Performance and perceived fatigability across the intensity spectrum: role of muscle mass during cycling.

The role of muscle mass in modulating performance and perceived fatigability across the entire intensity spectrum during cycling remains unexplored. We hypothesized that at task failure (Tlim), muscle contractile function would decline more following single- (SL) versus double-leg (DL) cycling within severe and extreme intensities, but not moderate and heavy intensities. After DL and SL ramp-incremental tests, on separate days, 11 recreationally active males (V̇o2max: 49.5 ± 7.7 mL·kg-1·min-1) completed SL and DL cycling until Tlim within each intensity domain. Power output for SL trials was set at 60% of the corresponding DL trial. Before and immediately after Tlim, participants performed an isometric maximal voluntary contraction (MVC) coupled with one superimposed and three resting femoral nerve stimulations [100 Hz; 10 Hz; single twitch (Qtw)] to measure performance fatigability. Perceived fatigue, leg pain, dyspnea, and effort were collected during trials. Tlim within each intensity domain was not different between SL and DL (all P > 0.05). MVC declined more for SL versus DL following heavy- (-42 ± 16% vs. -30 ± 18%; P = 0.011) and severe-intensity cycling (-41 ± 12% vs. -31 ± 15%; P = 0.036). Similarly, peak Qtw force declined more for SL following heavy- (-31 ± 12% vs. -22 ± 10%; P = 0.007) and severe-intensity cycling (-49 ± 13% vs. -40 ± 7%; P = 0.048). Except for heavy intensity, voluntary activation reductions were similar between modes. Similarly, except for dyspnea, which was lower for SL versus DL across all domains, ratings of fatigue, pain, and effort were similar at Tlim between exercise modes. Thus, the amount of muscle mass modulates the extent of contractile function impairment in an intensity-dependent manner.NEW & NOTEWORTHY We investigated the modulatory role of muscle mass on performance and perceived fatigability across the entire intensity spectrum. Despite similar time-to-task failure, single-leg cycling resulted in greater impairments in muscle contractile function within the heavy- and severe-intensity domains, but not the moderate- and extreme-intensity domains. Perceived fatigue, pain, and effort were similar between cycling modes. This indicates that the modulatory role of muscle mass on the extent of performance fatigability is intensity domain-dependent.

Hypertension Restricts Leg Blood Flow and Aggravates Neuromuscular Fatigue during Human Locomotion in Males.

Patients with hypertension (HTN) are characterized by exaggerated vascular resistance and mean arterial pressure (MAP), and a compromised leg blood flow (QL) response to exercise recruiting a small muscle mass. However, the impact of hypertension on peripheral hemodynamics and the development of neuromuscular fatigue during locomotor activities, which critically depends on QL, remain unknown. Eight HTN (143±11mmHg / 95±6mmHg; 45±13years) and 8 matched (age, activity) controls (120±6mmHg / 77±7mmHg; CTRL) performed constant-load cycling exercise at 25, 50, and 75W (for 4-min each), and at 165±41W (for 5-min). Exercise-induced locomotor muscle fatigue was quantified as the pre- to post-exercise change in quadriceps twitch-torque (∆Qtw, peripheral fatigue) and voluntary activation (∆VA%, central fatigue). QL (Doppler-ultrasound) and leg vascular conductance (LVC) were determined during cycling at 25, 50, and 75W. Heart Rate and ventilatory responses were recorded during all intensities. MAP during exercise was, on average, ~21mmHg higher (P=0.002) and LVC ~39% lower (P=0.001) in HTN compared to CTRL. QL was consistently between 20-30% lower (P=0.004) and heart rate was significantly higher in HTN. Exercise-induced peripheral (∆Qtw: -53±19% vs -25±23%) and central (∆VA%: -7±5% vs -3±2%) fatigue were significantly greater in HTN compared to CTRL. In addition to an exaggerated MAP, LVC and QL were lower during exercise in HTN compared to CTRL. Given the critical role of QL in determining the development of neuromuscular fatigue, these hemodynamic impairments likely accounted for the faster development of neuromuscular fatigue characterizing hypertensive individuals during locomotor exercise.

Activation of skeletal muscle mechanoreceptors and nociceptors reduces the exercise performance of the contralateral homologous muscles.

