Quadriceps Twitch Force Research Articles

Muscle fatigue, pedalling technique and the slow component during cycling.

Above the first lactate threshold, the steady-state is delayed or prevented due to the slow component ( ). This phenomenon has been associated with muscle fatigue, but evidence for a causal relationship is equivocal. Moreover, little is known about the contribution of pedalling technique adjustments to during fatiguing cycling exercise. Eleven participants completed constant power trials at 10% above the second lactate threshold. Muscle fatigue was assessed, utilizing femoral nerve stimulation and instrumented pedals, while , quadriceps oxygenation, electromyography (EMG) and pedal force components were measured. Correlations between physiological and mechanical variables were estimated at group and individual levels. Group correlations revealed moderate values for with quadriceps twitch force (r=-0.51) and muscle oxygenation (r=-0.52), while weak correlations were observed for EMG amplitude (r=0.26) and EMG mean power frequency (r=-0.16), and with pedalling mechanical variables such as peak total downstroke force (r=-0.16), minimum total upstroke force (r=-0.16) and upstroke index of effectiveness (r=0.16). The findings here align with prior literature reporting significant correlations between the magnitude of muscle fatigue and that of , although there was large interindividual variability for all the reported correlations. Considering the heterogeneity in the data, it is difficult to determine therelative impact of pedalling technique adjustments on overall, but the present study opens the possibility that in some cases, increases in secondary to technical adjustments may be 'superimposed' on the underlying .

Neural and Muscular Determinants of Performance Fatigability Are Independent of Work and Recovery Durations During High-Intensity Interval Exercise in Males

ABSTRACT The present study aimed to investigate the effect of two protocols of high-intensity interval exercise (HIIE) on performance fatigability and its neural and muscular determinants. On different days, 14 healthy males performed two HIIE protocols with different work and recovery durations (matched for total duration, work and recovery intensities, and density): 1) 4 × 4 min at 90% HRpeak,180-s recovery at 70% HRpeak; and 2) 16 × 1 min at 90% HRpeak, 45-s recovery at 70% HRpeak. Pre- to post-HIIE reduction in maximal voluntary isometric contraction (MVIC) was used as marker of performance fatigability, while voluntary activation (VA) and potentiated quadriceps twitch force (Qtw) as markers of the neural (i.e. central fatigue) and muscular (i.e. peripheral fatigue) determinants, respectively. In addition, pre- to post-HIIE reduction in twitch force stimulated at 100 Hz (Qtw100) and 10:100 Hz ratio (Qtw10:Qtw100) were used as markers of high- and low-frequency performance fatigability, respectively. The MVIC, VA, Tw, Qtw100, and Qtw10:Qtw100 ratio decreased similarly from pre- to post-HIIE in both HIIE protocols (p < .05). The rating of perceived effort, blood pH, and plasma lactate responses were similar between HIIE protocols (p > .05), but the heart rate was higher in the longer HIIE protocol (p < .05). In conclusion, performance fatigability and its neural and muscular determinants seemed to be independent of the work and recovery durations of the HIIE, at least when HIIE protocols were matched for total work duration, work and recovery intensities, and density. Further, HIIE with long work and recovery might be preferable when the intention is to stress the chronotropic response.

The validity and reliability of quadriceps twitch force as a measure of skeletal muscle fatigue while cycling.

The measurement of skeletal muscle fatigue in response to cycling exercise is commonly done in isometric conditions, potentially limiting its ecological validity, and creating challenges in monitoring the time course of muscle fatigue across an exercise bout. This study aimed to determine if muscle fatigue could be reliably assessed by measuring quadriceps twitch force evoked while pedaling, using instrumented pedals. Nine participants completed three laboratory visits: a step incremental test to determine power output at lactate threshold, and on separate occasions, two constant-intensity bouts at a power output 10% above lactate threshold. Femoral nerve electrical stimulation was applied to elicit quadriceps twitch force both while pedaling (dynamic) and at rest (isometric). The test-retest reliability of the dynamic twitch forces and the agreement between the dynamic and isometric twitch forces were evaluated. Dynamic twitch force was found to have excellent reliability in an unfatigued state (intraclass correlation coefficient (ICC)=0.920 and mean coefficient of variation (CV)=7.5%), and maintained good reliability at task failure (ICC=0.846 and mean CV=11.5%). When comparing dynamic to isometric twitch forces across the task, there was a greater relative decline in the dynamic condition (P=0.001). However, when data were normalized to the 5min timepoint when potentiation between conditions was presumed to be more similar, this difference disappeared (P=0.207). The reliability of this method was shown to be commensurate with the gold standard method utilizing seated isometric dynamometers and offers a new avenue to monitor the kinetics of muscle fatigue during cycling in real time.

