Neuromuscular fatigue occurs when an individual's capacity to produce force or power is impaired. Repeated sprint exercise requires an individual to physically exert themselves at near-maximal to maximal capacity for multiple short-duration bouts, is extremely taxing on the neuromuscular system, and consequently leads to the rapid development of neuromuscular fatigue. During repeated sprint exercise the development of neuromuscular fatigue is underlined by a combination of central and peripheral fatigue. However, there are a number of methodological considerations that complicate the quantification of the development of neuromuscular fatigue. The main goal of this review is to synthesize the results from recent investigations on the development of neuromuscular fatigue during repeated sprint exercise. Hence, we summarize the overall development of neuromuscular fatigue, explain how recovery time may alter the development of neuromuscular fatigue, outline the contributions of peripheral and central fatigue to neuromuscular fatigue, and provide some methodological considerations for quantifying neuromuscular fatigue during repeated sprint exercise.

The purpose of this study was to examine the effect of shoulder position on corticospinal excitability (CSE) of the biceps brachii during rest and a 10% maximal voluntary contraction (MVC). Participants ( = 9) completed two experimental sessions with four conditions: ) rest, 0° shoulder flexion;) 10% MVC, 0° shoulder flexion; ) rest, 90° shoulder flexion; and) 10% MVC, 90° shoulder flexion. Transcranial magnetic, transmastoid electrical, and Erb's point stimulation were used to induce motor-evoked potentials (MEPs), cervicomedullary MEPs (CMEPs), and maximal muscle compound potentials (M), respectively, in the biceps brachii in each condition. At rest, MEP, CMEP, and M amplitudes increased ( < 0.01) by 509.7 ± 118.3%, 113.3 ± 28.3%, and 155.1 ± 47.9%, respectively, at 90° compared with 0°. At 10% MVC, MEP amplitudes did not differ ( = 0.08), but CMEP and M amplitudes increased ( < 0.05) by 32.3 ± 10.5% and 127.9 ± 26.1%, respectively, at 90° compared with 0°. MEP/M increased ( < 0.01) by 224.0 ± 99.1% at rest and decreased ( < 0.05) by 51.3 ± 6.7% at 10% MVC at 90° compared with 0°. CMEP/M was not different ( = 0.22) at rest but decreased ( < 0.01) at 10% MVC by 33.6 ± 6.1% at 90° compared with 0°. EMG increased ( < 0.001) by 8.3 ± 2.0% at rest and decreased ( < 0.001) by 21.4 ± 4.4% at 10% MVC at 90° compared with 0°. In conclusion, CSE of the biceps brachii was dependent on shoulder position, and the pattern of change was altered within the state in which it was measured. The position-dependent changes in M amplitude, EMG, and CSE itself all contribute to the overall change in CSE of the biceps brachii. We demonstrate that when the shoulder is placed into two common positions for determining elbow flexor force and activation, corticospinal excitability (CSE) of the biceps brachii is both shoulder position and state dependent. At rest, when the shoulder is flexed from 0° to 90°, supraspinal factors predominantly alter CSE, whereas during a slight contraction, spinal factors predominantly alter CSE. Finally, the normalization techniques frequently used by researchers to investigate CSE may under- and overestimate CSE when shoulder position is changed.

Transcranial magnetic (TMS) and motor point stimulation have been used to determine voluntary activation (VA). However, very few studies have directly compared the two stimulation techniques for assessing VA of the elbow flexors. The purpose of this study was to compare TMS and motor point stimulation for assessing VA in non-fatigued and fatigued elbow flexors. Participants performed a fatigue protocol that included twelve, 15 s isometric elbow flexor contractions. Participants completed a set of isometric elbow flexion contractions at 100, 75, 50, and 25% of maximum voluntary contraction (MVC) prior to and following fatigue contractions 3, 6, 9, and 12 and 5 and 10 min post-fatigue. Force and EMG of the bicep and triceps brachii were measured for each contraction. Force responses to TMS and motor point stimulation and EMG responses to TMS (motor evoked potentials, MEPs) and Erb's point stimulation (maximal M-waves, Mmax) were also recorded. VA was estimated using the equation: VA% = (1−SITforce/PTforce) × 100. The resting twitch was measured directly for motor point stimulation and estimated for both motor point stimulation and TMS by extrapolation of the linear regression between the superimposed twitch force and voluntary force. MVC force, potentiated twitch force and VA significantly (p < 0.05) decreased throughout the elbow flexor fatigue protocol and partially recovered 10 min post fatigue. VA was significantly (p < 0.05) underestimated when using TMS compared to motor point stimulation in non-fatigued and fatigued elbow flexors. Motor point stimulation compared to TMS superimposed twitch forces were significantly (p < 0.05) higher at 50% MVC but similar at 75 and 100% MVC. The linear relationship between TMS superimposed twitch force and voluntary force significantly (p < 0.05) decreased with fatigue. There was no change in triceps/biceps electromyography, biceps/triceps MEP amplitudes, or bicep MEP amplitudes throughout the fatigue protocol at 100% MVC. In conclusion, motor point stimulation as opposed to TMS led to a higher estimation of VA in non-fatigued and fatigued elbow flexors. The decreased linear relationship between TMS superimposed twitch force and voluntary force led to an underestimation of the estimated resting twitch force and thus, a reduced VA.

Introduction The interactive effect of delayed-onset muscle soreness (DOMS) and a topical analgesic on corticospinal excitability was investigated. Methods Thirty-two participants completed Experiments A (no DOMS) and B (DOMS). For each experiment, participants were randomly assigned to two groups: 1) topical analgesic gel (topical analgesic, n = 8), or 2) placebo gel (placebo, n = 8) group. Before the application of gel (pregel), as well as 5, 15, 30, and 45 min postgel, motor-evoked potential (MEP) area, latency, and silent period, as well as cervicomedullary MEP and maximal compound motor unit action potential areas and latencies were measured. In addition, pressure–pain threshold (PPT) was measured pre-DOMS and at the same timepoints in experiment B. Results In experiment A, neither group showed a significant change for any outcome measure. In experiment B, both groups exhibited a significant decrease in PPT from pre-DOMS to pregel. After the application of topical analgesic, but not placebo, there was a significant increase in PPT at 45 min postgel, respectively, compared with pregel and a main effect of time for the silent period to increase compared with pregel. Participants with DOMS had reduced MEP and cervicomedullary MEP areas and increased corticospinal silent periods compared with those who did not have DOMS. Conclusions These findings suggest that DOMS reduced corticospinal excitability and after the administration of menthol-based topical analgesic, there was a reduction in pain, which was accompanied by increased corticospinal inhibition.

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