Development Of Peripheral Fatigue Research Articles

The influence of biological sex on the relationship between inorganic phosphates, hydrogen ions, and the peripheral component of neuromuscular fatigue

Background: In males, the relationship between peripheral fatigue development and intramuscular inorganic phosphate (Pi) accumulation is more robust than that with hydrogen ion (H+) accumulation. Based on previous findings of greater peripheral fatigability during exercise in males vs females (as pre-post %changes in twitch force, Qtw) and thus the potential for sex differences in the mechanisms of fatigue, we aimed to: 1) establish whether the relationship between peripheral fatigue development and Pi accumulation is more robust than that with H+ accumulation in females, and 2) determine whether females and males differ in the development of peripheral fatigue for a given Pi or H+ accumulation. Methods: Eleven recreationally active, healthy, young individuals (5 females) performed two consecutive (interspersed by 5-min of rest) intermittent isometric single-leg knee-extensor trials (60 maximal voluntary contractions; 3-s contraction, 2-s relaxation). Throughout both trials, quadriceps intramuscular [Pi] and [H+] were quantified using phosphorus magnetic resonance spectroscopy (31P-MRS), and quadriceps Qtw was measured using electrical femoral nerve stimulation. Peripheral fatigue was quantified as the exercise-induced decrease in Qtw. The relationships between Qtw and [Pi] and [H+] were analyzed using linear mixed-effects models for the portion of exercise where peripheral fatigue was developing ( i.e., decreasing Qtw). The results are presented as the Z-score β coeffcients and p-values. Results: The exercise-induced reduction in Qtw (thus peripheral fatigue) was larger in males compared to females (-65±16 vs -43±21%; p<0.05). During both trials, the decrease in Qtw for a given increase in [Pi] was not different between sexes, and these relationships were not altered from Trial 1 to Trial 2 (Female slope Trial 1: -1.5 vs Trial 2: -1.4; Male slope Trial 1: -1.7 vs Trial 2: -1.6, all p>0.3). The decrease in Qtw for a given increase in [H+] was greater for men compared to women in both trials (both p<0.01), and these relationships were not altered from Trial 1 to Trial 2 (both p>0.4) (Female slope Trial 1: -0.8 vs Trial 2: -0.9; Male slope Trial 1: -1.2 vs Trial 2: -1.3). The overall relationship ( i.e., y-intercept) between Qtw and [Pi] did not shift up or down across the consecutive trials for either sex (Females y-intercept Trial 1: -1.0 vs Trial 2: -1.3; Males y-intercept Trial 1: 0.8 vs Trial 2: 0.7, both p>0.2). In contrast, the overall relationship ( i.e., y-intercept) between Qtw and [H+] shifted down from Trial 1 to Trial 2 for both sexes (Females y-intercept Trial 1: 0.2 vs Trial 2: -0.3; Males y-intercept Trial 1: 0.3 vs Trial 2: -0.2, both p<0.01). Conclusions: In males and females, the relationship between the magnitude of Qtw and Pi is more robust compared to the relationship between the magnitude of Qtw and H+, suggesting Pi accumulation as the stronger mediator of peripheral fatigue in both sexes. Furthermore, the susceptibility of Qtw to decrease in response to a given increase in Pi was not different between sexes. The difference in peripheral fatigability between males and females are therefore likely due to differences in [Pi] and factors determining the magnitude of its accumulation ( e.g., force output, muscle fiber type distribution, or O2 transport and utilization). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Does creatine supplementation affect recovery speed of impulse above critical torque?

