. These effects seemed specific to walking, as similar changes in TA MEP were not seen when seated subjects were tested during static dorsiflexion. These observations suggest that the corticospinal tract contributes to the adaptation of walking to an external force field.     

Short-term adaptations in spinal cord circuits evoked by repetitive transcranial magnetic stimulation: possible underlying mechanisms

Repetitive transcranial magnetic stimulation (rTMS) has been shown to induce adaptations in cortical neuronal circuitries. In the present study we investigated whether rTMS, through its effect on corticospinal pathways, also produces adaptations at the spinal level, and what the neuronal mechanisms involved in such changes are. rTMS (15 trains of 20 pulses at 5 Hz) was applied over the leg motor cortical area in ten healthy human subjects. At rest motor evoked potentials (MEPs) in the soleus and tibialis anterior muscles were facilitated by rTMS (at 1.2×MEP threshold). In contrast, the soleus H-reflex was depressed for 1 s at stimulus intensities from 0.92 to 1.2×MEP threshold. rTMS increased the size of the long-latency depression of the soleus H-reflex evoked by common peroneal nerve stimulation and decreased the femoral nerve facilitation of the soleus H-reflex. These observations suggest that the depression of the H-reflex by rTMS can be explained, at least partly, by an increased presynaptic inhibition of soleus Ia afferents. In contrast, rTMS had no effect on disynaptic reciprocal Ia inhibition from ankle dorsiflexors to plantarflexors. We conclude that a train of rTMS may modulate transmission in specific spinal circuitries through changes in corticospinal drive. This may be of relevance for future therapeutic strategies in patients with spasticity.     

Changes in spinal but not cortical excitability following combined electrical stimulation of the tibial nerve and voluntary plantar-flexion

Unilateral training involving voluntary contractions, neuromuscular electrical stimulation (NMES), or a combination of the two can increase the excitability of neural circuits bilaterally within the CNS. Many rehabilitation programs are designed to promote such “neuroplasticity” to improve voluntary movement following CNS damage. While much is known about this type of activity-dependent plasticity for the muscles that dorsi-flex the ankle, similar information is not available for the plantar-flexors. Presently, we assessed the excitability of corticospinal (CS) and spinal circuits for both soleus (SOL) muscles before and after voluntary contractions of the right plantar-flexors (VOL; 5?s on–5?s off, 40?min), NMES of the right tibial nerve (tnNMES; 5?s on–5?s off, 40?min), or both together (V?+?tnNMES). CS excitability for the right (rSOL) and left SOL (lSOL) muscles was assessed by quantifying motor evoked potentials elicited by transcranial magnetic stimulation. Spinal excitability was assessed using measures from the ascending limb of the M-wave versus H-reflex recruitment curve. CS excitability did not change for rSOL (the activated muscle) or lSOL following any condition. In contrast, there was a marked increase in spinal excitability for rSOL, but only following V?+?tnNMES; the slope of the M-wave versus H-reflex recruitment curve increased?approximately twofold (pre?=?7.9; post?=?16.2) and H-reflexes collected when the M-wave was?~5?% of the maximal M-wave (M_max) increased by?~1.5×?(pre?=?19?% M_max, post?=?29?% M_max). Spinal excitability for lSOL did not change following any condition. Thus, only voluntary contractions that were coupled with NMES increased CNS excitability, and this occurred only in the ipsilateral spinal circuitry. These results are in marked contrast to previous studies showing NMES-induced changes in CS excitability for every other muscle studied and suggest that the mechanisms that regulate activity-dependent neuroplasticity are different for SOL than other muscles. Further, while rehabilitation strategies involving voluntary training and/or NMES of the plantar-flexors may be beneficial for producing movement and reducing atrophy, a single session of low-intensity NMES and voluntary training may not be effective for strengthening CS pathways to the SOL muscle.     

