The effects of pain induced by blood flow occlusion in one leg on exercise tolerance and corticospinal excitability and inhibition of the contralateral leg in males.

Experiencing pain in one leg can alter exercise tolerance and neuromuscular fatigue (NMF) responses in the contralateral leg; however, the corticospinal modulations to nonlocal experimental pain induced by blood flow occlusion remain unknown. In three randomized visits, 13 male participants performed 25% of isometric maximal voluntary contraction (25%IMVC) to task failure with one leg preceded by (i) 6-min rest (CON), (ii) cycling at 80% of peak power output until task failure with the contralateral leg (CYCL), or (iii) CYCL followed by blood flow occlusion (OCCL) during 25%IMVC. NMF assessments (IMVC, voluntary activation [VA], and potentiated twitch [Qtw]) were performed at baseline and task failure. During the 25%IMVC, transcranial magnetic stimulations were performed to obtain motor-evoked potential (MEP), silent period (SP), and short intracortical inhibition (SICI). 25%IMVC was the shortest in OCCL (105 ± 50s) and shorter in CYCL (154 ± 68 s) than CON (219 ± 105 s) (p < 0.05). IMVC declined less after OCCL (-24 ± 19%) and CYCL (-27 ± 18%), then CON (-35 ± 11%) (p < 0.05). Qtw declined less in OCCL (-40 ± 25%) compared to CYCL (-50 ± 22%) and CON (-50 ± 21%) (p < 0.05). VA was similar amongst conditions. MEP and SP increased and SICI decreased throughout the task, while SP was longer for OCCL compared to CYC condition (p < 0.05). The results suggest that pain in one leg diminishes contralateral limb exercise tolerance and NMF development and modulate corticospinal inhibition in males. Novelty: Pain in one leg diminished MVC and twitch force decline in the contralateral limb. Experimental pain induced by blood flow occlusion may modulation corticospinal inhibition of the neural circuitries innervating the contralateral exercise limb.

Power loss is attenuated following a second bout of high-intensity eccentric contractions due to the repeated bout effect's protection of rate of torque and velocity development.

High-intensity unaccustomed eccentric contractions result in weakness and power loss because of fatigue and muscle damage. Through the repeated bout effect (RBE), adaptations occur, then damage and weakness are attenuated following a subsequent bout. However, it is unclear whether the RBE protects peak power output. We investigated the influence of the RBE on power production and estimated fatigue- and damage-induced neuromuscular impairments following repeated high-intensity eccentric contractions. Twelve healthy adult males performed 5 sets of 30 maximal eccentric elbow flexions and repeated an identical bout 4 weeks later. Recovery was tracked over 7 days following both bouts. Reduced maximum voluntary isometric contraction torque, and increased serum creatine kinase and self-reported soreness indirectly inferred muscle damage. Peak isotonic power, time-dependent measures - rate of velocity development (RVD) and rate of torque development (RTD) - and several electrophysiological indices of neuromuscular function were assessed. The RBE protected peak power, with a protective index of 66% 24 h after the second eccentric exercise bout. The protection of power also related to preserved RVD (R2 = 0.61, P < 0.01) and RTD (R2 = 0.39, P < 0.01). Furthermore, the RBE's protection against muscle damage permitted the estimation of fatigue-associated neuromuscular performance decrements following eccentric exercise. Novelty: The repeated bout effect protects peak isotonic power. Protection of peak power relates to preserved rates of torque and velocity development, but more so rate of velocity development. The repeated bout effect has little influence on indices of neuromuscular fatigue.

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.

Caffeine increases peripheral fatigue in low- but not in high-performing cyclists.