Concerns over the Utility of Phase Angle and its Association with Muscle Function

Introduction: Phase angle (PhA) derived from bioelectrical impedance analysis (BIA) has been used as an indicator of cellular hydration, muscle function, and nutritional status. Positive relationships between PhA and various measures of muscle function have been reported but it remains unclear whether PhA retains its predictive utility of muscle function, or whether it performs better than fat-free mass (FFM) in the context of muscle function. Methods: This perspective highlights secondary analyses of data collected during a randomized, double-blind, placebo-controlled trial that examined indices of recovery with different whey protein supplements after muscle-damaging exercise among resistance-trained adults. Results: Bivariate correlations between phase angle and quadriceps twitch force were positively correlated at baseline, 24-h, and 72-h post-exercise. In linear regression, FFM was shown to account for nearly 44% (partial r = 0.662) of the variance in quadriceps twitch force independent of phase angle at 24-h. A similar pattern emerged at 48-h and 72-h post-exercise Conclusions: Within this framework, these data demonstrate that: 1) PhA exhibits a weaker correlation to quadriceps twitch force compared to FFM and 2) in the context of muscle function, PhA does not provide additional information beyond that of FFM alone. Investigators should consider adjusting for FFM when evaluating the relationship between PhA and muscle function outcomes.

Hemodynamic and neuromuscular basis of reduced exercise capacity in patients with end-stage renal disease.

The present study aimed to characterize the exercise-induced neuromuscular fatigue and its possible links with cerebral and muscular oxygen supply and utilization to provide mechanistic insights into the reduced exercise capacity characterizing patients with end-stage renal disease (ESRD). Thirteen patients with ESRD and thirteen healthy males (CTR group) performed a constant-force sustained isometric contraction at 50% of their maximal voluntary isometric contraction (MVC) until exhaustion. Quadriceps muscle activation during exercise was estimated from vastus lateralis, vastus medialis, and rectus femoris EMG. Central and peripheral fatigue were quantified via changes in pre- to postexercise quadriceps voluntary activation (ΔVA) and quadriceps twitch force (ΔQtw,pot) evoked by supramaximal electrical stimulation, respectively. To assess cerebral and muscular oxygenation, throughout exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin (∆O2Hb), deoxyhemoglobin (∆HHb), and total hemoglobin (∆THb) in the prefrontal cortex and in the vastus lateralis muscle. ESRD patients demonstrated lower exercise time to exhaustion than that of CTR (88.8 ± 15.3s and 119.9 ± 14.6s, respectively, P < 0.01). Following the exercise, MVC, Qtw,pot, and VA reduction were similar between the groups (P > 0.05). There was no significant difference in muscle oxygenation (∆O2Hb) between the two groups (P > 0.05). Cerebral and muscular blood volume (∆THb) and oxygen extraction (∆HHb) were significantly blunted in the ESRD group (P < 0.05). A significant positive correlation was observed between time to exhaustion and cerebral blood volume (∆THb) in both groups (r2 = 0.64, P < 0.01). These findings support cerebral hypoperfusion as a factor contributing to the reduction in exercise capacity characterizing ESRD patients.

Grass-Fed and Non-Grass-Fed Whey Protein Consumption Do Not Attenuate Exercise-Induced Muscle Damage and Soreness in Resistance-Trained Individuals: A Randomized, Placebo-Controlled Trial

Eccentric muscle contractions can cause structural damage to muscle cells resulting in temporarily decreased muscle force production and soreness. Prior work indicates pasture-raised dairy products from grass-fed cows have greater anti-inflammatory and antioxidant properties compared to grain-fed counterparts. However, limited research has evaluated the utility of whey protein from pasture-raised, grass-fed cows to enhance recovery compared to whey protein from non-grass-fed cows. Therefore, using a randomized, placebo-controlled design, we compared the effect of whey protein from pasture-raised, grass-fed cows (PRWP) to conventional whey protein (CWP) supplementation on indirect markers of muscle damage in response to eccentric exercise-induced muscle damage (EIMD) in resistance-trained individuals. Thirty-nine subjects (PRWP, n = 14; CWP, n = 12) completed an eccentric squat protocol to induce EIMD with measurements performed at 24, 48, and 72 h of recovery. Dependent variables included: delayed onset muscle soreness (DOMS), urinary titin, maximal isometric voluntary contraction (MIVC), potentiated quadriceps twitch force, countermovement jump (CMJ), and barbell back squat velocity (BBSV). Between-condition comparisons did not reveal any significant differences (p ≤ 0.05) in markers of EIMD via DOMS, urinary titin, MIVC, potentiated quadriceps twitch force, CMJ, or BBSV. In conclusion, neither PRWP nor CWP attenuate indirect markers of muscle damage and soreness following eccentric exercise in resistance-trained individuals.