ABSTRACT We previously reported that creatine supplementation improved intermittent isometric exercise performance by augmenting the total impulse performed above end-test torque (total IET′). However, our previous analyses did not enable mechanistic assessments. The objective of this study was to determine if creatine supplementation affected the IET′ speed of recovery. To achieve this objective, we retrospectively analyzed our data using the IET′ balance model to determine the time constant for the recovery of IET′ (τIET′). Sixteen men were randomly allocated into creatine (N = 8) or placebo (N = 8) groups. Prior to supplementation, participants performed quadriceps all-out exercise to determine end-test torque (ET) and IETʹ. Participants then performed quadriceps exercise at ET + 10% until task-failure before supplementation (Baseline), until task-failure after supplementation (Creatine or Placebo), and until the Baseline time after supplementation (Creatine- or Placebo-Isotime). τIET′ was faster than Baseline for Creatine (669 ± 98 vs 470 ± 66 s), but not Placebo (792 ± 166 vs 786 ± 161 s). The creatine-induced change in τIET′ was inversely correlated with the creatine-induced changes in both the rate of peripheral fatigue development and time to task-failure. τIET′ was inversely correlated with total IET′ and ET in all conditions, but creatine supplementation shifted this relationship such that τIET′ was faster for a given ET. Creatine supplementation, therefore, sped the recovery of IET′ during intermittent isometric exercise, which was inversely related to the improvement in exercise performance. These findings support that the improvement in exercise performance after creatine supplementation was, at least in part, specific to effects on the physiological mechanisms that determine the IET′ speed of recovery. HIGHLIGHTS Sixteen healthy participants were randomly allocated to creatine supplementation or placebo groups. Creatine supplementation accelerated the time constant for the recovery of IET′ (τIET′). The time constant for the recovery of IET′ (τIET′) was inversely related to both the rate of peripheral fatigue development and the time to task failure.

The completely recover of quadriceps muscle peripheral fatigue after running in Olympic but not in Sprint triathlon

ABSTRACT This study compared central and peripheral fatigue development between Sprint and Olympic distance triathlon. Fifteen male triathletes performed Sprint and Olympic triathlon simulations in a randomized and counterbalanced order. Central and peripheral fatigue was evaluated from changes in voluntary activation level (VAL) and twitch responses of quadriceps muscle (Qtw,pot), respectively. Qtw,pot reduced from baseline to post-swimming similarly between triathlon simulations (Sprint, −1711%; Olympic, −13%). In post-cycling, Qtw,pot further declined to a similar extent between triathlon distances (Sprint, −3115%; Olympic, −2811%). In post-running, Qtw,pot was fully recovered in Olympic triathlon (-410%), whereas there was only a partial recovery of Qtw,pot in Sprint triathlon (−2011%). VAL was not reduced in post-swimming, but reduction was similar between triathlon distances in post-cycling (Sprint, −109%; Olympic, −88%) and post-running (Sprint, −1514%; Olympic, −168%). In Sprint triathlon, the swimming speed (1.070.13 m ·s-1) was above (p.001) critical speed (1.010.14 m ·s-1), the cycling power (179.727.2W) was below the respiratory compensation point (216.327.8W, p.001) and running speed (13.71.05km·h-1) similar to the respiratory compensation point (13.20.70 km·h-1, p.124). In Olympic triathlon, swimming speed (1.030.13m·s-1) was similar to critical speed (p.392), and both cycling power (165.327.3W) and running speed (12.61.05km·h-1) were below the respiratory compensation point (p.007). In conclusion, peripheral fatigue progressed until post-cycling regardless of triathlon distances. However, peripheral fatigue was fully recovered after running in Olympic but not in Sprint triathlon. The central fatigue started in post-cycling and progressed until post-running regardless of triathlon distances.

Sex Differences in the Severe‐ and Extreme‐Intensity Power‐Duration Relationships

