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 central nervous system (CNS) takes advantage of a network of complex neural pathways and mechanisms in the control of normal human gait. One such mechanism is the use of afferent feedback from muscle, cutaneous and joint receptors. Our knowledge of the contribution of afferent information in human gait is still limited, although this has been an area of active research for many years (e.g. Dietz et al. 1985;Yang et al. 1991;Sinkjaer et al. 1996). Yang et al. (1991) and Sinkjaer et al. (1996) have shown that afferent-mediated feedback is used by the CNS in the control of gait when an unexpected stretch of the ankle extensors is imposed. More recently, Sinkjaer et al. (2000) provided evidence that during walking, up to 50 % of the background EMG from the soleus muscle can be attributed to afferent feedback. However, the relative importance of the separate afferent pathways may differ for the background locomotor EMG and the EMG that results from an imposed stretch.When the human soleus muscle is stretched in a seated subject, two distinct bursts, with average peak latencies of 59 and 86 ms are evident in the EMG (Toft et al. 1989). These bursts are often referred to as the short (SLR) and medium (MLR) reflex responses, respectively, and have also been labelled the M1 and M2 stretch reflex responses, respectively. The short latency response has an onset latency of approximately 40 ms and is attributed to monosynaptic excitation of spinal motoneurones from the large diameter group Ia afferent fibres (Taylor et al.Group II muscle afferents probably contribute to the medium latency soleus stretch reflex during walking in humans 1. The objective of this study was to determine which afferents contribute to the medium latency response of the soleus stretch reflex resulting from an unexpected perturbation during human walking.2. Fourteen healthy subjects walked on a treadmill at approximately 3.5 km h _1 with the left ankle attached to a portable stretching device. The soleus stretch reflex was elicited by applying small amplitude (~8 deg) dorsiflexion perturbations 200 ms after heel contact.3. Short and medium latency responses were observed with latencies of 55 ± 5 and 78 ± 6 ms, respectively. The short latency response was velocity sensitive (P < 0.001), while the medium latency response was not (P = 0.725).4. Nerve cooling increased the delay of the medium latency component to a greater extent than that of the short latency component (P < 0.005).5. Ischaemia strongly decreased the short latency component (P = 0.004), whereas the medium latency component was unchanged (P = 0.437).6. Two hours after the ingestion of tizanidine, an a 2 -adrenergic receptor agonist known to selectively depress the transmission in the group II afferent pathway, the medium latency reflex was strongly depressed (P = 0.007), whereas the short latency component was unchanged (P = 0.653).7. An ankle block with lidocaine hydrochloride was performed to suppress the cutaneous afferents of the foot and ankle. Neither the short (P = 0.453) nor m...

Electrochemical and X-ray absorption techniques have been used to determine the influence of heat treatment in electrocatalytic activity for O2 reduction for two cobalt catalysts. The catalysts are cobalt phthalocyanine (catalyst 1) and polyacrylonitrile + cobalt acetate (catalyst 2) adsorbed on carbon black and heat treated at several temperatures. A maximum far the catalytic activity was obtained for PcCo at 850 "C and for the PAN + Co catalyst at 950 "C with subsequent decrease. The results obtained by XANES and EXAFS data clearly show that metallic cobalt aggregates with different size are synthetized in the range of increased activity. In the region of highest activity were observed the smallest cobalt clusters (20 A). For higher temperatures these cobalt aggregates became bigger (100-200 A), which corresponds to the decrease in the catalytic activity.TEM was utilized as a complementary technique and it confirms the influence of the annealing temperature in the size of the cobalt aggregates obtained. XANES measurements at the Co and N K edges confirm that CON, centers and nitrogen atoms are no longer detected after heat treatment in the region of increased activity. 7440-48-4; H,SO,, 7664-93-9; LiCIO,, 7791-03-9; cobalt acetate, 71-48-7; polypyrrole, 30604-8 1-0; pyrrole, 109-97-7; acetonitrile, 75-05-8; carbon, 7440-44-0.

The purpose of this study was to investigate whether repetitive electrical stimulation of the common peroneal nerve (CPN) is associated with changes in the motor response of the tibialis anterior (TA) muscle elicited by focal magnetic stimulation of the motor cortex. Motor evoked potentials (MEP) with a stimulation intensity of 125% of the threshold of the relaxed right TA were obtained before, during, and after repetitive electrical stimulation of the CPN (trains of five pulses of 1 ms, at a frequency of 200 Hz, repeated every second with a 30-min duration). The MEP of the TA muscle elicited after repetitive electrical stimulation were increased by 104% (range: 18-263%), and the increase was maintained for up to 110 min (range: 15-110 min) after the end of nerve stimulation. This increase in the MEP of the TA muscle was associated with a decrease in the threshold from the stimulation-response curve. Furthermore, during that period the early component of the TA stretch reflex as well as the latency of the MEP did not significantly change. To further test the origin of the increased MEP, complementary experiments showed that MEP elicited by transcranial electrical stimulation (TES) were also increased, but to a lesser degree (approximately 50%) than MEP elicited by TMS. It can be concluded that short-term nerve repetitive electrical stimulation of the lower extremities in healthy human participants can lead to a long-term increase in the contralateral MEP. As TES is believed to mainly activate the axon and not the soma of the cortical cells, the increased MEP cannot be explained exclusively by changes in the motor cortex cell excitability, but also by changes in subcortical neural structures involved in the excitation of spinal motoneurons. The results of this study allow the speculation that it would be possible to use repetitive electrical stimulation in the rehabilitation of patients with lower limb muscle weakness and spasticity.