Estimation of critical end-test torque using neuromuscular electrical stimulation of the quadriceps in humans.

Characterization of critical power/torque (CP/CT) during voluntary exercise requires maximal effort, making difficult for those with neuromuscular impairments. To address this issue we sought to determine if electrically stimulated intermittent isometric exercise resulted in a critical end-test torque (ETT) that behaved similar to voluntary CT. In the first experiment participants (n = 9) completed four bouts of stimulated exercise at a 3:2 duty cycle, at frequencies of 100, 50, 25 Hz, and a low frequency below ETT (Sub-ETT; ≤ 15 Hz). The second experiment (n = 20) consisted of four bouts at a 2:2 duty cycle-two bouts at 100 Hz, one at an intermediate frequency (15-30 Hz), and one at Sub-ETT. The third experiment (n = 12) consisted of two bouts at 50 Hz at a 3:2 duty* cycle with proximal blood flow occlusion during one of the bouts. ETT torque was similar (p ≥ 0.43) within and among stimulation frequencies in experiment 1. No fatigue was observed during the Sub-ETT bouts (p > 0.05). For experiment 2, ETT was similar at 100 Hz and at the intermediate frequency (p ≥ 0.29). Again, Sub-ETT stimulation did not result in fatigue (p > 0.05). Altering oxygen delivery by altering the duty cycle (3:2 vs. 2:2; p = 0.02) and by occlusion (p < 0.001) resulted in lower ETT values. Stimulated exercise resulted in an ETT that was consistent from day-to-day and similar regardless of initial torque, as long as that torque exceeded ETT, and was sensitive to oxygen delivery. As such we propose it represents a parameter similar to voluntary CT.

Voluntary muscle activation and evoked volitional-wave responses as a function of torque.

INTRODUCTION: This study employed a unique stimulation paradigm which allowed for the simultaneous assessment of voluntary activation levels (VA) via twitch-interpolation, and the evoked V-wave responses of the plantar flexors during submaximal and maximal contractions. Test-retest reliability was also examined. METHODS: Fourteen participants repeated a stimulation protocol over four visits to assess VA and evoked V-wave amplitude across torque levels ranging from 20% to 100% MVC. MVC torque and EMG amplitude were also measured. RESULTS: VA increased nonlinearly with torque production and plateaued by 80% MVC. V-wave amplitude increased linearly from 20% to 100% MVC. There were no differences in any dependent variable across visits (p > 0.05). VA demonstrated moderate to substantial reliability across all torque levels (ICC = 0.76-0.91) while V-wave amplitude exhibited fair to moderate reliability from 40% to 100% (ICC = 0.48-0.74). DISCUSSION: We were able to reliably collect VA and the V-wave simultaneously in the plantar flexors. Collection of VA and V-wave during the same contraction provides distinct information regarding the contribution of motor-unit recruitment and descending cortico-spinal drive/excitability to force production.

Adaptations in antagonist co-activation: Role in the repeated-bout effect.

