TIME-COURSE OF SET-RELATED CHANGES IN MUSCLE RESPONSES TO STANCE PERTURBATION IN HUMANS

1. In standing subjects, toe-down rotation of a supporting platform el icits a medium-latency response (MLR) in tibialis anterior (TA) muscle and a long-latency response (LLR) in soleus (Sol). Toe-up rotation in duces a short-latency response (SLR) in Sol and a LLR in TA. When subj ects steadily hold onto a stable frame, all responses are decreased, e xcept Sol SLR. The aim of this investigation was to assess whether the response modulation is dependent on information from the hand touchin g the frame, or whether it anticipates the holding task.2. The time co urse of the changes in response amplitude was studied in a time interv al centred around the act of holding, performed in a reaction-time mod e. Subjects kept their extended arm close to the frame in front of the m and brought the hand in contact with the frame in response to a visu al go-signal. The platform was moved at different intervals prior to o r after the go-signal. Surface EMGs of Sol, TA and deltoid (Delt) were recorded. 3. TA MLR began to decrease when the platform was displaced at an interval of 140 ms after the go-signal, about 200 ms before sub jects touched the frame and 120 ms before termination of Delt EMG. Fou r hundred milliseconds after the go-signal the response reached and ma intained maximal inhibition, similar to that occurring under the stati onary holding condition. The time course of inhibition of Sol LLR and TA LLR was similar to that of TA MLR, except that LLRs began to decrea se at an earlier interval. Due to the different response latency fr om the onset of the perturbations, the beginning of inhibition of both M LRs and LLRs occurred almost simultaneously. 4. The changes in amplitu de of leg muscle responses are not triggered by the go-signal, contact with the frame, or arm motion, suggesting that the modulation is rela ted to the transition to a new, stabilized postural 'set'. The similar extent and parallel time course of MLR and LLR suppression, possibly transmitted through different pathways, points to the spinal cord as t he site of action. The lack of depression of the monosynaptic SLR sugg ests an effect at premotoneuronal level. On the basis of selectivity, latency and time course of the effect, we favour the hypothesis that a monoaminergic pathway from the brainstem is involved.