Exacerbated central fatigue and reduced exercise capacity in early-stage breast cancer patients treated with chemotherapy

PurposeThe present study aimed to characterize the etiology of exercise-induced neuromuscular fatigue and its consequences on the force-duration relationship to provide mechanistic insights into the reduced exercise capacity characterizing early-stage breast cancer patients.MethodsFifteen early-stage breast cancer patients and fifteen healthy women performed 60 maximal voluntary isometric quadriceps contractions (MVCs, 3 s of contraction, 2 s of relaxation). The critical force was determined as the mean force of the last six contractions, while W’ was calculated as the force impulse generated above the critical force. Quadriceps muscle activation during exercise was estimated from vastus lateralis, vastus medialis and rectus femoris EMG. Central and peripheral fatigue were quantified via changes in pre- to postexercise quadriceps voluntary activation (ΔVA) and quadriceps twitch force (ΔQTw) evoked by supramaximal electrical stimulation, respectively.ResultsEarly-stage breast cancer patients demonstrated lower MVC than controls preexercise (− 15%, P = 0.022), and this reduction persisted throughout the 60-MVC exercise (− 21%, P = 0.002). The absolute critical force was lower in patients than in controls (144 ± 29N vs. 201 ± 47N, respectively, P < 0.001), while W’ was similar (P = 0.546), resulting in lower total work done (− 23%, P = 0.001). This was associated with lower muscle activation in the vastus lateralis (P < 0.001), vastus medialis (P = 0.003) and rectus femoris (P = 0.003) in patients. Immediately following exercise, ΔVA showed a greater reduction in patients compared to controls (− 21.6 ± 13.3% vs. − 12.6 ± 7.7%, P = 0.040), while ΔQTw was similar (− 60.2 ± 13.2% vs. − 52.8 ± 19.4%, P = 0.196).ConclusionThese findings support central fatigue as a primary cause of the reduction in exercise capacity characterizing early-stage breast cancer patients treated with chemotherapy.Clinical trials registration No. NCT04639609—November 20, 2020.

On the role of skeletal muscle acidosis and inorganic phosphates as determinants of central and peripheral fatigue: A 31 P-MRS study.

Intramuscular hydrogen ion (H+ ) and inorganic phosphate (Pi) concentrations were dissociated during exercise to challenge their relationships with peripheral and central fatigue in vivo. Ten recreationally active, healthy men (27±5years; 180±4cm; 76±10kg) performed two consecutive intermittent isometric single-leg knee-extensor trials (60 maximal voluntary contractions; 3s contraction, 2s relaxation) interspersed with 5min of rest. Phosphorus magnetic resonance spectroscopy (31 P-MRS) was used to continuously quantify intramuscular [H+ ] and [Pi] during both trials. Using electrical femoral nerve stimulation, quadriceps twitch force (Qtw ) and voluntary activation (VA) were quantified at rest and throughout both trials. Decreases in Qtw and VA from baseline were used to determine peripheral and central fatigue, respectively. Qtw was strongly related to both [H+ ] (β coefficient: -0.9, P<0.0001) and [Pi] (-1.1, P<0.0001) across trials. There was an effect of trial on the relationship between Qtw and [H+ ] (-0.5, P<0.0001), but not Qtw and [Pi] (0.0, P=0.976). This suggests that, unlike the unaltered association with [Pi], a given level of peripheral fatigue was associated with a different [H+ ] in Trial 1 vs. Trial 2. VA was related to [H+ ] (-0.3, P<0.0001), but not [Pi] (-0.2, P=0.243), across trials and there was no effect of trial (-0.1, P=0.483). Taken together, these results support intramuscular Pi as a primary cause of peripheral fatigue, and muscle acidosis, probably acting on group III/IV muscle afferents in the interstitial space,as a contributor to central fatigue during exercise. KEY POINTS: We investigated the relationship between intramuscular metabolites and neuromuscular function in humans performing two maximal, intermittent, knee-extension trials interspersed with 5min of rest. Concomitant measurements of intramuscular hydrogen (H+ ) and inorganic phosphate (Pi) concentrations, as well as quadriceps twitch-force (Qtw ) and voluntary activation (VA), were made throughout each trial using phosphorus magnetic resonance spectroscopy (31 P-MRS) and electrical femoral nerve stimulations. Although [Pi] fully recovered prior to the onset of the second trial, [H+ ] did not. Qtw was strongly related to both [H+ ] and [Pi] across both trials. However, the relationship between Qtw and [H+ ] shifted leftward from the first to the second trial, whereas the relationship between Qtw and [Pi] remained unaltered. VA was related to [H+ ], but not [Pi], across both trials. These in vivo findings support the hypotheses of intramuscular Pi as a primary cause of peripheral fatigue, and muscle acidosis, probably acting on group III/IV muscle afferents,as a contributor to central fatigue.