Eccentric exercise results in an adaptation which attenuates muscle damage from subsequent exercise-termed the "repeated-bout effect (RBE)." PURPOSE: Study examined antagonist co-activation and motor-unit recruitment strategy, assessed via dEMG, concomitant to the RBE. METHODS: Nine participants performed 5 sub-maximal isometric trapezoid (ramp-up, hold, ramp-down) contractions at force levels corresponding to 50% and 80% of maximal isometric strength (MVC). Surface EMG signals of the biceps brachii were decomposed into individual motor-unit action potential trains. The relationship between mean firing rate (MFR) of each motor-unit and its recruitment threshold (RT) was examined using linear regression. Eccentric exercise was then performed until biceps brachii MVC had decreased by ~40%. Surface EMG of the biceps and triceps were collected during eccentric exercise. MVC, range-of-motion (ROM), and delayed onset muscle soreness (DOMS) were measured 24-hours, 72-hours, and 1-week following eccentric exercise. Three weeks later all procedures were repeated. RESULTS: Changes in MVC (-32±14% vs -25±10%; p = 0.034), ROM (-11% vs 6%; p = 0.01), and DOMS (31.0±19mm vs 19±12mm; p = 0.015) were attenuated following the second bout of exercise. Triceps EMG was reduced (16.8±9.5% vs. 12.6±7.2%; p = 0.03) during the second bout of eccentric exercise. The slope (-0.60±0.13 vs -0.70±0.18; p = 0.029) and y-intercept (46.5±8.3 vs 53.3±8.8; p = 0.020) of the MFR vs. RT relationship was altered during contractions at 80% of MVC prior to the second bout of eccentric exercise. No changes were observed at 50% of MVC. CONCLUSION: A reduction in antagonist co-activation during the second bout of eccentric exercise suggests less total force was required to move an identical external load. This finding is supported by the increased negative slope coefficient and an increased y-intercept of the linear relationship between RT and MFR.

The effects of caffeine ingestion on exercise-induced hypoalgesia: A pilot study.

Exercise acutely reduces pain sensitivity, termed exercise-induced hypoalgesia (EIH). The mechanisms underlying EIH remain unclear. Caffeine, a non-specific adenosine receptor antagonist has been shown to attenuate EIH in animals-suggesting the involvement of the adenosinergic system. This pilot study investigated the effects of caffeine on pain sensitivity following cycling exercise in college-aged men. Pressure pain threshold (PPT) and thermal pain threshold (TPT) were assessed in thirteen low caffeine consuming men prior to ingestion of a counter-balanced 5mg·kg(-1) dose of caffeine or a placebo (Pre), 60min following ingestion (Post-In), and then following a 15min bout of cycling exercise (Post-Ex) at an intensity eliciting a quadriceps muscle pain rating of 3 out of 10. Nine of the men completed follow-up testing which was identical except that the exercise consisted of 10min of cycling eliciting a pain rating of 5 out of 10. Caffeine had no effect compared to placebo on PPT (p≥0.15) or TPT (p≥0.41) 60min following ingestion and following exercise. PPT increased from 599±176kPa to 648±202kPa (p=0.009) and from 578±217kPa to 666±278kPa (p=0.01) following 15 and 10min of cycling, respectively. TPT increased from 46.2±2.9°C to 46.8±2.6°C (p=0.008) following the 15min exercise bout, but did not change (46.4±3.6°C vs. 46.8±3.3°C; p=0.24) following the shorter, higher intensity exercise bout. The results from this study indicate cycling exercise reduces pain sensitivity, especially to pressure stimuli. Caffeine ingestion did not alter the EIH response-suggesting adenosine may not play a prominent role in the EIH response in humans.

Time-course of recovery of peak oxygen uptake after exercise-induced muscle damage.

V̇O2 peak has been shown to be reduced 48 h following exercise-induced muscle damage (EIMD), but it is unclear how long this reduction may persist. In this study eight endurance trained participants (21.5 ± 1.1 years old) performed a maximal exercise tests over 10-days followings EIMD. Cardiorespiratory variables were collected via open-circuit spirometry and soreness, maximal strength (MVC), motor-unit recruitment, and contractile properties were assessed prior to each test. MVC was reduced for up to 4-days (p ≤ 0.05) and soreness was evident for 10-days in the quadriceps (p < 0.05). V̇O2peak was reduced 7.4% 2-days post EIMD (55.5 ± 6.0 vs. 51.3 ± 5.8; p = 0.006) and remained reduced in 6 of 8 participants at 10-days post (p = 0.005). No relationship was found between changes in MVC, soreness, motor-unit recruitment, and contractile properties and changes in V̇O2peak (p > 0.05). EIMD resulted in small, but prolonged reductions in V̇O2peak. Our findings suggest mechanisms aside from force loss and soreness are primarily responsible for the reductions in V̇O2peak after EIMD.