Increasing evidence suggests that activation of muscle nerve afferents may inhibit central motor drive, affecting contractile performance of remote exercising muscles. Although these effects are well documented for metaboreceptors, very little is known about the activation of mechano- and mechanonociceptive afferents on performance fatigability. Therefore, the purpose of the present study was to examine the influence of mechanoreceptors and nociceptors on performance fatigability. Eight healthy young males undertook four randomized experimental sessions on separate occasions in which the experimental knee extensors were the following: 1) resting (CTRL), 2) passively stretched (ST), 3) resting with delayed onset muscle soreness (DOMS), or 4) passively stretched with DOMS (DOMS+ST), whereas the contralateral leg performed an isometric time to task failure (TTF). Changes in maximal voluntary contraction (ΔMVC), potentiated twitch force (ΔQtw,pot), and voluntary muscle activation (ΔVA) were also assessed. TTF was reduced in DOMS+ST (-43%) and ST (-29%) compared with CTRL. DOMS+ST also showed a greater reduction of VA (-25% vs. -8%, respectively) and MVC compared with CTRL (-28% vs. -45%, respectively). Rate of perceived exertion (RPE) was significantly increased at the initial stages (20-40-60%) of the TTF in DOMS+ST compared with all conditions. These findings indicate that activation of mechanosensitive and mechanonociceptive afferents of a muscle with DOMS reduces TTF of the contralateral homologous exercising limb, in part, by reducing VA, thereby accelerating mechanisms of central fatigue.NEW & NOTEWORTHY We found that activation of mechanosensitive and nociceptive nerve afferents of a rested muscle group experiencing delayed onset muscle soreness was associated with reduced exercise performance of the homologous exercising muscles of the contralateral limb. This occurred with lower muscle voluntary activation of the exercising muscle at the point of task failure.

Decreased neural drive affects the early rate of force development after repeated burst-like isometric contractions.

The neural drive to the muscle is the primary determinant of the rate of force development (RFD) in the first 50 ms of a rapid contraction. It is still unproven if repetitive rapid contractions specifically impair the net neural drive to the muscles. To isolate the fatiguing effect of contraction rapidity, 17 male adult volunteers performed 100 burst-like (i.e., brief force pulses) isometric contractions of the knee extensors. The response to electrically-evoked single and octet femoral nerve stimulation was measured with high-density surface electromyography (HD-sEMG) from the vastus lateralis and medialis muscles. Root mean square (RMS) of each channel of HD-sEMG was normalized to the corresponding M-wave peak-to-peak amplitude, while muscle fiber conduction velocity (MFCV) was normalized to M-wave conduction velocity to compensate for changes in sarcolemma properties. Voluntary RFD 0-50 ms decreased (d = -0.56, p < 0.001) while time to peak force (d = 0.90, p < 0.001) and time to RFDpeak increased (d = 0.56, p = 0.034). Relative RMS (d = -1.10, p = 0.006) and MFCV (d = -0.53, p = 0.007) also decreased in the first 50 ms of voluntary contractions. Evoked octet RFD 0-50 ms (d = 0.60, p = 0.020), M-wave amplitude (d = 0.77, p = 0.009) and conduction velocity (d = 1.75, p < 0.001) all increased. Neural efficacy, i.e., voluntary/octet force ratio, largely decreased (d = -1.50, p < 0.001). We isolated the fatiguing impact of contraction rapidity and found that the decrement in RFD, particularly when calculated in the first 50 ms of muscle contraction, can mainly be explained by a decrease in the net neural drive.

Peripheral fatigue regulation during knee extensor exercise in type 1 diabetes and consequences on the force-duration relationship.

PURPOSE: This study aimed to examine if peripheral fatigue is adjusted during knee extensor (KE) exercise in order not to surpass a critical threshold patient with type 1 diabetes (T1D) and the consequences of this mechanism on the force-duration relationship. METHODS: Eleven T1D individuals randomly performed two different sessions in which they performed 60 maximum voluntary contractions (MVC; 3 s contraction, 2 s relaxation). One trial was performed in the non-fatigued state (CTRL) and another after fatiguing neuromuscular stimulation of the KE (FNMES). Peripheral and central fatigue were quantified by the difference between pre and post exercise in quadriceps voluntary activation (ΔVA) and potentiated twitch (ΔPtw). Critical torque (CT) was determined as the average force of the last 12 contractions, whereas W' was calculated as the area above the CT. RESULTS: Although FNMES led to a significant decrease in potentiated twitch (Ptw) before performing the 60-MVCs protocol (p < 0.05), ΔVA (∼ -7.5%), ΔPtw (∼ -39%), and CT (∼816 N) post-MVCs were similar between the two conditions. The difference in W' between CTRL and FNMES was correlated with the level of pre-fatigue induced in FNMES (r2 = 0.60). In addition, W' was correlated with ΔPtw (r2 = 0.62) in the CTRL session. CONCLUSION: Correlative results in the present study indicate that regulating peripheral fatigue mechanisms at a critical threshold limit W'. Additionally, peripheral fatigue during KE exercise is limited to an individual threshold in T1D patients.

No sex differences in time-to-task failure and neuromuscular patterns of response during submaximal, bilateral, isometric leg extensions.