Does Standard Physical Therapy Increase Quadriceps Strength in Chronically Ventilated Patients? A Pilot Study.

Physical therapy is standard care for mechanically ventilated patients, but there is no evidence, using nonvolitional, objective measurements, that physical therapy increases muscle strength in this population. The present study tested the hypothesis that 2 weeks of standard, conventional physical therapy provided at a ventilator weaning facility would increase quadriceps strength in mechanically ventilated patients. Prospective observational study. Ventilator weaning unit. Patients who were transferred from an acute care hospital because of failure to wean from mechanical ventilation and who were receiving physical therapy as prescribed by facility staff. None. We employed a novel, nonvolitional objective technique, quadriceps twitch force generation in response to femoral nerve magnetic stimulation, to assess leg strength before and after 2 weeks of conventional physical therapy. The duration and specific exercises provided to patients were also recorded. In a subset of patients, we measured muscle activation intensity using wireless electromyogram recordings. Indices of respiratory function (maximum inspiratory pressure generation and the rapid shallow breathing index) were also assessed. Patients' responses to 2 weeks of physical therapy were poor; on average, quadriceps twitch fell by -1.02 ± 0.71 Newtons. Neither physical therapy duration nor specific forms of exercise were identified to positively impact quadriceps twitch. Electromyogram recordings indicated that during training, muscle activation was poor. Consequently, therapists spent substantial time performing exercises that elicited little muscle activation. Physical therapy did not improve respiratory function. Standard physical therapy delivered in a ventilator weaning facility failed to improve quadriceps leg strength in a majority of mechanically ventilated patients. The fact that mechanically ventilated patients fail to achieve high levels of muscle activation during physical therapy provides a potential explanation as to why physical therapy may often be ineffective. We speculate that use of novel methods which increase muscle activation during exercise may improve responses of mechanically ventilated patients to physical therapy.

Respiratory Muscle Fatigue Alters Cycling Performance and Locomotor Muscle Fatigue.

This study aimed to determine if preexisting respiratory muscle fatigue (RMF) alters motoneuronal output, locomotor muscle fatigue, and cycling performance. Eight trained male cyclists performed 5-km cycling time trials after a resistive breathing task that induced RMF and under control conditions (CON). Motoneuronal output was estimated using vastus lateralis surface electromyography, and locomotor muscle fatigue was quantified as the change in potentiated quadriceps twitch force from preexercise to postexercise. Time to complete the time trial was 1.9% ± 0.9% longer in RMF compared with CON (P < 0.001). Estimated motoneuronal output was lower in RMF compared with CON during 1 km (45% ± 11% vs 53% ± 13%, P = 0.004) and 2 km (45% ± 14% vs 51% ± 14%, P = 0.008), but was not different thereafter. Ventilation was lower in RMF compared with CON during 1 km (114 ± 19 vs 135 ± 24 L·min, P = 0.003) and 2 km (136 ± 23 vs 152 ± 31 L·min, P = 0.009); however, ratings of dyspnea were similar. After the 5-km time trial, locomotor muscle fatigue was attenuated in RMF compared with CON (-22% ± 6%, vs -28% ± 7%, P = 0.02). Alterations to dyspnea for a given ventilation seem to have constrained power output during cycling exercise, thereby limiting the development of locomotor muscle fatigue. These findings indicate that the respiratory system is an integral component in a global feedback loop that regulates exercise performance and the development of locomotor muscle fatigue.

Cardiorespiratory Response during the 1-min Sit-to-Stand Test in Chronic Obstructive Pulmonary Disease.