We have previously shown that, similar to the severe‐intensity power duration relationship (i.e., W’sev), there exists a separate, smaller power‐duration relationship for the extreme‐intensity domain (W’­ext) in men. We have also shown that there may be differences in contributions of central and peripheral fatigue between men and women during and immediately following extreme‐intensity exercise. The current study tested the hypotheses that 1) the W’extwould be significantly less than W’sev in both sexes, but not different between men and women, 2) absolute Maximum Voluntary Contractions (MVC) would be reduced to greater extent at end‐exercise following severe‐ and extreme‐intensity exercise in men compared to women but not when scaled relative to baseline, and 3) peripheral fatigue would be greater at task failure (Tlim) in men compared to women following severe‐intensity exercise, with no sex difference following extreme‐intensity exercise. Following familiarization, 7 men and 7 women completed three severe‐ (Tlim: 2‐4 min, S3; 5‐7 min, S2; 8‐12 min, S1) and three extreme‐intensity (70, 80, 90% MVC) isometric knee‐extension bouts to task failure. MVC and potentiated twitch force (Qpot) were measured and compared at baseline, task failure, and 150 s of recovery. W’ext was significantly smaller compared to W’sev in men (2.4 ± 1.2 kJ vs 3.9 ± 1.3 kJ; p = 0.03) and in women (1.6 ± 0.8 kJ vs 2.9 ± 1.7 kJ; p = 0.05), however there were no sex differences in either W’extor W’­sev. There were no sex differences in MVC at task failure following severe‐intensity exercise. However, MVC was lower in women following extreme‐intensity exercise compared to men, although there were no sex differences in MVC relative to baseline. Further, there were no differences in MVC by the end of recovery compared to baseline in men or women following extreme‐intensity exercise.Qpot was not different at task failure following severe‐ and extreme‐intensity exercise between men and women. However, men showed lower Qpot relative to baseline, suggesting greater peripheral fatigue development, with the exception of exercise at 90% MVC. These data provide evidence that important sex differences exist in the contributions of peripheral fatigue to task failure and in recovery from exercise which depend on exercise intensity. Therefore, practitioners need to consider exercise intensity and the time course of recovery when prescribing exercise to men and women.

The effects of exercise intensity and duration on the relationship between the slow component of V̇O2 and peripheral fatigue.

If the development of the oxygen uptake slow component (V̇O2SC ) and muscle fatigue are related, these variables should remain coupled in a time- and intensity-dependent manner. 16 participants (7 females) visited the laboratory on 7 separate occasions: (1) three 6-minutes moderate-intensity cycling exercise bouts proceeded by a ramp incremental test; (2-3) 30-minutes constant power output (PO) exercise bout to determine the maximal lactate steady state (MLSS); (4-7) constant-PO exercise bouts to task failure (TTF), pseudorandomized order, at (i) 15% below the PO at MLSS; (ii) 10W below MLSS; (iii) MLSS; (iv) 10W above MLSS (first intensity and randomized order thereafter). Neuromuscular fatigue was characterized by isometric maximal voluntary contractions and femoral nerve electrical stimulation of knee extensors to measure peripheral fatigue at baseline, at min 5, 10, 20, 30 and TTF. Pulmonary oxygen uptake (V̇O2 ) was continuously recorded during the constant-PO bouts and V̇O2SC was characterized based on each individual V̇O2 kinetics during moderate transitions. The development of V̇O2SC and peripheral fatigue were correlated across time (r2 adj range of 0.64-0.80) and amongst each exercise intensity (r2 adj range of 0.26-0.30) (all P<.001). Also, TTF was correlated with V̇O2SC and neuromuscular fatigue parameters (r2 adj range of 0.52-0.82, all P<.001). The V̇O2SC and peripheral fatigue development are correlated throughout the exercise in a time- and intensity-dependent manner, suggesting that the V̇O2SC may depend on muscle fatigue even if the mechanisms of reduced contractile function are different amongst intensities.

Effects of caffeine on central and peripheral fatigue following closed- and open-loop cycling exercises.

We examined whether endurance performance and neuromuscular fatigue would be affected by caffeine ingestion during closed- and open-loop exercises. Nine cyclists performed a closed-loop (4,000-m cycling time trial) and an open-loop exercise (work rate fixed at mean power of the closed-loop trial) 60 min after ingesting caffeine (CAF, 5 mg/kg) or placebo (PLA, cellulose). Central and peripheral fatigue was quantified via pre- to post-exercise decrease in quadriceps voluntary activation and potentiated twitch force, respectively. Test sensitivity for detecting caffeine-induced improvements in exercise performance was calculated as the mean change in time divided by the error of measurement. Caffeine ingestion reduced the time of the closed-loop trial (PLA: 375.1±14.5 s vs CAF: 368.2±14.9 s, P=0.024) and increased exercise tolerance during the open-loop trial (PLA: 418.2±99.5 s vs CAF: 552.5±106.5 s, P=0.001), with similar calculated sensitivity indices (1.5, 90%CI: 0.7-2.9 vs 2.8, 90%CI: 1.9-5.1). The reduction in voluntary activation was more pronounced (P=0.019) in open- (-6.8±8.3%) than in closed-loop exercises (-1.9±4.4%), but there was no difference between open- and closed-loop exercises for the potentiated twitch force reduction (-25.6±12.8 vs -26.6±12.0%, P>0.05). Caffeine had no effect on central and peripheral fatigue development in either mode of exercise. In conclusion, caffeine improved endurance performance in both modes of exercise without influence on post-exercise central and peripheral fatigue, with the open-loop exercise imposing a greater challenge to central fatigue tolerance.

