Fatigue and muscle pain induced in a remote muscle group has been shown to alter neuromuscular performance in exercising muscles. Inhibitory neural feedback associated with activation of mechano- and metabo-sensitive muscle afferents has been implicated in this phenomenon. The present study aimed to quantify and compare the effects of pre-induced fatigue and concurrent rising pain (evoked by muscle ischaemia) on the contralateral leg exercise capacity, neuromuscular performance, and corticomotor excitability and inhibition of knee extensor muscles. Pre-induced fatigue in one leg had a greater detrimental effect than the concurrent rising pain on the contralateral limb cycling capacity. Furthermore, pre-induced fatigue, but not concurrent rising pain, reduced corticospinal inhibition recorded from tested contralateral muscles. Regardless of the origin or mechanisms modulating sensory afferents during single-leg cycling exercise (i.e. pre-induced fatigue vs. concurrent rising pain), the limit of exercise tolerance remained the same and exercise was terminated upon achievement of a sensory tolerance limit. Individuals often need to maintain voluntary contractions during high intensity exercise in the presence of fatigue and pain. This investigation examined the effects of pre-induced fatigue and concurrent rising pain (evoked by muscle ischaemia) in one leg on motor fatigability and corticospinal excitability/inhibition of the contralateral limb. Twelve healthy males undertook four experimental protocols including unilateral cycling to task failure at 80% of peak power output with: (i) the right-leg (RL); (ii) the left-leg (LL); (iii) RL immediately preceded by LL protocol (FAT-RL); and (iv) RL when blood flow was occluded in the contralateral (left) leg (PAIN-RL). Participants performed maximal and submaximal 5s right-leg knee extensions during which transcranial magnetic and femoral nerve electrical stimuli were delivered to elicit motor-evoked and compound muscle action potentials, respectively. The pre-induced fatigue reduced the right leg cycling time-to-task failure (mean±SD; 332±137s) to a greater extent than concurrent pain (460±158s), compared to RL (580±226s) (P< 0.001). The maximum voluntary contraction force declined less following FAT-RL (P<0.019) and PAIN-RL (P<0.032) compared to RL. Voluntary activation declined and the corticospinal excitability recorded from knee extensors increased similarly after the three conditions (P<0.05). However, the pre-induced fatigue, but not concurrent pain, reduced corticospinal inhibition compared to RL (P<0.05). These findings suggest that regardless of the origin and/or mechanisms modulating sensory afferent feedback during single-leg cycling (e.g. pre-induced fatigue vs. concurrent rising pain), the limit of exercise tolerance remains the same, suggesting that exercise will be terminated upon achievement of sensory tolerance limit.
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