During hopping an early burst can be observed in the EMG from the soleus muscle starting about 45 ms after touch-down. It may be speculated that this early EMG burst is a stretch reflex response superimposed on activity from a supra-spinal origin. We hypothesised that if a stretch reflex indeed contributes to the early EMG burst, then advancing or delaying the touch-down without the subject's knowledge should similarly advance or delay the burst. This was indeed the case when touch-down was advanced or delayed by shifting the height of a programmable platform up or down between two hops and this resulted in a correspondent shift of the early EMG burst. Our second hypothesis was that the motor cortex contributes to the first EMG burst during hopping. If so, inhibition of the motor cortex would reduce the magnitude of the burst. By applying a low-intensity magnetic stimulus it was possible to inhibit the motor cortex and this resulted in a suppression of the early EMG burst. These results suggest that sensory feedback and descending drive from the motor cortex are integrated to drive the motor neuron pool during the early EMG burst in hopping. Thus, simple reflexes work in concert with higher order structures to produce this repetitive movement.

Flexion and extension movements are organized reciprocally, so that extensor motoneurones in the spinal cord are inhibited when flexor muscles are active and vice versa. During and just prior to dorsiflexion of the ankle, soleus motoneurones are thus inhibited as evidenced by a depression of the soleus H-reflex. It is therefore surprising that soleus motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) have been found not to be reduced and even facilitated during a voluntary dorsiflexion. The objective of this study was to investigate if MEPs, evoked by TMS, show a similar facilitation prior to and at the onset of contraction of muscles that are antagonists to the muscle in which the MEP is evoked and if so, examine the origin of such a facilitatory motor programme. Eleven seated subjects reacted to an auditory cue by contracting either the tibialis anterior (TA) or soleus muscle of the left ankle. TMS was applied to the hotspot of TA and soleus muscles on separate days. Stimuli were delivered prior to and at the beginning of contraction. Soleus MEPs were significantly facilitated when TMS was applied 50 ms prior to onset of plantar flexion. Surprisingly, soleus MEPs were also facilitated (although to a lesser extent) at a similar time in relation to the onset of dorsiflexion. TA MEPs were facilitated 50 ms prior to onset of dorsiflexion and neither depressed nor facilitated prior to plantar flexion. No difference was found between the facilitation of the soleus MEP and motor evoked responses to cervicomedullary stimulation prior to dorsiflexion, suggesting that the increased soleus MEPs were not caused by changes at a cortical level. This was confirmed by the observation that short-latency facilitation of the soleus H-reflex by subthreshold TMS was increased prior to plantar flexion, but not prior to dorsiflexion. These findings suggest that voluntary contraction at the ankle is accompanied by preceding facilitation of antagonists by a subcortical motor programme. This may help to ensure that the direction of movement may be changed quickly and efficiently during functional motor tasks.

A rapid plantar flexion perturbation in the early stance phase of walking elicits a large stretch reflex in tibialis anterior (TA). In this study we use repetitive transcranial magnetic stimulation (rTMS) to test if this response is mediated through a transcortical pathway. TA stretch reflexes were elicited in the early stance phase of the step cycle during treadmill walking. Twenty minutes of 1 Hz rTMS at 115% resting motor threshold (MT r ) significantly decreased (P < 0.05) the magnitude of the later component of the reflex at a latency of ∼100 ms up to 25 min after the rTMS. Control experiments in which stretch reflexes were elicited during sitting showed no effect on the spinally mediated short and medium latency stretch reflexes (SLR and MLR) while the long latency stretch reflex (LLR) and the motor-evoked potential (MEP) showed a significant decrease 10 min after 115% MT r rTMS. This study demonstrates that 1 Hz rTMS applied to the leg area of the motor cortex can suppress the long latency TA stretch reflex during sitting and in the stance phase of walking. These results are in line with the hypothesis that the later component of the TA stretch reflex in the stance phase of walking is mediated by a transcortical pathway. An alternative explanation for the observed results is that the reflex is mediated by subcortical structures that are affected by the rTMS. This study also shows that rTMS may be used to study the neural control of walking.