During fatiguing voluntary contractions, the excitability of motoneurons innervating arm muscles decreases. However, the behavior of motoneurons innervating quadriceps muscles is unclear. Findings may be inconsistent because descending cortical input influences motoneuron excitability and confounds measures during exercise. To overcome this limitation, we examined effects of fatigue on quadriceps motoneuron excitability tested during brief pauses in descending cortical drive after transcranial magnetic stimulation (TMS). Participants ( n = 14) performed brief (~5-s) isometric knee extension contractions before and after a 10-min sustained contraction at ~25% maximal electromyogram (EMG) of vastus medialis (VM) on one ( n = 5) or two ( n = 9) days. Electrical stimulation over thoracic spine elicited thoracic motor evoked potentials (TMEP) in quadriceps muscles during ongoing voluntary drive and 100 ms into the silent period following TMS (TMS-TMEP). Femoral nerve stimulation elicited maximal M-waves (M). On the 2 days, either large (~50% M) or small (~15% M) TMS-TMEPs were elicited. During the 10-min contraction, VM EMG was maintained ( P = 0.39), whereas force decreased by 52% (SD 13%) ( P < 0.001). TMEP area remained unchanged ( P = 0.9), whereas large TMS-TMEPs decreased by 49% (SD 28%) ( P = 0.001) and small TMS-TMEPs by 71% (SD 22%) ( P < 0.001). This decline was greater for small TMS-TMEPs ( P = 0.019; n = 9). Therefore, without the influence of descending drive, quadriceps TMS-TMEPs decreased during fatigue. The greater reduction for smaller responses, which tested motoneurons that were most active during the contraction, suggests a mechanism related to repetitive activity contributes to reduced quadriceps motoneuron excitability during fatigue. By contrast, the unchanged TMEP suggests that ongoing drive compensates for altered motoneuron excitability. NEW & NOTEWORTHY We provide evidence that the excitability of quadriceps motoneurons decreases with fatigue. Our results suggest that altered intrinsic properties brought about by repetitive activation of the motoneurons underlie their decreased excitability. Furthermore, we note that testing during voluntary contraction may not reflect the underlying depression of motoneuron excitability because of compensatory changes in ongoing voluntary drive. Thus, this study provides evidence that processes intrinsic to the motoneuron contribute to muscle fatigue of the knee extensors.

PurposeTo examine quadriceps muscle fatigue and central motor output during fatiguing single joint exercise at 40% and 80% maximal torque output in resistance trained men.MethodTen resistance trained men performed fatiguing isometric knee extensor exercise at 40% and 80% of maximal torque output. Maximal torque, rate of torque development, and measures of central motor output and peripheral muscle fatigue were recorded at two matched volumes of exercise, and after a final contraction performed to exhaustion. Central motor output was quantified from changes in voluntary activation, normalized surface electromyograms (EMG), and V-waves. Quadriceps muscle fatigue was assessed from changes in the size and shape of the resting potentiated twitch (Q.pot.tw). Central motor output during the exercise protocols was estimated from EMG and interpolated twitches applied during the task (VAsub).ResultsGreater reductions in maximal torque and rate of torque development were observed during the 40% protocol (p<0.05). Maximal central motor output did not change for either protocol. For the 40% protocol reductions from pre-exercise in rate and amplitude variables calculated from the Q.pot.tw between 66.2 to 70.8% (p<0.001) exceeded those observed during the 80% protocol (p<0.01). V-waves only declined during the 80% protocol between 56.8 ± 35.8% to 53.6 ± 37.4% (p<0.05). At the end of the final 80% contraction VAsub had increased from 91.2 ± 6.2% to 94.9 ± 4.7% (p = 0.005), but a greater increase was observed during the 40% contraction where VAsub had increased from 67.1 ± 6.1% to 88.9 ± 9.6% (p<0.001).ConclusionMaximal central motor output in resistance trained men is well preserved despite varying levels of peripheral muscle fatigue. Upregulated central motor output during the 40% contraction protocol appeared to elicit greater peripheral fatigue. V-waves declines during the 80% protocol suggest intensity dependent modulation of the Ia afferent pathway.