Differential changes in corticospinal and Ia input to tibialis anterior and soleus motor neurones during voluntary contraction in man

Motor-evoked potentials (MEPs) were recorded in the tibialis anterior and soleus muscles following transcranial magnetic stimulation (TMS) of the motor cortex. In the soleus, the H-reflex amplitude increased with the contraction level to the same extent as that of MEPs, whereas in the tibialis anterior, the H-reflex amplitude increased significantly less than that of MEPs. The latency of the MEPs decreased with contraction, whereas this was not the case of the H-reflexes. In the tibialis anterior, the response probability of single-motor units (SMU) to TMS increased more substantially during voluntary contraction than following stimulation of the peroneal nerve. In the tibialis anterior, the response probability of SMU increased more substantially during voluntary contraction than following stimulation of the peroneal nerve. The short-latency facilitation, presumably monosynaptic of origin, of the soleus H-reflex evoked by subthreshold TMS increased as a function of the plantarflexion force. This was not the case for the heteronymous Ia facilitation of the soleus H-reflex following stimulation of the femoral nerve. It is concluded that the corticospinal input to lower limb motor neurones generated by TMS increases with the level of voluntary contraction, whereas this is true only to a limited extent for the synaptic input from Ia afferents. It is suggested that this reflects changes in the susceptibility of corticospinal cells to TMS during voluntary contraction.     

Force-length characteristics of in vivo human skeletal muscle

In the present study, the in vivo force-length relations of the human soleus (SOL) and tibialis anterior (TA) muscles were estimated. Measurements were taken in six men at ankle angles from 30 degrees of dorsiflexion to 45 degrees of plantarflexion in steps of 15 degrees, and involved dynamometry, electrical stimulation, ultrasonography and magnetic resonance imaging (MRI). For each muscle and ankle angle studied the following three measurements were carried out: (1) dynamometry-based measurement of maximal voltage tetanic moment, (2) ultrasound-based measurement of pennation angle and fibre length and (3) MRI-based measurement of tendon moment arm length. Tendon forces were calculated dividing moments by moment arm lengths, and muscle forces were calculated dividing tendon forces by the cosine of pennation angles. In the transition from 30 degrees of dorsiflexion to 45 degrees of plantarflexion the SOL muscle fibre length decreased from 3.8 to 2.4 cm and its force decreased from 3330 to 290 N. Over the same range of ankle angles the TA muscle fibre length increased from 3.7 to 6 cm and its force increased from 157 to 644 N. Over the longest muscle fibre lengths reached the force of both muscles remained approximately constant. These results indicate that the intact human SOL and TA muscles operate in the ascending limb and plateau region of the force-length relationship. Similar conclusions were reached when calculating the theoretical operating range of the two muscle sarcomeres in the study.     

Posture-related changes in heteronymous recurrent inhibition from quadriceps to ankle muscles in humans

The possibility was investigated that changes in heteronymous recurrent inhibition (RI) from quadriceps (Q) to soleus (Sol) and tibialis anterior (TA) motoneurons (MNs) occur during postural tasks requiring cocontraction of Q with one of these muscles. Stimulation of the femoral nerve (FN), which elicited a Q H-reflex discharge, was used to activate Renshaw cells. The resulting inhibition of TA and Sol MNs was assessed using three test responses: (1) the rectified and averaged ongoing electromyogram (EMG) activity in TA or Sol; (2) the motor-evoked potential (MEP) elicited by cortical stimulation in these muscles; and (3) the Sol H reflex. The characteristics of the depression (appearance and increase with the conditioning reflex discharge, short central delay and long duration) are consistent with a Renshaw origin. In addition, results obtained in control experiments (no change in the EMG suppression after an ischaemic blockade of group-I afferents from the leg, time course of the FN-induced depression of the MEP similar to that of the ongoing EMG) made a significant contribution from other pathways activated by FN stimulation unlikely. Posture-related heteronymous RI from Q was compared in different postural tasks at matched levels of background EMG activity: voluntary co-contraction of Q and of the relevant ankle muscle while sitting (control situation), postural co-contraction of Q and TA (while leaning backwards during stance), or contraction of Sol with (preparation for hopping) and without (standing on tip of toes and leaning forwards during stance) associated contraction of the Q. During stance, heteronymous RI from Q was reduced to TA (but not to Sol) while leaning backwards and to Sol in preparation for hopping, but not in the other situations. Thus, RI from Q to TA or Sol was specifically decreased when a co-contraction of the Q and of the relevant muscle operating at the ankle was required to maintain bipedal stance. It is argued that this control of Renshaw cells is descending in origin and contributes to selection of the appropriate synergism in various postural tasks.