Electrically induced quadriceps fatigue in the contralateral leg impairs ipsilateral knee extensors performance.

Muscle fatigue induced by voluntary exercise, which requires central motor drive, causes central fatigue that impairs endurance performance of a different, nonfatigued muscle. This study investigated the impact of quadriceps fatigue induced by electrically induced (no central motor drive) contractions on single-leg knee-extension (KE) performance of the subsequently exercising ipsilateral quadriceps. On two separate occasions, eight males completed constant-load (85% of maximal power-output) KE exercise to exhaustion. In a counterbalanced manner, subjects performed the KE exercise with no pre-existing quadriceps fatigue in the contralateral leg on one day (No-PreF), whereas on the other day, the same KE exercise was repeated following electrically induced quadriceps fatigue in the contralateral leg (PreF). Quadriceps fatigue was assessed by evaluating pre- to postexercise changes in potentiated twitch force (ΔQtw,pot; peripheral fatigue), and voluntary muscle activation (ΔVA; central fatigue). As reflected by the 57 ± 11% reduction in electrically evoked pulse force, the electrically induced fatigue protocol caused significant knee-extensors fatigue. KE endurance time to exhaustion was shorter during PreF compared with No-PreF (4.6 ± 1.2 vs 7.7 ± 2.4 min; P < 0.01). Although ΔQtw,pot was significantly larger in No-PreF compared with PreF (-60% vs -52%, P < 0.05), ΔVA was greater in PreF (-14% vs -10%, P < 0.05). Taken together, electrically induced quadriceps fatigue in the contralateral leg limits KE endurance performance and the development of peripheral fatigue in the ipsilateral leg. These findings support the hypothesis that the crossover effect of central fatigue is mainly mediated by group III/IV muscle afferent feedback and suggest that impairments associated with central motor drive may only play a minor role in this phenomenon.

Heart failure with preserved ejection fraction diminishes peripheral hemodynamics and accelerates exercise-induced neuromuscular fatigue.

This study investigated the impact of HFpEF on neuromuscular fatigue and peripheral hemodynamics during small muscle mass exercise not limited by cardiac output. Eight HFpEF patients (NYHA II-III, ejection-fraction: 61 ± 2%) and eight healthy controls performed dynamic knee extension exercise (80% peak workload) to task failure and maximal intermittent quadriceps contractions (8 × 15 s). Controls repeated knee extension at the same absolute intensity as HFpEF. Leg blood flow (QL) was quantified using Doppler ultrasound. Pre/postexercise changes in quadriceps twitch torque (ΔQtw; peripheral fatigue), voluntary activation (ΔVA; central fatigue), and corticospinal excitability were quantified. At the same relative intensity, HFpEF (24 ± 5 W) and controls (42 ± 6 W) had a similar time-to-task failure (∼10 min), ΔQtw (∼50%), and ΔVA (∼6%). This resulted in a greater exercise-induced change in neuromuscular function per unit work in HFpEF, which was significantly correlated with a slower QL response time. Knee extension exercise at the same absolute intensity resulted in an ∼40% lower QL and greater ΔQtw and ΔVA in HFpEF than in controls. Corticospinal excitability remained unaltered during exercise in both groups. Finally, despite a similar ΔVA, ΔQtw was larger in HFpEF versus controls during isometric exercise. In conclusion, HFpEF patients are characterized by a similar development of central and peripheral fatigue as healthy controls when tested at the same relative intensity during exercise not limited by cardiac output. However, HFpEF patients have a greater susceptibility to neuromuscular fatigue during exercise at a given absolute intensity, and this impairs functional capacity. The patients' compromised QL response to exercise likely accounts, at least partly, for the patients' attenuated fatigue resistance.NEW & NOTEWORTHY The susceptibility to neuromuscular fatigue during exercise is substantially exaggerated in individuals with heart failure with a preserved ejection fraction. The faster rate of fatigue development is associated with the compromised peripheral hemodynamic response characterizing these patients during exercise. Given the role of neuromuscular fatigue as a factor limiting exercise, this impairment likely accounts for a significant portion of the exercise intolerance typical for this population.