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Acute intermittent hypoxia (AIH) induces persistent increases in output from rat phrenic motoneurones. Studies in people with spinal cord injury (SCI) suggest that AIH improves limb performance, perhaps via postsynaptic changes at corticomotoneuronal synapses. We assessed whether limb motoneurone output in response to reflex and descending synaptic activation is facilitated after one session of AIH in healthy able-bodied volunteers. Fourteen participants completed two experimental days, with either AIH or a sham intervention (randomised crossover design). We measured H-reflex recruitment curves and homosynaptic post-activation depression (HPAD) of the H-reflex in soleus, and motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation (TMS) and their recruitment curves in first dorsal interosseous. All measurements were performed at rest and occurred at baseline, 0, 20, 40 and 60 min post-intervention. The intervention was 30 min of either normoxia (sham, F iO 2 ≈ 0.21) or AIH (alternate 1-min hypoxia [F iO 2 ≈ 0.09], 1-min normoxia). After AIH, the H-reflex recruitment curve shifted leftward. Lower stimulation intensities were needed to evoke 5%, 50% and 99% of the maximal H-reflex at 40 and 60 min after AIH (P < 0.04). The maximal H-reflex, recruitment slope and HPAD were unchanged after AIH. MEPs evoked by constant intensity TMS were larger 40 min after AIH (P = 0.027).There was no change in MEP recruitment or the maximal MEP. In conclusion, some measures of the evoked responses from limb motoneurones increased after a single AIH session, but only at discrete time points. It is unclear to what extent these changes alter functional performance.

PurposeIn two concurrent studies, we aimed to a) confirm the acute effect of 0.3 g·kg-1 body weight (BW) sodium bicarbonate (NaHCO3) supplementation on central and peripheral mechanisms associated with explosive power (Study 1) and b) determine whether chronic NaHCO3 supplementation would improve the adaptive response of the neuromuscular system during a 10-week resistance training program (Study 2).MethodsEight resistance trained participants volunteered after providing written consent. The experimental design consisted of a week of baseline testing, followed by ten weeks of training with progress measures performed in Week 5. Study 1 involved neuromuscular measurements before and after the leg extension portion of a power based training session performed in Week 1. Changes in maximal torque (MVT) and rates of torque development (RTD), along with other variables derived from femoral nerve stimulation (e.g. voluntary activation, neural recruitment) were analysed to determine the extent of fatigue under NaHCO3 or placebo conditions. Changes in these same variables, coupled with functional 1-repetition maximum leg extension strength, were measured in Study 2 from baseline (Week 0) to Week 5, and again at Week 10.Results and conclusionIn Study 1, we observed a decline after the leg extension task in both MVT (~ 30%) and rates of torque production (RTD) irrespective of acid-base status, however the decline in maximal RTD (RTDMAX) was nearly 20% less in the NaHCO3 condition when compared to placebo (mean difference of 294.8 ± 133.4 Nm·s-1 (95% CI -583.1 to -6.5 Nm, p < 0.05)). The primary finding in Study 2, however, suggests that introducing NaHCO3 repeatedly during a 10-week RT program does not confer any additional benefit to the mechanisms (and subsequent adaptive processes) related to explosive power production.