This study aimed to assess the cardiorespiratory response during a 1-min sit-to-stand test (1STS) in comparison with cycling cardiopulmonary exercise test (CPET) in people with chronic obstructive pulmonary disease (COPD) and in healthy subjects and to evaluate whether 1STS may induce leg fatigue in these individuals. Fourteen people with severe COPD and 12 healthy subjects performed a 1STS and a CPET during which cardiorespiratory response, perception of dyspnea, and leg fatigue were assessed. Quadriceps strength was assessed before and after 1STS, and contractile fatigue was defined as a postexercise fall in quadriceps twitch force greater than 15% of resting values. In COPD, peak V˙O2, V˙E, and HR achieved during 1STS reached 113%, 103%, and 93% of the corresponding values during CPET, respectively. Decrease in SpO2 from preexercise to peak exercise and the magnitude of dynamic hyperinflation were similar between 1STS and CPET. Borg dyspnea and leg fatigue scores were higher for CPET than 1STS. In healthy subjects, peak cardiorespiratory demand and symptom scores were higher during CPET compared with 1STS. A V˙O2 overshoot during recovery was observed only in people with COPD. After 1STS, the V˙O2 half-time recovery of COPD was 152 ± 25 s compared with 74 ± 18 in healthy subjects (P < 0.01). Ten people with COPD and five healthy subjects were considered as fatiguers. The 1STS induced a similar cardiorespiratory stress to that of CPET and was associated with contractile quadriceps fatigue in people with severe COPD. The V˙O2 overshoot and slower recovery time of cardiorespiratory variables seen in COPD demonstrate the clinical relevance of monitoring the recovery phase of exercise.

Centrally-mediated regulation of peripheral fatigue during knee extensor exercise and consequences on the force-duration relationship in older men

The aim of the present study was to investigate the existence of a critical threshold beyond which peripheral fatigue would not further decrease during knee extensor (KE) exercise in older men, and the consequences of this mechanism on the force-duration relationship. Twelve old men (59 ± 2 years) randomly performed two different sessions, in which they performed 60 maximum voluntary contractions (MVC; 3s contraction, 2s relaxation). One trial was performed in the unfatigued state (CTRL) and one other following fatiguing neuromuscular electrical stimulation of the KE (FNMES). Peripheral and central fatigue were quantified via pre/post-exercise decreases in quadriceps twitch-force (Δ Ptw) and voluntary activation (ΔVA). Critical torque (CT) was determined as the mean force of the last 12 contractions while W′ was calculated as the area above CT. Compared with CTRL, pre-fatigue (Δ Ptw = −10.3 ± 6.2%) resulted in a significant (p < 0.05) reduction in W’ (−18.2 ± 1.6%) in FNMES. However, CT (∼964 N), ΔVA (∼15%) and Δ Ptw (∼25%) post-MVCs were similar between both conditions. In CTRL, W’ was correlated with Δ Ptw (r 2 = 0.78). Moreover, the difference in W’ between CTRL and FNMES was correlated with the level of pre-fatigue induced in FNMES (r 2 = 0.76). These findings document that peripheral fatigue is confined to an individual threshold during KE exercise in older men. Furthermore, correlative results suggest that mechanisms regulating peripheral fatigue to a critical threshold also restrict W’, and therefore play a role in exercise capacity in older men.

Stretch-shortening cycle exercise produces acute and prolonged impairments on endurance performance: is the peripheral fatigue a single answer?

This study aimed to verify the acute and prolonged effects of stretch-shortening cycle exercise (SSC) on performance and neuromuscular function following a 4-km cycling time trial (4-km TT). On separate days, individuals performed a 4-km TT without any previous exercise (CON), immediately (ACUTE) and 48h after (PROL) SSC protocol (i.e., 100-drop jumps). Neuromuscular function was measured at baseline SSC (baseline), before (pre-TT) and after (post-TT) 4-km TT. Muscle soreness and inflammatory responses also were assessed. The endurance performance was impaired in both ACUTE (- 2.3 ± 1.8%) and PROL (- 1.8 ± 2.4%) compared with CON. The SSC protocol caused also an acute reduction in neuromuscular function, with a greater decrease in potentiated quadriceps twitch-force (Qtw.pot - 49 ± 16%) and voluntary activation (VA - 6.5 ± 7%) compared for CON and PROL at pre-TT. The neuromuscular function was fully recovered 48h after SSC protocol. Muscle soreness and IL-10 were elevated only 48h after SSC protocol. At post-TT, Qtw.pot remained lower in ACUTE (- 52 ± 14%) compared to CON (- 29 ± 7%) and PROL (- 31 ± 16%). These findings demonstrate that impairment in endurance performance induced by prior SSC protocol was mediated by two distinct mechanisms, where the acute impairment was related to an exacerbated degree of peripheral and central fatigue, and the prolonged impairment was due to elevated perceived muscle soreness.

The magnitude of neuromuscular fatigue is not intensity dependent when cycling above critical power but relates to aerobic and anaerobic capacities.

