Modulation of transmission in the corticospinal and group Ia afferent pathways to soleus motoneurons during bicycling.

Transmission in the corticospinal and Ia pathways to soleus motoneurons was investigated in healthy human subjects during bicycling. Soleus H reflexes and motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) were modulated similarly during the crank cycle being large during downstroke [concomitant with soleus background electromyographic (EMG) activity] and small during upstroke. Tibialis anterior MEPs were in contrast large during upstroke and small during downstroke. The soleus H reflexes and MEPs were also recorded during tonic plantarflexion at a similar ankle joint position, corresponding ankle angle, and matched background EMG activity as during the different phases of bicycling. Relative to their size during tonic plantarflexion, the MEPs were found to be facilitated in the early part of downstroke during bicycling, whereas the H reflexes were depressed in the late part of downstroke. The intensity of TMS was decreased below MEP threshold and used to condition the soleus H reflex. At short intervals (conditioning-test intervals of -3 to -1 ms), TMS produced a facilitation of the H reflex that is in all likelihood caused by activation of the fast monosynaptic corticospinal pathway. This facilitation was significantly larger in the early part of downstroke during bicycling than during tonic plantarflexion. This suggests that the increased MEP during downstroke was caused by changes in transmission in the fast monosynaptic corticospinal pathway. To investigate whether the depression of H reflexes in the late part of downstroke was caused by increased presynaptic inhibition of Ia afferents, the soleus H reflex was conditioned by stimulation of the femoral nerve. At a short interval (conditioning-test interval: -7 to -5 ms), the femoral nerve stimulation produced a facilitation of the H reflex that is mediated by the heteronymous monosynaptic Ia pathway from the femoral nerve to soleus motoneurons. Within the initial 0.5 ms after its onset, the size of this facilitation depends on the level of presynaptic inhibition of the Ia afferents, which mediate the facilitation. The size of the facilitation was strongly depressed in the late part of downstroke, compared with the early part of downstroke, suggesting that increased presynaptic inhibition was indeed responsible for the depression of the H reflex. These findings suggest that there is a selectively increased transmission in the fast monosynaptic corticospinal pathway to soleus motoneurons in early downstroke during bicycling. It would seem likely that one cause of this is increased excitability of the involved cortical neurons. The increased presynaptic inhibition of Ia afferents in late downstroke may be of importance for depression of stretch reflex activity before and during upstroke.