Sensory feedback plays a major role in the regulation of the spinal neural locomotor circuitry in cats. The present study investigated whether sensory feedback also plays an important role during walking in 20 healthy human subjects, by arresting or unloading the ankle extensors 6 deg for 210 ms in the stance phase of gait. During the stance phase of walking, unloading of the ankle extensors significantly (P < 0·05) reduced the soleus activity by 50 % in early and mid‐stance at an average onset latency of 64 ms. The onset and amplitude of the decrease in soleus activity produced by the unloading were unchanged when the common peroneal nerve, which innervates the ankle dorsiflexors, was reversibly blocked by local injection of lidocaine (n= 3). This demonstrated that the effect could not be caused by a peripherally mediated reciprocal inhibition from afferents in the antagonist nerves. The onset and amplitude of the decrease in soleus activity produced by the unloading were also unchanged when ischaemia was induced in the leg by inflating a cuff placed around the thigh. At the same time, the group Ia‐mediated short latency stretch reflex was completely abolished. This demonstrated that group Ia afferents were probably not responsible for the decrease of soleus activity produced by the unloading. The findings demonstrate that afferent feedback from ankle extensors is of significant importance for the activation of these muscles in the stance phase of human walking. Group II and/or group Ib afferents are suggested to constitute an important part of this sensory feedback.

The cerebellum has been proposed to be a crucial component in the state estimation process that combines information from motor efferent and sensory afferent signals to produce a representation of the current state of the motor system. Such a state estimate of the moving human arm would be expected to be used when the arm is rapidly and skillfully reaching to a target. We now report the effects of transcranial magnetic stimulation (TMS) over the ipsilateral cerebellum as healthy humans were made to interrupt a slow voluntary movement to rapidly reach towards a visually defined target. Errors in the initial direction and in the final finger position of this reach-to-target movement were significantly higher for cerebellar stimulation than they were in control conditions. The average directional errors in the cerebellar TMS condition were consistent with the reaching movements being planned and initiated from an estimated hand position that was 138 ms out of date. We suggest that these results demonstrate that the cerebellum is responsible for estimating the hand position over this time interval and that TMS disrupts this state estimate.

In human subjects, stretch applied to ankle dorsiflexors elicited three bursts of reflex activity in the tibialis anterior (TA) muscle (labelled M1, M2 and M3) at mean onset latencies of 44, 69 and 95 ms, respectively. The possibility that the later of these reflex bursts is mediated by a transcortical pathway was investigated. The stretch evoked a cerebral potential recorded from the somatosensory cortex at a mean onset latency of 47 ms in nine subjects. In the same subjects a compound motor‐evoked potential (MEP) in the TA muscle, evoked by magnetic stimulation of the motor cortex, had a mean onset latency of 32 ms. The M1 and the M2 reflexes thus had too short a latency to be caused by a transcortical pathway (minimum latency, 79 ms (47 + 32)), whereas the later part of the M2 and all of the M3 reflex had a sufficiently long latency. When the transcranial magnetic stimulation was timed so that the MEP arrived in the TA muscle at the same time as the M1 or M2 reflexes, no extra increase in the potential was observed. However, when the MEP arrived at the same time as the M3 reflex a significant (P < 0.01) extra‐facilitation was observed in all twelve subjects investigated. Peaks evoked by transcranial magnetic stimulation in the post‐stimulus time histogram of the discharge probability of single TA motor units (n= 28) were strongly facilitated when they occurred at the same time as the M3 response. This was not the case for the first peaks evoked by electrical transcranial stimulation in any of nine units investigated. We suggest that these findings are explained by an increased cortical excitability following TA stretch and that this supports the hypothesis that the M3 response in the TA muscle is ‐ at least partly ‐ mediated by a transcortical reflex.

The cerebral activation during bicycle movements was investigated by oxygen-15-labelled H2O positron emission tomography (PET) in seven healthy human subjects. Compared to rest active bicycling significantly activated sites bilaterally in the primary sensory cortex, primary motor cortex (M1) and supplementary motor cortex (SMA) as well as the anterior part of cerebellum. Comparing passive bicycling movements with rest, an almost equal activation was observed. Subtracting passive from active bicycle movements, significant activation was only observed in the leg area of the primary motor cortex and the precuneus, but not in the primary sensory cortex (S1). The M1 activation was positively correlated (alpha=0.75-0.85, t=6.4, P<10(-5)) with the rate of the active bicycle movements. Imagination of bicycle movements compared to rest activated bilaterally sites in the SMA. It is suggested that the higher motor centres, including the primary and supplementary motor cortices as well as the cerebellum, take an active part in the generation and control of rhythmic motor tasks such as bicycling.