What is the central question of this study? Is the magnitude of neuromuscular fatigue dependent upon exercise intensity above critical power (CP) when W' (the curvature constant of the power-duration relationship) is depleted? What is the main finding and its importance? The magnitude of neuromuscular fatigue is the same after two bouts of supra-CP cycling (3 versus 12min) when controlling for W' depletion but is larger for individuals of greater anaerobic capacity after the shorter bout and smaller for individuals of greater aerobic capacity after the longer exercise bout. These findings provide new insight into the mechanisms underpinning exercise above CP. The aim of the present study was to test whether the development of neuromuscular fatigue within the severe-intensity domain could be linked to the depletion of the curvature constant (W') of the power-duration relationship. Twelve recreationally active men completed tests to determine peak oxygen consumption, critical power (CP) and W', followed by two randomly assigned constant-load supra-CP trials set to deplete W' fully in 3 (P-3) and 12min (P-12). Pre- to postexercise changes in maximal voluntary contraction, potentiated quadriceps twitch force evoked by single (Qpot ) and paired high- (PS100) and low-frequency (PS10) stimulations and voluntary activation were determined. Cycling above CP reduced maximal voluntary contraction (P-3, -20± 10% versus P-12, -15± 7%), measures associated with peripheral fatigue (Qpot , -35± 13 versus -31± 14%; PS10, -38± 13 versus -37± 17%; PS100, -18± 9 versus -13± 8% for P-3 and P-12, respectively) and voluntary activation (P-3, -12± 3% versus P-12, -13± 3%; P< 0.05), with no significant difference between trials (P> 0.05). Changes in maximal voluntary contraction and evoked twitch forces were inversely correlated with CP and peak oxygen consumption after P-12, whereas W' was significantly correlated with changes in Qpot and PS10 after P-3 (P< 0.05). Therefore, the magnitude of neuromuscular fatigue does not depend on exercise intensity when W' is fully exhausted during severe-intensity exercise; nonetheless, exploration of inter-individual variations suggests that mechanisms underpinning exercise tolerance within this domain differ between short- and long-duration exercise.

Neuromuscular Fatigue and Recovery after Heavy Resistance, Jump, and Sprint Training.

Training methods that require maximal intensity efforts against light and heavy resistance are commonly used for athletic development. Typically, these sessions are separated by at least 48 h recovery on the assumption that such efforts elicit marked fatigue of the central nervous system (CNS), but this posit has not been well studied. The aim of the study was to assess the etiology and recovery of fatigue after heavy-resistance (strength), jump, and sprint training methods. Ten male athletes completed three training sessions requiring maximal efforts that varied in their loading characteristics: (i) heavy-resistance exercise (10 × 5 back squats at 80% one-repetition maximum [1RM]) (STR), (ii) jumping exercise (10 × 5 jump squats) (JUMP), and (iii) maximal sprinting (15 × 30 m) (SPR). Preparticipants, postparticipants, and 24-, 48-, and 72-h postparticipants completed a battery of tests to measure neuromuscular function using electrical stimulation of the femoral nerve, and single- and paired-pulse magnetic stimulation of the motor cortex, with evoked responses recorded from the knee extensors. Fatigue was self-reported at each time point using a visual analog scale. Each intervention elicited fatigue that resolved by 48 (JUMP) and 72 h (STR and SPR). Decrements in muscle function (reductions in the potentiated quadriceps twitch force) persisted for 48 h after all exercise. Reductions in voluntary activation were present for 24 h after JUMP and SPRINT, and 48 h after STR. No other differences in CNS function were observed as a consequence of training. Strength, jump, and sprint training requiring repeated maximum efforts elicits fatigue that requires up to 72 h to fully resolve, but this fatigue is not primarily underpinned by decrements in CNS function.

Effect of carbohydrate ingestion on central fatigue during prolonged running exercise in moderate hypoxia

To determine whether acute exposure to moderate hypoxia alters central and peripheral fatigue and to test whether carbohydrate ingestion impacts fatigue characteristics, 12 trained runners completed three running trials lasting 1 h each at 65% of normoxic maximum oxygen uptake. The first trial was performed in normoxia [inspired O2 fraction ( ) = 0.21], and the last two trials were completed in hypoxia ( = 0.15). Participants ingested a placebo drink in normoxia (NORM-PLA), a placebo drink in hypoxia (HYP-PLA), or a carbohydrate solution in hypoxia (HYP-CHO). HYP conditions were randomized. Peripheral [change in potentiated quadriceps twitch force (ΔQtw,pot)] and central [change in voluntary activation (ΔVA)] fatigue were assessed via preexercise-to-postexercise changes in magnetically evoked quadriceps twitch. In HYP, blood was drawn to determine the ratio of free-tryptophan (f-TRP) to branched-chain amino acids (BCAA). After exercise, peripheral fatigue was reduced to a similar degree in normoxia and hypoxia (ΔQtw,pot = -4.5 ± 1.3% and -4.0 ± 1.5% in NORM-PLA and HYP-PLA, respectively; P = 0.61). Central fatigue was present after normoxic and hypoxic exercise but to a greater degree in HYP-PLA compared with NORM-PLA (ΔVA: -4.7 ± 0.9% vs. -1.9 ± 0.7%; P < 0.01). Carbohydrate ingestion did not influence central fatigue (ΔVA in HYP-CHO: -5.7 ± 1.2%; P = 0.51 vs. HYP-PLA). After exercise, no differences were observed in the ratio of f-TRP to BCAA between HYP-PLA and HYP-CHO ( P = 0.67). Central fatigue increased during prolonged running exercise in moderate hypoxia although the ratio of f-TRP to BCAA remained unchanged. Ingesting carbohydrates while running in hypoxia did not influence fatigue development. NEW & NOTEWORTHY Hypoxic exposure influences the origin of exercise-induced fatigue and the rate of fatigue development depending on the severity of hypoxia. Our data suggest that moderate hypoxia increases central, but not peripheral, fatigue in trained runners exercising at 65% of normoxic maximum oxygen uptake. The increase in central fatigue was unaffected by carbohydrate intake and occurred although the ratio of free tryptophan to branched-chain amino acids remained unchanged.

