Neuromuscular fatigue of the elbow flexors during repeated maximal arm cycling sprints: the effects of forearm position.

Repeated sprint exercise (RSE) is often used to induce neuromuscular fatigue (NMF). It is currently not known whether NMF is influenced by different forearm positions during arm cycling RSE. The purpose of this study was to investigate the effects of a pronated versus supinated forearm position on elbow flexor NMF during arm cycling RSE. Participants (n = 12) completed ten 10-s maximal arm cycling sprints interspersed by 60 s of rest on 2 separate days using either a pronated or supinated forearm position. All sprints were performed on an arm cycle ergometer in a reverse direction. Prior to and following RSE, NMF measurements (i.e., maximal voluntary contraction (MVC), potentiated twitch (PT), electromyography median frequencies) were recorded. Sprint performance measures, ratings of perceived exertion (RPE) and pain were also recorded. Irrespective of forearm position, sprint performance decreased as sprint number increased. These decreases were accompanied by significant increases in RPE (p < 0.001, ηp2 = 0.869) and pain (p < 0.001, ηp2 = 0.745). Participants produced greater power output during pronated compared with supinated sprinting (p < 0.001, ηp2 = 0.728). At post-sprinting, the percentage decrease in elbow flexor MVC and PT force from pre-sprinting was significantly greater following supinated than pronated sprinting (p < 0.001), suggesting greater peripheral fatigue occurred in this position. The data suggest that supinated arm cycling RSE results in inferior performance and greater NMF compared with pronated arm cycling RSE. Novelty: NMF of the elbow flexors is influenced by forearm position during arm cycling RSE. Supinated arm cycling sprints resulted in worse repeated sprint performance and also greater NMF than pronated RSE.

Delayed-Onset Muscle Soreness and Topical Analgesic Alter Corticospinal Excitability of the Biceps Brachii.

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.

The effect of shoulder position on motor evoked and maximal muscle compound action potentials of the biceps brachii.

The purpose of the study was to assess the effect of shoulder position, 0° versus 90° shoulder flexion, on stimulation intensity and maximal muscle compound action potentials (Mmax) and motor evoked potentials (MEP) of the biceps brachii during both rest and 10% maximum voluntary contraction (MVC). Nine participants completed two experimental sessions with four conditions. During each condition, transcranial magnetic (TMS) and Erb's point stimulation were used to elicit MEPs and Mmax, respectively. During rest, the TMS intensity to elicit a MEP response (p<0.001), was significantly lower by 28.6±6.8%, in the 90° compared to the 0° position, but the stimulation intensity to elicit a Mmax was not different. MEP (p<0.001) and Mmax (p<0.001) amplitudes were significantly higher by 212.4±43.3% and 86.5±38.0%, respectively in the 90° compared to the 0° position. During 10% MVC the Mmax stimulation intensity (p=0.022), but not TMS intensity, was significantly lower by 7.4±3.8% in the 90° compared to the 0° position. Mmax (p<0.001) amplitudes were significantly higher by 92.2±20.2% in the 90° compared to the 0° position whereas MEP (p<0.001) amplitudes were significantly lower by 24.5±6.0% in the 90° compared to the 0° position. In conclusion, TMS intensity and Mmax intensity were both shoulder-position and state-dependent, whereas MEP and Mmax amplitudes were only shoulder position-dependent.

Neuromuscular fatigue during repeated sprint exercise: underlying physiology and methodological considerations.

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.

Upper and lower body responses to repeated cyclical sprints.

PURPOSE: To compare the physiological and perceptual responses of the upper and lower body to all-out cyclical sprints with short or long rest periods between sprints. METHODS: Ten recreationally trained males completed four 10 × 10 s sprint protocols in a randomized order: upper body with 30 s and 180 s of rest between sprints, and lower body with 30 s and 180 s of rest between sprints. Additionally, maximum voluntary contractions (MVC) were measured at pre-sprint and post-sprints 5 and 10. Normalized (% of first sprint) peak power, MVC, heart rate (HR) and rating of perceived exertion (RPE) were compared between upper and lower body within the same recovery period, and absolute values (Watts, bpm, RPE scores) were compared within the same body part and between recovery periods. RESULTS: Trivial differences were identified in normalized peak power, HR and RPE values between the upper and lower body in both recovery conditions (<2%, d ≤ 0.1), but MVC forces were better maintained with the upper body (∼9.5%, d = 1.0) in both recovery conditions. Absolute peak power was lower (∼147 Watts, d = 1.3), and HR was higher (∼10 bpm, d = 0.73) in the 30 s compared to 180 s condition in both the upper and lower body whereas RPE scores were similar (<0.6 RPE units, d ≤ 0.1). Despite the reductions in peak power, MVC forces were better maintained in the 30 s condition in both upper (2.5 kg, d = 0.4) and lower (7.5 kg, d = 0.7) body. CONCLUSIONS: Completing a commonly used repeated sprint protocol with the upper and lower body results in comparable normalized physiological and perceptual responses.

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.

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.

Corticospinal excitability to the biceps brachii and its relationship to postactivation potentiation of the elbow flexors.

We examined the effects of a submaximal voluntary elbow flexor contraction protocol on measures of corticospinal excitability and postactivation potentiation of evoked muscle forces and if these measures were state-dependent (rest vs. voluntary muscle contraction). Participants completed four experimental sessions where they rested or performed a 5% maximum voluntary contraction (MVC) of the elbow flexors prior to, immediately, and 5 min following a submaximal contraction protocol. During rest or 5% MVC, transcranial magnetic stimulation, transmastoid electrical stimulation, electrical stimulation of biceps brachii motor point and Erb's point were elicited to induce motor-evoked potentials (MEPs), cervicomedullary MEPs (CMEPs), potentiated twitch (PT) force, and maximal muscle compound action potential (Mmax), respectively prior to, immediately, and 5 min postcontraction protocol. MEP amplitudes increased (215 and 165%Mmax, P ≤ 0.03) only at 1 and 6s postcontraction protocol, respectively during rest but not 5% MVC CMEP amplitudes decreased during rest and 5% MVC (range:21-58%Mmax, P ≤ 0.04) for up to 81 sec postcontraction protocol. Peak twitch force increased immediately postcontraction protocol and remained elevated for 90 sec (range:122-147% increase, P < 0.05). There was a significant positive correlation between MEP and PT force during rest (r = 0.88, P = 0.01) and a negative correlation between CMEP and PT force during rest (r = -0.85, P < 0.02 and 5% MVC (r = -0.96, P < 0.01) immediately postcontraction protocol. In conclusion, the change in corticospinal and spinal excitability was state- and time-dependent whereas spinal excitability and postactivation potentiation were time-dependent following the contraction protocol. Changes in corticospinal excitability and postactivation potentiation correlated and were also state-dependent.