Abstract

PurposeThis study investigated the supraspinal processes of fatigue of the quadriceps muscle in response to repeated cycling sprints.MethodsTwelve active individuals performed 10 × 6-s “all-out” sprints on a cycle ergometer (recovery = 30 s), followed 6 min later by 5 × 6-s sprints (recovery = 30 s). Transcranial magnetic and electrical femoral nerve stimulations during brief (5-s) and sustained (30-s) isometric contractions of the knee extensors were performed before and 3 min post-exercise.ResultsMaximal strength of the knee extensors decreased during brief and sustained contractions (∼11% and 9%, respectively; P<0.001). Peripheral and cortical voluntary activation, motor evoked potential amplitude and silent period duration responses measured during briefs contractions were unaltered (P>0.05). While cortical voluntary activation declined (P<0.01) during the sustained maximal contraction in both test sessions, larger reductions occurred (P<0.05) after exercise. Lastly, resting twitch amplitude in response to both femoral nerve and cortical stimulations was largely (> 40%) reduced (P<0.001) following exercise.ConclusionThe capacity of the motor cortex to optimally drive the knee extensors following a repeated-sprint test was shown in sustained, but not brief, maximal isometric contractions. Additionally, peripheral factors were largely involved in the exercise-induced impairment in neuromuscular function, while corticospinal excitability was well-preserved.

Highlights

  • Most previous explanations of fatigue during repeated-sprint exercise have focused on muscular factors associated with cellular mechanisms [1]

  • Fatigue induced by repeated-sprint efforts has been related to neural factors, as demonstrated by reduced muscle activation levels inferred from muscle functional magnetic resonance imaging [4], surface EMG [5,6] or peripheral motor nerve (PMN) stimulation techniques

  • A decrease in raw EMG activity across repetitions could be due to peripheral alterations in the transmission and propagation of the EMG signal, this study reported a significant decrement in both the normalized EMG activity (RMS/M-wave ratio) and the percentage of voluntary activation (VA) during a subsequent maximal isometric voluntary contraction [7]

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Summary

Introduction

Most previous explanations of fatigue during repeated-sprint exercise have focused on muscular factors associated with cellular mechanisms [1]. A decrease in raw EMG activity across repetitions could be due to peripheral alterations in the transmission and propagation of the EMG signal, this study reported a significant decrement in both the normalized EMG activity (RMS/M-wave ratio) and the percentage of voluntary activation (VA) during a subsequent maximal isometric voluntary contraction [7] Taken together, these observations suggest that the decrement in EMG induced by repeated sprints was partly linked to a central deficit in muscle activation. These observations suggest that the decrement in EMG induced by repeated sprints was partly linked to a central deficit in muscle activation This was further evidenced by a significant decrease in both the percentage of peripheral voluntary activation (VA) and normalized EMG activity (RMS/M-wave ratio) during a maximal isometric voluntary contraction of the knee extensors performed within 5 min of the last sprint bout [7]. A limitation of these conventional methods is that the precise locus of the impaired neural drive to the muscle, which can theoretically be mediated at any site proximal to the motor axons, cannot be ascertained [8]

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