Caffeine increases both total work performed above critical power and peripheral fatigue during a 4-km cycling time trial.

The link between total work performed above critical power (CP) and peripheral muscle fatigue during self-paced exercise is unknown. We investigated the influence of caffeine on the total work done above CP during a 4-km cycling time trial (TT) and the subsequent consequence on the development of central and peripheral fatigue. Nine cyclists performed three constant-load exercise trials to determine CP and two 4-km TTs ~75 min after oral caffeine (5 mg/kg) or cellulose (placebo) ingestion. Neuromuscular functions were assessed before and 50 min after supplementation and 1 min after TT. Oral supplementation alone had no effect on neuromuscular function ( P > 0.05). Compared with placebo, caffeine increased mean power output (~4%, P = 0.01) and muscle recruitment (as inferred by EMG, ~17%, P = 0.01) and reduced the time to complete the TT (~2%, P = 0.01). Work performed above CP during the caffeine trial (16.7 ± 2.1 kJ) was significantly higher than during the placebo (14.7 ± 2.1 kJ, P = 0.01). End-exercise decline in quadriceps twitch force (pre- to postexercise decrease in twitch force at 1 and 10 Hz) was more pronounced after caffeine compared with placebo (121 ± 13 and 137 ± 14 N vs. 146 ± 13 and 156 ± 11 N; P < 0.05). There was no effect of caffeine on central fatigue. In conclusion, caffeine increases muscle recruitment, which enables greater work performed above CP and higher end-exercise peripheral locomotor muscle fatigue. NEW & NOTEWORTHY The link between total work done above critical power and peripheral fatigue during a self-paced, high-intensity exercise is unclear. This study revealed that caffeine ingestion increases muscle recruitment, which enables greater work done above critical power and a greater degree of end-exercise decline in quadriceps twitch force during a 4-km cycling time trial. These findings suggest that caffeine increases performance at the expense of greater locomotor muscle fatigue.

Skeletal muscle bioenergetics during all-out exercise: mechanistic insight into the oxygen uptake slow component and neuromuscular fatigue.

Although all-out exercise protocols are commonly used, the physiological mechanisms underlying all-out exercise performance are still unclear, and an in-depth assessment of skeletal muscle bioenergetics is lacking. Therefore, phosphorus magnetic resonance spectroscopy (31P-MRS) was utilized to assess skeletal muscle bioenergetics during a 5-min all-out intermittent isometric knee-extensor protocol in eight healthy men. Metabolic perturbation, adenosine triphosphate (ATP) synthesis rates, ATP cost of contraction, and mitochondrial capacity were determined from intramuscular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), diprotonated phosphate ([Formula: see text]), and pH. Peripheral fatigue was determined by exercise-induced alterations in potentiated quadriceps twitch force (Qtw) evoked by supramaximal electrical femoral nerve stimulation. The oxidative ATP synthesis rate (ATPOX) attained and then maintained peak values throughout the protocol, despite an ~63% decrease in quadriceps maximal force production. ThusATPOX normalized to force production (ATPOX gain) significantly increased throughout the exercise (1st min: 0.02 ± 0.01, 5th min: 0.04 ± 0.01 mM·min-1·N-1), as did the ATP cost of contraction (1st min: 0.048 ± 0.019, 5th min: 0.052 ± 0.015 mM·min-1·N-1). Additionally, the pre- to postexercise change in Qtw (-52 ± 26%) was significantly correlated with the exercise-induced change in intramuscular pH (r = 0.75) and [Formula: see text] concentration (r = 0.77). In conclusion, the all-out exercise protocol utilized in the present study elicited a "slow component-like" increase in intramuscular ATPOX gain as well as a progressive increase in the phosphate cost of contraction. Furthermore, the development of peripheral fatigue was closely related to the perturbation of specific fatigue-inducing intramuscular factors (i.e., pH and [Formula: see text] concentration).NEW & NOTEWORTHY The physiological mechanisms and skeletal muscle bioenergetics underlying all-out exercise performance are unclear. This study revealed an increase in oxidative ATP synthesis rate gain and the ATP cost of contraction during all-out exercise. Furthermore, peripheral fatigue was related to the perturbation in pH and deprotonated phosphate ion. These findings support the concept that the oxygen uptake slow component arises from within active skeletal muscle and that skeletal muscle force generating capacity is linked to the intramuscular metabolic milieu.

