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  • Title: Decline in voluntary activation contributes to reduced maximal performance of fatigued human lower limb muscles.
    Author: Mileva KN, Sumners DP, Bowtell JL.
    Journal: Eur J Appl Physiol; 2012 Dec; 112(12):3959-70. PubMed ID: 22434254.
    Abstract:
    In upper limb muscles, altered corticospinal excitability and reduction in neural drive are observed in parallel with peripheral fatigue during prolonged and/or repeated contractions. However, the fatigue-induced adaptations of central and peripheral elements and their relative contribution to lower limb muscle performance are yet to be fully explored. In the present study, corticospinal excitability and peripheral contractility of ankle flexor muscles were quantified before, during and after repeated brief unilateral maximal dorsiflexions to fatigue in eleven healthy volunteers. Transcranial magnetic stimulation of the motor cortex area related to lower limb muscles was performed, and the evoked twitch and EMG responses in tibialis anterior (TA) and soleus (SOL) were measured. The motor evoked potentials (MEPs) in fatigued TA during post-exercise maximal dorsiflexions were smaller (-20 ± 6 %, p = 0.026) and remained depressed for at least 5 min. Post-exercise MEPs in fatigued SOL and silent periods in TA and SOL were not different compared to pre-exercise. These changes were accompanied by lower voluntary torque (-8 ± 3 %, p = 0.013), estimated resting twitch (-36 ± 5 %, p = 0.003) and voluntary activation (-17 ± 9 %, p = 0.021) versus pre-exercise. During last versus first maximal contraction in the fatiguing protocol lower voluntary torque (-40 ± 4 %, p = 0.003), higher MEP amplitudes (>+49 %, p < 0.021) and longer silent periods (>+24 %, p < 0.004) were recorded in both muscles. Decreased corticospinal excitability contributes significantly to the reduced maximal performance of fatigued lower limb muscles. During prolonged intermittent maximal dorsiflexions the performance of ankle muscles declines despite enhanced corticospinal excitability presumably due to deficient descending drive and/or spinal motoneuron responsiveness to the cortical drive.
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