The effect of transcranial magnetic stimulation (TMS) on the soleus H reflex was investigated in the stance phase of walking in seventeen human subjects. For comparison, measurements were also made during quiet standing, matched tonic plantar flexion and matched dynamic plantar flexion. During walking and dynamic plantar flexion subliminal (0.95 times threshold for a motor response in the soleus muscle) TMS evoked a large short‐latency facilitation (onset at conditioning‐test interval: −5 to −1 ms) of the H reflex followed by a later (onset at conditioning‐test interval: 3–16 ms) long‐lasting inhibition. In contrast, during standing and tonic plantar flexion the short‐latency facilitation was either absent or small and the late inhibition was replaced by a long‐lasting facilitation. When grading the intensity of TMS it was found that the short‐latency facilitation had a lower threshold during walking than during standing and tonic plantar flexion. Regardless of the stimulus intensity the late facilitation was never seen during walking and dynamic plantar flexion and the late inhibition was not seen, except for one subject, during standing and tonic plantar flexion. A similar difference in the threshold of the short‐latency facilitation between walking and standing was not observed when the magnetic stimulation was replaced by transcranial electrical stimulation. The lower threshold of the short‐latency facilitation evoked by magnetic but not electrical transcranial stimulation during walking compared with standing suggests that cortical cells with direct motoneuronal connections increase their excitability in relation to human walking. The significance of the differences in the late facilitatory and inhibitory effects during the different tasks is unclear.

Time- and frequency-domain analysis of the coupling between pairs of electromyograms (EMG) recorded from leg muscles was investigated during walking in healthy human subjects. For two independent surface EMG signals from the tibialis anterior (TA) muscle, coupling estimated from coherence measurements was observed at frequencies

The sensitivity of soleus H-reflexes, T-reflexes, and short-latency stretch reflexes (M1) to presynaptic inhibition evoked by a weak tap applied to the biceps femoris tendon or stimulation of the common peroneal nerve (CPN) was compared in 17 healthy human subjects. The H-reflex was strongly depressed for a period lasting up to 300-400 ms (depression to 48 +/- 23%, mean +/- SD, of control at a conditioning test interval of 70 ms) by the biceps femoris tendon tap. In contrast, the short-latency soleus stretch reflex elicited by a quick passive dorsiflexion of the ankle joint was not depressed. The soleus T-reflex elicited by an Achilles tendon tap was only weakly depressed (92 +/- 8%). The H-reflex was also significantly more depressed than the T-reflex at long intervals (>15 ms) after stimulation of CPN (H-reflex 63 +/- 14%, T-reflex 91 +/- 13%; P < 0. 01). However, the short-latency (2 ms) disynaptic reciprocal Ia inhibition evoked by stimulation of CPN was equally strong for H- and T-reflexes (H-reflex 72 +/- 10%, T-reflex 67 +/- 13%; P = 0.07). Peaks in the poststimulus time histogram (PSTH) of the discharge probability of single soleus motor units (n = 53) elicited by an Achilles tendon tap had a longer duration than peaks evoked by electrical stimulation of the tibial nerve (on average 5.0 ms as compared with 2.7 ms). All parts of the electrically evoked peaks were depressed by the conditioning biceps femoris tendon tap (average depression to 55 +/- 27% of control; P < 0.001). A similar depression was observed for the initial 2 ms of the peaks evoked by the Achilles tendon tap (69 +/- 48%; P < 0.001), but the last 2 ms were not depressed. Conditioning stimulation of the CPN at long intervals (>15 ms) also depressed all parts of the electrically evoked PSTH peaks (n = 34; average 65%; P < 0.001) but had only a significant effect on the initial 2 ms of the peaks evoked by the Achilles tendon tap (85%; P < 0.001). We suggest that the different sensitivity of mechanically and electrically evoked reflexes to presynaptic inhibition is caused by a difference in the shape and composition of the excitatory postsynaptic potentials underlying the two reflexes. This difference may be explained by a different composition and/or temporal dispersion of the afferent volleys evoked by electrical and mechanical stimuli. We conclude that it is not straightforward to predict the modulation of stretch reflexes based on observations of H-reflex modulation.

Stretch of the ankle dorsiflexors was applied at different times of the walking cycle in 17 human subjects. When the stretch was applied in the swing phase, only small and variable reflex responses were observed in the active tibialis anterior (TA) muscle. Two of the reflex responses that could be distinguished had latencies which were comparable with the early (M1) and late (M3)components of the three reflex responses (M1, M2 and M3) observed during tonic dorsiflexion in sitting subjects. In the stance phase a single very large response was consistently observed in the inactive TA muscle. The peak of this response had the same latency as the peak of M3, but in the majority of subjects the onset latency was shorter than that of M3. The TA reflex response in the stance phase was abolished by ischaemia of the lower leg at the same time as the soleus H‐reflex, suggesting that large muscle afferents were involved in the generation of the response. Motor‐evoked potentials (MEPs) elicited in the TA by transcranial magnetic stimulation (TMS) were strongly facilitated corresponding to the peak of the stretch response in the stance phase and the late reflex response in the swing phase. A similar facilitation was not observed corresponding to the earlier responses in the swing phase and the initial part of the response in stance. Prior stretch did not facilitate MEPs evoked by transcranial electrical stimulation in the swing phase of walking. However, in the stance phase MEPs elicited by strong electrical stimulation were facilitated by prior stretch to the same extent as the MEPs evoked by TMS. The large responses to stretch seen in the stance phase are consistent with the idea that stretch reflexes are mainly involved in securing the stability of the supporting leg during walking. It is suggested that a transcortical reflex pathway may be partly involved in the generation of the TA stretch responses during walking.