No Influence of Transcutaneous Electrical Nerve Stimulation on Exercise-Induced Pain and 5-Km Cycling Time-Trial Performance.

Introduction: Afferent information from exercising muscle contributes to the sensation of exercise-induced muscle pain. Transcutaneous electrical nerve stimulation (TENS) delivers low–voltage electrical currents to the skin, inhibiting nociceptive afferent information. The use of TENS in reducing perceptions of exercise-induced pain has not yet been fully explored. This study aimed to investigate the effect of TENS on exercise-induced muscle pain, pacing strategy, and performance during a 5-km cycling time trial (TT).Methods: On three separate occasions, in a single-blind, randomized, and cross-over design, 13 recreationally active participants underwent a 30-min TENS protocol, before performing a 5-km cycling TT. TENS was applied to the quadriceps prior to exercise under the following conditions; control (CONT), placebo with sham TENS application (PLAC), and an experimental condition with TENS application (TENS). Quadriceps fatigue was assessed with magnetic femoral nerve stimulation assessing changes in potentiated quadriceps twitch force at baseline, pre and post exercise. Subjective scores of exertion, affect and pain were taken every 1-km.Results: During TTs, application of TENS did not influence pain perceptions (P = 0.68, = 0.03). There was no significant change in mean power (P = 0.16, = 0.16) or TT duration (P = 0.17, = 0.14), although effect sizes were large for these two variables. Changes in power output were not significant but showed moderate effect sizes at 500-m ( = 0.10) and 750-m ( = 0.10). Muscle recruitment as inferred by electromyography data was not significant, but showed large effect sizes at 250-m ( = 0.16), 500-m ( = 0.15), and 750-m ( = 0.14). This indicates a possible effect for TENS influencing performance up to 1-km.Discussion: These findings do not support the use of TENS to improve 5-km TT performance.

Fatigue diminishes motoneuronal excitability during cycling exercise.

Exercise-induced fatigue influences the excitability of the motor pathway during single-joint isometric contractions. This study sought to investigate the influence of fatigue on corticospinal excitability during cycling exercise. Eight men performed fatiguing constant-load (80% Wpeak; 241 ± 13 W) cycling to exhaustion during which the percent increase in quadriceps electromyography (ΔEMG; vastus lateralis and rectus femoris) was quantified. During a separate trial, subjects performed two brief (∼45 s) nonfatiguing cycling bouts (244 ± 15 and 331 ± 23W) individually chosen to match the ΔEMG across bouts to that observed during fatiguing cycling. Corticospinal excitability during exercise was quantified by transcranial magnetic, electric transmastoid, and femoral nerve stimulation to elicit motor-evoked potentials (MEP), cervicomedullary evoked potentials (CMEP), and M waves in the quadriceps. Peripheral and central fatigue were expressed as pre- to postexercise reductions in quadriceps twitch force (ΔQtw) and voluntary quadriceps activation (ΔVA). Whereas nonfatiguing cycling caused no measureable fatigue, fatiguing cycling resulted in significant peripheral (ΔQtw: 42 ± 6%) and central (ΔVA: 4 ± 1%) fatigue. During nonfatiguing cycling, the area of MEPs and CMEPs, normalized to M waves, similarly increased in the quadriceps (∼40%; P < 0.05). In contrast, there was no change in normalized MEPs or CMEPs during fatiguing cycling. As a consequence, the ratio of MEP to CMEP was unchanged during both trials (P > 0.5). Therefore, although increases in muscle activation promote corticospinal excitability via motoneuronal facilitation during nonfatiguing cycling, this effect is abolished during fatigue. We conclude that the unaltered excitability of the corticospinal pathway from start of intense cycling exercise to exhaustion is, in part, determined by inhibitory influences on spinal motoneurons obscuring the facilitating effects of muscle activation.