Exercise intolerance and fatigue in chronic heart failure: is there a role for group III/IV afferent feedback?

Exercise intolerance and early fatiguability are hallmark symptoms of chronic heart failure. While the malfunction of the heart is certainly the leading cause of chronic heart failure, the patho-physiological mechanisms of exercise intolerance in these patients are more complex, multifactorial and only partially understood. Some evidence points towards a potential role of an exaggerated afferent feedback from group III/IV muscle afferents in the genesis of these symptoms. Overactivity of feedback from these muscle afferents may cause exercise intolerance with a double action: by inducing cardiovascular dysregulation, by reducing motor output and by facilitating the development of central and peripheral fatigue during exercise. Importantly, physical inactivity appears to affect the progression of the syndrome negatively, while physical training can partially counteract this condition. In the present review, the role played by group III/IV afferent feedback in cardiovascular regulation during exercise and exercise-induced muscle fatigue of healthy people and their potential role in inducing exercise intolerance in chronic heart failure patients will be summarised.

Influence of blood flow occlusion on muscular recruitment and fatigue during maximal-effort small muscle-mass exercise.

The heavy-to-severe intensity exercise threshold (i.e. critical force) distinguishes between steady-state and progressive metabolic and neuromuscular responses to exercise. High levels of skeletal muscle sensory feedback related to peripheral fatigue development are thought to restrict motor unit activation and limit exercise tolerance. Utilizing limb blood flow occlusion, we demonstrate that critical force reflects an oxygen-delivery-dependent balance between motor unit activation and peripheral fatigue development. Our findings suggest that mechanisms which determine the total force-producing capacity of exercising skeletal muscle are significantly altered during blood flow occlusion. These findings may have widespread implications for exercise tolerance in patient populations who experience partial vascular occlusion or altered neuromuscular reflexes. High levels of muscle sensory feedback restrict motor unit activation and limit exercise tolerance. The roles of muscle fatigue development and motor unit activation in determining the heavy- to severe-intensity threshold (critical force; CF) remain unclear. This study utilized blood flow occlusion (OCC) to determine relationships between muscle fatigue development and motor unit activation during the determination of CF. We hypothesized that (1) OCC would exacerbate peripheral fatigue development and increase the rate of motor unit deactivation, and (2) blood flow reperfusion (REP) would result in muscle recovery and re-recruitment of motor units despite continuous maximal effort, (3) resulting in an end-exercise force not different from CF. Seven young, healthy subjects performed maximal-effort rhythmic handgrip exercise for 5min under control conditions (CON) and during OCC and REP. Peripheral fatigue development and motor unit activation were measured via electrical stimulation and electromyography, respectively, during each test. OCC resulted in significantly greater peripheral fatigue development than CON (54.3±34.8%;P<0.001). Motor unit deactivation was only observed during OCC (P<0.001). REP resulted in significant peripheral recovery (P<0.001) and the re-recruitment of motor units (P<0.001) to levels not different from CON. While OCC resulted in a significantly greater reduction in force production compared to CON (65.7±35.6%;P<0.001), REP resulted in the restoration of maximal-effort force production (266±19N;P<0.001) to levels not different from CF (276±55N).These data suggest that CF reflects an oxygen-delivery-dependent balance between motor unit activation and peripheral fatigue development. Furthermore, this study established that mechanisms which determine the total force-producing capacity of exercising skeletal muscle are altered during OCC.

On the Influence of Group III/IV Muscle Afferent Feedback on Endurance Exercise Performance.

