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Foot equilibrium position controls partition of voluntary command to antagonists during foot oscillations
Fausto Baldissera1, Paolo Cavallari, Roberto Esposti
1Istituto di Fisiologia Umana II, Università degli Studi, Via Mangiagalli 32, 20113 Milano, Italy. fausto.baldissera@unimi.it
Abstract:
During low-frequency (< 1.5 Hz) voluntary oscillations of the foot, placed on a rotating platform, onset of the Tibialis Anterior (TA) EMG paradoxically phase-lags the onset of dorsiflexion, suggesting that initial dorsiflexion is sustained by recoil of elastic structures that were stretched during plantarflexion. It is argued that the lag would disappear if the EMG onset were referred to the foot passive equilibrium position rather than to the movement onset. This hypothesis was tested in ten subjects who, after assessment of foot equilibrium position, voluntarily oscillated their foot at various frequencies (0.2-3 Hz) over three angular ranges: a mid range (foot crossing the equilibrium symmetrically), a high range (whole excursion above equilibrium) and a low range (whole excursion below equilibrium). In the mid range, phase relations were measured between the crossing of equilibrium position and the onset of the TA EMG during dorsiflexion or the onset of Soleus EMG during plantarflexion. In both cases, the paradoxical lag of EMG on movement was absent, phase curves started around zero and could be well fitted by a second order model. Phase curves with similar features were also obtained in the high and low ranges (no crossing of equilibrium) but correlating the onset of the EMG burst to the onset of the related movement. Altogether, these findings show that in all ranges of the joint excursion, the homology is between the EMG onset and the moment when the foot draws away from equilibrium. Based on the observed pattern of muscular activation, we suggest that voluntary foot oscillation in any movement range is sustained by one sinusoidal central command that, when equilibrium is crossed, is clipped in two half-waves reciprocally distributed to the couple of antagonist muscles. A simple neural circuit for this operation is proposed.
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