The influence of cyclists' performance levels on caffeine-induced increases in neuromuscular fatigue after a 4-km cycling time trial (TT) was investigated. Nineteen cyclists performed a 4-km cycling TT 1 h after ingesting caffeine (5 mg·kg-1) or placebo (cellulose). Changes from baseline to after exercise in voluntary activation (VA) and potentiated 1 Hz force twitch (Qtw,pot) were used as markers of central and peripheral fatigue, respectively. Participants were classified as "high performing" (HP, n = 8) or "low performing" (LP, n = 8) in accordance with their performance in a placebo trial. Compared with placebo, caffeine increased the power, anaerobic mechanical power, and anaerobic work, reducing the time to complete the trial in both groups (p < 0.05). There was a group versus supplement and a group versus supplement versus trial interaction for Qtw,pot, in which the postexercise reduction was greater after caffeine compared with placebo in the LP group (Qtw,pot = -34% ± 17% vs. -21% ± 11%, p = 0.02) but not in the HP group (Qtw,pot = -22% ± 8% vs. -23% ± 10%, p = 0.64). There was no effect of caffeine on VA, but there was a group versus trial interaction with lower postexercise values in the LP group than in the HP group (p = 0.03). Caffeine-induced improvement in 4-km cycling TT performance seems to come at the expense of greater locomotor muscle fatigue in LP but not in HP cyclists. Novelty Caffeine improves exercise performance at the expense of a greater end-exercise peripheral fatigue in low-performing athletes. Caffeine-induced improvement in exercise performance does not affect end-exercise peripheral fatigue in high-performing athletes. High-performing athletes seem to have augmented tolerance to central fatigue during a high-intensity time trial.

Acetaminophen ingestion improves muscle activation and performance during a 3-min all-out cycling test.

Acute acetaminophen (ACT) ingestion has been shown to enhance cycling time-trial performance. The purpose of this study was to assess whether ACT ingestion enhances muscle activation and critical power (CP) during maximal cycling exercise. Sixteen active male participants completed two 3-min all-out tests against a fixed resistance on an electronically braked cycle ergometer 60 min after ingestion of 1 g of ACT or placebo (maltodextrin, PL). CP was estimated as the mean power output over the final 30 s of the test and W' (the curvature constant of the power-duration relationship) was estimated as the work done above CP. The femoral nerve was stimulated every 30 s to measure membrane excitability (M-wave) and surface electromyography (EMGRMS) was recorded continuously to infer muscle activation. Compared with PL, ACT ingestion increased CP (ACT: 297 ± 32 W vs. PL: 288 ± 31 W, P < 0.001) and total work done (ACT: 66.4 ± 6.5 kJ vs. PL: 65.4 ± 6.4 kJ, P = 0.03) without impacting W' (ACT: 13.1 ± 2.9 kJ vs. PL: 13.6 ± 2.4 kJ, P = 0.19) or the M-wave amplitude (P = 0.66) during the 3-min all-out cycling test. Normalised EMGRMS amplitude declined throughout the 3-min protocol in both PL and ACT conditions; however, the decline in EMGRMS amplitude was attenuated in the ACT condition, such that the EMGRMS amplitude was greater in ACT compared with PL over the last 60 s of the test (P = 0.04). These findings indicate that acute ACT ingestion might increase performance and CP during maximal cycling exercise by enhancing muscle activation.

Acute ibuprofen ingestion does not attenuate fatigue during maximal intermittent knee extensor or all-out cycling exercise.

Recent research suggests that acute consumption of pharmacological analgesics can improve exercise performance, but the ergogenic potential of ibuprofen (IBP) administration is poorly understood. This study tested the hypothesis that IBP administration would enhance maximal exercise performance. In one study, 13 physically active males completed 60 × 3-s maximal voluntary contractions (MVCs) of the knee extensors interspersed with 2-s passive recovery periods, on 2 occasions, with the critical torque (CT) estimated as the mean torque over the last 12 contractions (part A). In another study, 16 active males completed two 3-min all-out tests against a fixed resistance on an electronically braked cycle ergometer, with the critical power estimated from the mean power output over the final 30 s of the test (part B). All tests were completed 60 min after ingestion of maltodextrin (placebo, PL) or 400 mg of IBP. Peripheral nerve stimulation was administered at regular intervals and electromyography was measured throughout. For part A, mean torque (IBP: 60% ± 13% of pre-exercise MVC; PL: 58% ± 14% of pre-exercise MVC) and CT (IBP: 41% ± 16% of pre-exercise MVC; PL: 40% ± 15% of pre-exercise MVC) were not different between conditions (P > 0.05). For part B, end-test power output (IBP: 292 ± 28 W; PL: 288 ± 31 W) and work done (IBP: 65.9 ± 5.9 kJ; PL: 65.4 ± 6.4 kJ) during the 3-min all-out cycling tests were not different between conditions (all P > 0.05). For both studies, neuromuscular fatigue declined at a similar rate in both conditions (P > 0.05). In conclusion, acute ingestion of 400 mg of IBP does not improve single-leg or maximal cycling performance in healthy humans.