This review discusses evidence suggesting that group III/IV muscle afferents affect locomotor performance by influencing neuromuscular fatigue. These neurons regulate the hemodynamic and ventilatory response to exercise and, thus, assure appropriate locomotor muscle O2 delivery, which optimizes peripheral fatigue development and facilitates endurance performance. In terms of central fatigue, group III/IV muscle afferents inhibit motoneuronal output and thereby limit exercise performance.

Electrical Stimulation-induced Fatigue In The Contralateral Leg Impairs Endurance Exercise Performance

During fatiguing exercise, the development of peripheral fatigue and the associated increased firing of group III/IV afferent fibres, promote central fatigue. PURPOSE: The aim of this study was to assess whether peripheral fatigue in the contralateral leg induced by electrical quadriceps stimulation to bypass central command, would impair endurance performance of the subsequently exercising ipsilateral leg. METHODS: Eight young healthy males were recruited for this study. After completing an incremental test to exhaustion on a single-leg knee extensor ergometer, the subjects performed two tests on separate days. On the first day, they performed a time-to-exhaustion test at 85% of their maximal power output (No-PreF trial). Exercise-induced quadriceps muscle fatigue was assessed by supramaximal electrical femoral nerve stimulation evaluating changes in the potentiated resting twitch force (Qtw,pot), maximal voluntary contraction (MVC) and voluntary activation (VA) from pre to post exercise. On the second day, the same exercise bout was preceded by the induction of fatigue in the contralateral quadriceps through electrical stimulation (PreF trial). The pre-fatiguing protocol was terminated once the subjects reached the maximum tolerance score on a 1-10 visual analogue scale (duration: 6.6 ± 0.9 min). Integrated electromyography (iEMG) was recorded and used to estimate spinal motoneuronal output. RESULTS: Time to exhaustion in the PreF trial was reduced by 41% (9.1 ± 1.5 to 5.4 ± 1.2 min, p < 0.05). The reduction in MVC (-36 ± 8 vs -23 ± 10%, p < 0.05) and Qtw,pot (-53 ± 3 to -39 ± 9% p < 0.05) was more accentuated in the No-PreF trial compared to PreF. Conversely, VA was more affected in PreF than in No-PreF (-20 ± 7 vs -14 ± 5%, p < 0.05). At every submaximal time point, iEMG was significantly higher in PreF compared to No-PreF, while at exhaustion it was higher in the latter (p<0.05). CONCLUSIONS: Pre-induced muscle fatigue in the contralateral limb impairs endurance performance of the exercising ipsilateral limb. This cross-over effect of fatigue is likely mediated by the inhibitory influence associated with group III/IV muscle afferent feedback and not related to changes associated with central command.Funding: No funding was received for this study

The female menstrual cycle: impact on cardiovascular, ventilatory and neuromuscular responses to whole body exercise

BACKGROUNDThe female menstrual cycle (MC) is characterized by varying levels of endogenous sex hormones. Previous investigations have indicated that fluctuating levels of estrogen and progesterone may influence vascular function, ventilatory chemosensitivity, and exercise‐induced fatigue throughout the MC. However, a comprehensive analysis of the role of these sex hormones on determining cardiovascular, ventilatory, and neuromuscular responses during whole body exercise is currently lacking. Therefore, the purpose of this study was to investigate cardiovascular, ventilatory and neuromuscular responses to submaximal cycling exercise of eumenorrheic females throughout the MC.METHODSFemales were studied during three MC phases: early follicular (EF; days 1–4), late follicular (LF; days 8–12), and mid luteal (ML; days 8–10 post LH peak). Prior to exercise, venous blood was collected each visit to characterize endogenous hormone concentrations. Subjects cycled at 50 W, 75 W, 100 W, and 80% Wpeak (129 ± 12 W) for 4 min per stage. Heart rate (HR), mean arterial pressure (MAP), femoral artery blood flow (QL, Doppler ultrasound), minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), and estimated arterial hemoglobin saturation (SpO2) were quantified throughout all cycling trials. Preto post‐exercise changes in potentiated quadriceps twitches (ΔQtw) were used to quantify peripheral locomotor muscle fatigue.RESULTSHR, MAP, and QL were not different at any intensity throughout the MC (P &gt; 0.4). VE, VO2, VCO2 were also not different throughout the MC (P &gt; 0.2). Furthermore, neither hemoglobin content, nor SpO2 and arterial oxygen content changed significantly across the MC (P &gt; 0.1). Consequently, leg O2 delivery during exercise at all intensities were similar during the MC. Finally, exercise‐induced peripheral fatigue was not different throughout the MC (ΔQtw: ~47%; P = 0.2).CONCLUSIONFluctuating endogenous female sex hormones do not significantly influence central or peripheral hemodynamics or the ventilatory response to submaximal whole‐body exercise. Similarly, the exercise‐induced development of peripheral fatigue also remains unaltered across the MC during submaximal cycling exercise of the same duration and intensity. Although depending on the research question, these data suggest that controlling for MC phase may not be necessary when examining cardioventailtory or neuromuscular responses to whole body exercise in females, and should encourage the participation of more females in these types of studies.Support or Funding InformationNational Heart, Lung, and Blood Institute (HL‐116579)