The premise of eliciting the greatest acute fatigue is accepted and used for designing programs that include excessive, potentially dangerous volumes of high-intensity resistance exercise. There is no evidence examining acute fatigue and neuromuscular responses throughout multiple sets of moderate-to-high intensity resistance exercise. Fifteen resistance-trained male subjects performed a single exercise session using 8 sets of Bulgarian split squats performed at 75% maximal force output. Maximal force output (N) was measured after every set of repetitions. Electromyographic (EMG) activity of vastus lateralis was monitored during all force trials and exercise repetitions. Repetitions per set decreased from the first to the third set (p< 0.001). Maximal force output decreased from preexercise to set 4 (p < 0.001). Electromyographic amplitudes during exercise did not change. Secondary subgroup analysis was performed based on the presence, or not, of a fatigue plateau (<5% reductions in maximal force output in subsequent sets). Nine participants exhibited a fatigue plateau, and 6 did not. Participants who plateaued performed less first-set repetitions, accrued less total volume, and did not exhibit increases in EMG amplitudes during exercise. Initial strength levels and neuromuscular demand of the exercise was the same between the subgroups. These data suggest that there are individual differences in the training session responses when prescribing based off a percentage of maximal strength. When plateaus in fatigue and repetitions per set are reached, subsequent sets are not likely to induce greater fatigue and muscle activation. High-volume resistance exercise should be carefully prescribed on an individual basis, with intrasession technique and training responsiveness continually monitored.

Introduction Fatigue-related group III/IV muscle afferent firing from agonist, antagonist or distal muscles impairs the ability to drive the elbow flexors maximally, that is, reduces voluntary activation. In the lower limb, the effect of feedback from distal muscles on the proximal knee extensors is unknown. Here, we test whether maintained group III/IV afferent feedback from the plantarflexor muscles reduces voluntary activation of the knee extensors. Methods On 2 d, voluntary activation of the knee extensors during maximal voluntary contractions (MVCs) was assessed in 12 participants before and after a 3-min fatiguing task of the plantarflexors. On 1 d, an inflatable cuff around the calf occluded blood flow for 2 min immediately postexercise (cuff day). The other day had no occlusion (no-cuff day). Supramaximal stimulation of the femoral nerve elicited superimposed twitches during MVC of the knee extensors and resting twitches 2 to 3 s after relaxation. Pain (0–10 point scale) was reported throughout. Results In the 2 min after the 3-min fatiguing plantarflexor task, voluntary activation was 5.3% (SD, 7%) lower on the cuff day than on the no-cuff day (P = 0.045), and MVC force was reduced by 13% (SD, 16%) (P = 0.021). The resting twitch was similar on both days (P = 0.98). Pain rated 4.9 points higher with the cuff inflated (P = 0.001). Conclusions Maintained group III/IV afferent feedback from the fatigued plantarflexor muscles reduced maximal force and voluntary activation of the unfatigued knee extensors, suggesting that afferents from the calf act centrally to inhibit the ability to drive the motoneurones of the knee extensors.

We examined if transcranial magnetic stimulation (TMS) is a valid tool for assessment of voluntary activation of the knee extensors in healthy individuals. Maximal M-waves (Mmax) of vastus lateralis (VL) were evoked with electrical stimulation of femoral nerve (FNS); Mmax of medial hamstrings (HS) was evoked with electrical stimulation of sciatic nerve branches; motor evoked potentials (MEPs) of VL and HS were evoked with TMS; superimposed twitches (SIT) of knee extensors were evoked with FNS and TMS. In Study 1, TMS intensity (69% output(SD 5)) was optimized for MEP sizes, but guidelines for test validity could not be met. Agonist VL MEPs were too small (51.4% Mmax(SD 11.9); guideline ≥70% Mmax) and antagonist HS MEPs were too big (16.5% Mmax(SD 10.3); guideline <10% Mmax). Consequently, the TMS estimated resting twitch (99.1 N(SD 37.2)) and FNS resting twitch (142.4 N(SD 41.8)) were different. In Study 2, SITs at 90% maximal voluntary contraction (MVC) were similar between TMS (16.1 N(SD 10.3)) and FNS (20.9 N(SD 16.7)), when TMS intensity was optimized for this purpose, suggesting a procedure that combines TMS SITs with FNS resting twitches could be valid. In Study 3, which tested the TMS intensity (56% output(SD 18)) that evoked the largest SIT at 90%MVC, voluntary activation from TMS (87.3%(SD 7.1)) and FNS (84.5%(SD 7.6)) were different. In sum, the contemporary procedure for TMS-based voluntary activation of the knee extensors is invalid. A modified procedure improves validity, but only in individuals who meet rigorous inclusion criteria for SITs and MEPs.