2 research outputs found

    Maximal Voluntary Activation of the Elbow Flexors Is under Predicted by Transcranial Magnetic Stimulation Compared to Motor Point Stimulation Prior to and Following Muscle Fatigue

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    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

    Understanding corticospinal excitability to the biceps brachii during maximal repeated arm-cycling sprints

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    Studies investigating neuromuscular fatigue (NMF) induced by repeated sprint exercise primarily use a tonic contraction to assess corticospinal excitability (CSE). There is a lack of information about how CSE transiently changes with rapidly changing fatigue levels. Previous research has shown that CSE is dependent on a variety of factors, such as the targeted muscle, mode of exercise, hand position, cadence, cycling direction, and level of fatigue. No study has assessed CSE during repeated maximal arm-cycling sprints. The current study circumvents the limitations of a tonic contraction to assess CSE. We performed maximal repeated arm-cycling sprints using a custom-built cycle ergometer. Transcranial magnetic stimulation (TMS), transmastoid electrical stimulation (TMES), and brachial plexus stimulation (Erb’s point) were given during each sprint to determine how CSE to the biceps brachii was modulated during 5, approximately 20 second repeated sprints. The sprint protocol induced NMF as evidenced by mean power (p < 0.0001) and total work (p < 0.0001) dropping by 36.8% from sprint one to five respectively. There was a 4.57% decrease in TMES intensity required for the active motor threshold (AMT) from pre- (134.00 ± 31.52 mA) to post sprinting (124.17 ± 30.08 mA), t (12) = 3.445, p = 0.0055. Our findings suggest that our protocol increased spinal and peripheral excitability from pre to post sprinting, but not cortical because of the absence in change in MEP amplitudes from pre to post sprinting Changes at the spinal motoneuron and post-activation potentiation are likely mechanisms associated with the modulations
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