Effects of Nonstationarity on Muscle Force Signals Regularity During a Fatiguing Motor Task.

Physiological signals present fluctuations that can be assessed from their temporal structure, also termed complexity. The complexity of a physiological signal is usually quantified using entropy estimators, such as Sample Entropy. Recent studies have shown a loss of force signal complexity with the development of neuromuscular fatigue. However, these studies did not consider the stationarity of the force signals which is an important prerequisite of Sample Entropy measurements. Here, we investigated the effect of the potential nonstationarity of force signals on the kinetics of neuromuscular fatigue-induced change in force signal's complexity. Eleven men performed submaximal intermittent isometric contractions of knee extensors until exhaustion. Neuromuscular fatigue was assessed from changes in voluntary and electrically evoked contractions. Sample Entropy values were computed from submaximal force signals throughout the fatiguing task. The Dickey-Fuller test was used to statistically investigate the stationarity of force signals and the Empirical Mode Decomposition was applied to detrend these signals. Maximal voluntary force, central voluntary activation and muscle twitch decreased throughout the task (all ), indicating the development of global, central and peripheral fatigue, respectively. We found an increase in Sample Entropy with fatigue ( p = 0.024 ) when not considering the nonstationarity of force signals (i.e., 43% of nonstationary signals). After applying the Empirical Mode Decomposition, we found a decrease in Sample Entropy with fatigue ( p = 0.002 ). These findings confirm the presence of nonstationarity in force signals during submaximal isometric contractions which influences the kinetics of Sample Entropy with neuromuscular fatigue.

Repetitive Activation Compromises Motoneuron Excitability During Fatiguing Exercise

Although fatiguing exercise is known to decrease motoneuronal excitability, the mechanisms underlying this impact remain unclear. PURPOSE: To investigate the role of repetitive motoneuron activation in determining the decrease of motoneuronal excitability during fatiguing exercise. METHODS: On 2 separate days, healthy young subjects (26 ± 6 yrs) performed intermittent isometric knee extensions (at 20% of maximal voluntary quadriceps torque): 1) voluntarily (VOL; i.e. requiring repetitive motoneuron activation), and 2) electrically-evoked (EVO, femoral motor nerve stimulation at 20 Hz; no motoneuron activation). The exercise consisted of 50 s contractions followed by 10 s breaks during which potentiated twitches (Qtw) were assessed to monitor the development of peripheral fatigue during each trial. Exercise continued in each trial until the goal of achieving a similar ~40% reduction in Qtw (ΔQtw) was reached. Before and immediately after exercise, cervicomedullary stimulations (CMS) were used to elicit unconditioned (CMS only) and conditioned (transcranial magnetic stimulation followed by CMS, 100 ms interval) cervicomedullary motor-evoked potentials (CMEPs). All CMEPs were normalized to M-waves and evoked during a constant electromyographic (EMG) activity corresponding to 20% of the EMG obtained during pre-exercise MVCs. RESULTS: In both trials, ΔQtw was, per design, comparable (~40%; P = 0.9) and unconditioned CMEPs were similar before and after exercise (P = 0.23). Conditioned CMEPs were decreased following VOL (-79%, P < 0.05). While conditioned CMEPs were also significantly decreased following EVO (-62%), the exercise-induced reduction was substantially smaller compared to VOL. CONCLUSION: Repetitive activation of the motoneurons contributes to the decrease in motoneuronal excitability during voluntary exercise. It remains unclear whether motoneuronal responsiveness to synaptic input and/or the efficacy of the corticomotoneuronal synapse account for the repetitive activation-related depression. However, as motoneuron excitability still falls during evoked exercise, other mechanisms, potentially related to neural feedback, also contribute to the exercise-induced fall in motoneuronal excitability.

