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1 Laboratory of Applied Biology, Universite Libre de Bruxelles, Brussels, Belgium
2 Department of Physical Education and Sport Science, Aristotle University of Thessaloniki, Thessaloniki, Greece
* To whom correspondence should be addressed. E-mail: jduchat{at}ulb.ac.be.
This study examined the involvement of spinal mechanisms in the control of coactivation during a sustained contraction of the ankle dorsiflexors at 50% of maximal voluntary contraction (MVC). Changes in the surface electromyogram (EMG) of the tibialis anterior (TA) and of two antagonist muscles, the soleus (Sol) and lateral gastrocnemius (LG), were investigated during and after a fatigue task. Concurrently, the compound action potential (M-wave) and the Hoffmann reflex (H-reflex) of the Sol and LG were recorded. The results showed that the torque of the ankle dorsiflexors and the average EMG (aEMG) of the TA during MVC declined by 40.9 ± 17.7% (mean ± SD; P< 0.01) and 37.0 ± 19.9% (P<0.01), respectively, at task failure. During the submaximal fatiguing contraction, the aEMG of both the agonist and antagonist muscles increased, leading to a nearly constant ratio at the end of the contraction when normalized to post-fatigue values. In contrast to the monotonic increase in aEMG of the antagonist muscles, the excitability of their spinal reflex pathways exhibited a biphasic modulation. The amplitude of the Sol and LG H-reflexes increased to 147.5 ± 52.9% (P<0.05) and 166.7 ± 74.9% (P<0.01), respectively, during the first 20% of the contraction and then subsequently declined to 66.3 ± 44.8 % and 74.4 ± 44.2% of their initial values. In conclusion, the results show that antagonist coactivation did not contribute to task failure. The different changes in voluntary EMG activity and spinal reflex excitability in the antagonist muscles during the fatiguing contraction support the concept that the level of coactivation is controlled by supraspinal rather than spinal mechanisms. The findings indicate, however, that antagonist coactivation cannot simply be mediated by a central descending "common drive" to the motor neuron pools of the agonistantagonist muscle pairs. Rather they suggest a more subtle regulation of the drive, possibly through presynaptic mechanisms, to the motor neurons that innervate the antagonist muscles.
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