Experiments were done to determine the extent to which the corticospinal tract is linked with the segmental motor circuits controlling ankle flexors and extensors during human walking compared with voluntary motor tasks requiring attention to the level of motor activity. The motor cortex was activated transcranially using a focal magnetic stimulation coil. For each subject, the entire input-output (I-O) curve [i.e., the integral of the motor evoked-potential (MEP) versus stimulus strength] was measured during a prescribed tonic voluntary contraction of either the tibialis anterior (TA) or the soleus. Similarly, I-O curves were measured in the early part of the swing phase, or in the early part of the stance phase of walking. The I-O data points were fitted by the Boltzmann sigmoidal function, which accounted for >/=80% of total data variance. There was no statistically significant difference between the I-O curves of the TA measured during voluntary ankle dorsiflexion or during the swing phase of walking, at matched levels of background electromyographic (EMG) activity. Additionally, there was no significant difference in the relation between the coefficient of variation and the amplitude of the MEPs measured in each task, respectively. In comparison, during the stance phase of walking the soleus MEPs were reduced on average by 26% compared with their size during voluntary ankle plantarflexion. Furthermore, during stance the MEPs in the inactive TA were enhanced relative to their size during voluntary ankle plantarflexion and in four of six subjects the TA MEPs were larger than those of the soleus. Finally, stimulation of the motor cortex at various phases of the step cycle did not reset the cycle. The time of the next step occurred at the expected moment, as determined from the phase-resetting curve. One interpretation of this result is that the motor cortex may not be part of the central neural system involved in timing the motor bursts during the step cycle. We suggest that during walking the corticospinal tract is more closely linked with the segmental motor circuits controlling the flexor, TA, than it is with those controlling the extensor, soleus. However, during voluntary tasks requiring attention to the level of motor activity, it is equally linked with the segmental motor circuits of ankle flexors or extensors.

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Human subjects are able to prepare cognitively to resist an involuntary movement evoked by a suprathreshold transcranial magnetic stimulation (TMS) applied over the primary motor cortex (M1) by anticipatory selective modulation of corticospinal excitability. Uncovering how the sensorimotor cortical network is involved in this process could reveal directly how a prior intention can tune the intrinsic dynamics of M1 before any peripheral intervention. Here, we used combined TMS-EEG to study the cortical integrative processes that are engaged both in the preparation to react to TMS (Resist vs. Assist) and in the subsequent response to it. During the preparatory period, the contingent negative variation (CNV) amplitude was found to be smaller over central electrodes (FC1, C1, Cz) when preparing to resist compared with preparing to assist the evoked movement whereas alpha-oscillation power was similar in the two conditions. Following TMS, the amplitude of the TMS evoked-N100 component was higher in the Resist than in the Assist condition for some central electrodes (FCz, C1, Cz, CP1, CP3). Moreover, for six out of eight subjects, a single-trial-based analysis revealed a negative correlation between CNV amplitude and N100 amplitude. In conclusion, prior intention can tune the excitability of M1. When subjects prepare to resist a TMS-evoked movement, the anticipatory processes cause a decreased cortical excitability by locally increasing the inhibitory processes.

This experiment investigates the interaction of different sensory cues in the control of propulsive forces in human gait which in turn allow the body's forward progression to be regulated. The aim of this work was to determine how optic flow and leg-somatosensory feedback interact in this control. We therefore determined whether the responses to sinusoidal perturbations of optic flow were accentuated when leg-somatosensory feedback was modified by varying the support resistance. Subjects walked on a treadmill which was driven by their own locomotor activity (1) with a sinusoidal variation of optic flow velocity, (2) with a sinusoidal variation of support resistance which modified leg-somatosensory information and (3) with both visual and leg-somatosensory modification at different frequencies. The response of the subject was measured as changes in speed and propulsive power. The response to sinusoidal perturbations of optic flow was found to be increased and time delayed when visual perturbations are coupled with support perturbations in comparison with the response observed with visual perturbations only. This result shows the influence of leg-somatosensory feedback on the weighting of optic flow. Inversely, it was also found that the motor response to support perturbation was different when the flow was congruent (i.e., corresponding to the subject's virtual speed) and when it was not. This latter result shows the influence of optic flow on the weighting of leg-somatosensory feedback. The interaction between optic flow and leg-somatosensory feedback argues in favor of a multimodal sensory control of propulsive forces. This multimodal sensory control would be based on all the sensory feedback and all their mutual sensorial interaction. Therefore, the modification of one sensory input modifies not only this input but also the integration of the other inputs.

The aim of this study was to determine the relative involvement of the corticospinal (CS) pathway in voluntarily controlled walking compared to unconstrained walking. In the voluntarily controlled walking condition, subjects had to walk at the same speed as in unconstrained walking with a mechanical constraint, which is known to affect specifically the upper-leg muscles. The motor cortex was activated transcranially using a focal magnetic stimulation coil in order to elicit motor evoked potentials (MEPs) in the rectus femoris (RF) and the biceps femoris (BF). The magnetic stimulation was delivered at the end of the swing (at 90% of the cycle duration), when the EMG backgrounds were similar in the two experimental conditions. For each subject in each condition, MEPs were measured for several stimulus intensities in order to establish the input/output (I/O) curve (MEPs amplitude plotted against stimulus strength). The results showed a significant increase in the MEPs amplitude of both the RF and BF in voluntarily controlled walking compared to unconstrained walking, which is the first evidence of cofacilitation of MEPs in antagonist upper-leg muscles during human gait. In conclusion, although a lot of studies have emphasized a privileged input of the corticospinal pathway to the distal lower-leg muscles, this study shows that, if a locomotory task requires fine control of the proximal upper-leg muscles, a selective facilitation of MEPs is observed in these muscles.

The intentional control of stride length is a fundamental basis for the adaptation of the stride to environmental constraints (obstacle avoidance, for example). Controlling the propulsive forces during the stance and/or controlling the pendular movement of the oscillating leg constitute the two potential and non-exclusive mechanisms underlying intentional stride length modulation. The present experiment was conducted in order to determine if these two mechanisms contribute to voluntary length modulation and, if so, how they cooperate according to whether the subject has to lengthen or shorten a stride and how these mechanisms are implemented at the neuromuscular level. Subjects had to produce a temporarily modulated stride of the same length, but originating from two different initial steady-states: one from shorter stride length and one from longer stride length. We found that the shortening was essentially realized by a swing-duration decrease (an increased activity in the hip extensor--biceps femoris--during the swing of the ipsilaterally shortened stride stopped the pendular leg movement earlier). The lengthening was realized by two mechanisms: (1) an increase in the propulsive forces (via an increased activity of the ankle extensor muscles--soleus--and the hip extensors--biceps femoris--from the stance of the ipsilaterally modulated stride, which was prolonged during the following stance of the contralateral leg), and (2) an increase in swing duration on the ipsilateral leg (an increased activity in hip and ankle flexors--rectus femoris and tibialis anterior--maintained the ipsilateral leg in flexion during the lengthened swing so that the foot landed later). In this experiment, the subjects were faced with a spatial constraint of the same magnitude in the direction of stride lengthening and stride shortening. However, under these conditions, subjects used a different balance between swing control (that directly modifies the foot trajectory without affecting the trajectory of the head-arm-trunk system) and/or the control of propulsive forces (that indirectly influences foot trajectory by modifying the trajectory of the head-arm-trunk system). In the first case, this concerns a voluntary control of gesture produced by the legs and usually implicated in the locomotor pointing; in the second case, this concerns a voluntary control of propulsive forces.

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