Mental fatigue does not alter performance or neuromuscular fatigue development during self-paced exercise in recreationally trained cyclists.

The purpose of this study was to investigate the effects of mental fatigue, characterized by a subjective feeling of tiredness, on the development of neuromuscular fatigue during a 4-km cycling time trial (4-km TT). Eight recreationally trained male cyclists performed a 4-km TT after either performing a prolonged cognitive task (mental fatigue) or after viewing emotionally neutral documentaries (control). The neuromuscular function of the knee extensors was assessed using electrical nerve stimulation at baseline, before (pre-TT), and after (post-TT) the 4-km TT. Rating of perceived exertion (RPE) and physiological variables were periodically measured during 4-km TT. Subjective ratings of fatigue increased significantly only after a prolonged cognitive task (P = 0.022). Neuromuscular function at baseline was similar between conditions and remained unchanged at pre-TT. Time to complete the 4-km TT was similar between control (376 ± 27s) and mental fatigue (376 ± 26s). There was no significant difference between conditions for RPE, [Formula: see text], [Formula: see text], and HR throughout the exercise. The 4-km TT-induced similar decrease (from baseline to post-TT) in maximal voluntary contraction (mental fatigue - 11 ± 10%, control - 16 ± 12%), twitch force (mental fatigue - 26 ± 16%, control - 24 ± 17%), and voluntary activation (mental fatigue - 5 ± 7%, control - 3 ± 2%) for both conditions. Mental fatigue induced by prolonged cognitive task does not impair performance nor alter the degree of central and peripheral fatigue development during self-paced exercise in recreationally trained cyclists.

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.

Resistance training and exercise tolerance during high-intensity exercise: moving beyond just running economy and muscle strength.

Resistance training and exercise tolerance during high-intensity exercise: moving beyond just running economy and muscle strength.

Central and peripheral fatigue development in the shoulder muscle with obesity during an isometric endurance task

BackgroundFatigue increases the likelihood of developing work-related musculoskeletal disorders and injury. Due to the physiological and neuromuscular changes that accompany obesity, it may alter the fatigue development mechanism and exacerbate injury risk. The upper extremities have the highest incidence rates for work-related musculoskeletal disorders. Therefore, the goals of this study were to investigate the effect of obesity on central vs. peripheral fatigue as well as on the physical signs of fatigue on the middle deltoid muscle.MethodsA measure of central activation ratio was used to quantify central fatigue by considering the increment in the torque output by superimposed twitch relative to its corresponding maximum voluntary contraction. For this purpose, electrical stimulation was delivered at the middle deltoid muscles of 22 non-obese (18 < body mass index (BMI) < 25 kg/m2) and 17 obese (30 < BMI < 40 kg/m2) individuals aged 18-32 years old. Participants completed superimposed maximum voluntary isometric contractions of shoulder abduction before and after a sustained isometric fatiguing task at either 30 or 60% of the muscle capacity. Differences in endurance time, torque fluctuation, torque loss, and muscle activity measured by an electromyography sensor were also investigated.ResultsA greater reduction of voluntary activation of motor units (p = 0.001) with fatigue was observed for individuals who are obese. Contrary to the effect of obesity on central fatigue, a trend toward reduced peripheral fatigue (p = 0.06) was observed for the obese group compared to the non-obese group. On average, a 14% higher rate of torque loss per second was observed among individuals with obesity in comparison to non-obese participants.ConclusionsThe observed greater contribution of central fatigue during the sustained endurance tasks suggests that among young healthy obese individuals, the faster fatigue development with obesity, commonly reported in the literature, is most likely due to the central elements rather than the peripheral factors. This finding has implications for fatigue prevention programs during sustained exertions and can help to develop training, work, and rest schedules considering obesity.

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.