Group I projections from intrinsic foot muscles to motoneurones of leg andthigh muscles in humans

1. Group I projections from intrinsic plantar muscles to motoneurones (MNs) of human leg and thigh muscles were investigated. Changes in firing probab ility of single motor units (MUs) in the tibialis anterior (TA), peroneus b revis (Per brev), soleus (Sol), gastrocnemius medialis (GM), vastus lateral is (VL), semitendinosus (ST) and biceps (Bi) were studied after electrical stimuli applied to: (i) the tibial nerve (TN) at ankle level, (ii) the corr esponding homonymous nerve, and (iii) the skin of the heel, to mimic the TN -induced cutaneous sensation. 2. Homonymous facilitation, attributable to monosynaptic Ia excitation, was found in all the sampled units. Early heteronymous excitation elicited by TN stimulation was found in many MUs. Later effects (3-5 ins central delay) were bigger and more frequently observed: excitation in most TA and Per br ev MUs, and inhibition in most Sol, GM and Bi MUs and in many ST and VI, MU s. The low threshold (similar to0.5-0.6 X motor threshold) and the inabilit y of a pure cutaneous stimulation to reproduce these effects (except the la te excitation in TA MUs) indicate that they were due to stimulation of grou p I muscle afferents. 3. The early excitation was accepted to be monosynaptic when its central de lay differed from that of the homonymous la excitation by less than 0.5 ms. Such a significant TN-induced belonging to all leg and thigh motor nuclei monosynaptic Ta excitation was found ill MIT, tested. Although its mean str ength was relatively weak, it is argued that these monosynaptic connections might affect already depolarized MNs. 4. The late excitation found in TA and Per brev MUs is argued to be mediate d through interneurones located rostral to MNs. 5. The late suppression, found in most Sol, GM and Bi MUs, and in many ST a nd VL, MUs, was the dominant effect. It was accompanied by an inhibition of the Sol and quadriceps H reflexes at rest, and therefore reflects an inhib ition directed to MNs. Its long latency is argued to reflect transmission b y interneurones located rostral to MNs (the inhibitory counterpart of nonmo nosynaptic excitation). 6. The functional implications of these connections are discussed with resp ect to the requirements of the stance phase of human walking and running.