BACKGROUND: In general, it has been suggested that females are more fatigue-resistant than males, with the magnitude of difference being most pronounced during low-intensity sustained contractions. However, the mechanisms for the apparent sex difference have not yet been fully elucidated in the literature. This study aimed to examine sex-related differences in fatigability and patterns of neuromuscular responses for surface electromyographic (sEMG) and mechanomyographic (sMMG) amplitude and frequency (MPF) characteristics during a sustained submaximal bilateral, isometric leg extension muscle action. METHODS: A sample of 20 young recreationally active males and females with previous resistance training experience performed a sustained, submaximal, bilateral isometric leg extension until task failure. Time-to-task failure was compared using a nonparametric bootstrap of the 95% confidence interval for the mean difference between males and females. Additionally, patterns of response for sEMG and sMMG amplitude and MPF of the dominant limb were examined using linear mixed effect models. RESULTS: There were no differences in time-to-task failure between males and females. Additionally, neuromuscular responses revealed similar patterns of responses between males and females. Interestingly, sEMG amplitude and sMMG amplitude and MPF all revealed non-linear responses, while sEMG MPF demonstrated linear responses. CONCLUSION: These data revealed that time-to-task failure was not different between males and females during sustained submaximal bilateral, isometric leg extension. Interestingly, the parallel, non-linear, increases in sEMG and sMMG amplitude may indicate fatigue induced increases in motor unit recruitment, while the parallel decreases in sMMG MPF may be explained by the intrinsic properties of later recruited motor units, which may have inherently lower firing rates than those recruited earlier.

A Single Bout of On-Ice Training Leads to Increased Interlimb Asymmetry in Competitive Youth Hockey Athletes.

Interlimb asymmetry (ILA) refers to an anatomical or physiological imbalance between contralateral limbs, which can influence neuromuscular function. Investigating the influence of neuromuscular fatigue on ILA may be critical for optimizing training programs, injury rehabilitation, and sport-specific performance. The purpose of this study was to determine if a single bout of ice hockey-specific exercise creates or exacerbates lower-limb ILA. Before and after an on-ice training session, 33 youth ice-hockey athletes (14.9 [1.7] y; 11 females) performed 3 repetitions of a maximal vertical countermovement jump (CMJ), an eccentric hamstring contraction, and maximal isometric hip adduction and abduction contractions. Force- and power-related variables were analyzed to determine limb-specific neuromuscular function. The on-ice session reduced maximal isometric hip adduction (left: 7.3% [10.3%]; right: 9.5% [9.6%]) and abduction (left: 4.9% [6.9%]; right: 5.0% [8.1%]) force, but did not impair (P ≥ .10) CMJ performance (jump height, relative peak power, braking duration, and total duration). After the on-ice session, ILA was greater for CMJ propulsive impulse (6.3% [2.9%] vs 5.1% [2.6%]), CMJ braking rate of force development (19.3% [7.6%] vs 15.2% [6.4%]), and peak isometric hip adduction force (6.7% [5.5%] vs 6.1% [4.1%]). In conclusion, hockey-specific exercise leads to increased ILA for multiple force-related metrics, which may be a compensatory mechanism to maintain bilateral task performance when fatigued.

Acute and prolonged competing effects of activation history on human motor unit firing rates during contractile impairment and recovery.

The purpose of this study was to investigate the effect of inducing post-activation potentiation (PAP) during prolonged low-frequency force depression (PLFFD) on motor unit (MU) firing rates. In 10 participants, grouped firing rates of 3027 MUs from the tibialis anterior were recorded with tungsten microelectrodes. Baseline MU firing rates at 25% isometric maximal voluntary contraction (MVC) were ∼14 Hz. A 1 min dorsiflexion MVC reduced torque and maximal MU firing rates (36 Hz) by 49% and 52%, respectively. Following task completion, firing rates at 25% of baseline MVC torque and torque in response to electrically evoked (single twitch, 10 Hz and 50 Hz) stimulation were assessed before and after a 5 s MVC (to induce PAP) every 10 min for 60 min. From 10 to 60 min after task completion, the torque ratios (twitch:50 Hz and 10:50 Hz) were depressed (∼30%) relative to baseline (P < 0.001), indicating PLFFD; and firing rates were higher by ∼15% relative to baseline (P < 0.001). This occurred despite recovery of MVC rates (∼99%) and torque (∼95%) by 10 min (P > 0.3). Inducing PAP during PLFFD increased both low to high torque ratios (twitch and 10:50 Hz) by ∼200% and ∼135%, respectively (P < 0.001) and firing rates were ∼18% lower relative to PLFFD rates (P < 0.001), despite a speeding of evoked contractile properties (P = 0.001). Thus, firing rates appear strongly matched to alterations in torque, rather than contractile speed when modified by contractile history, and lower rates during PAP may be a mechanism to mitigate effects of PLFFD. The effect of activation history on contractile function demonstrates acute compensatory responses of motoneuron output. KEY POINTS: Prolonged low frequency force depression (PLFFD) following a sustained 1 min isometric maximal voluntary contraction causes an increase in submaximal mean motor unit (MU) firing rates. Inducing post-activation potentiation (PAP) during PLFFD, however, causes a reduction in mean submaximal MU firing rates to a level below those at baseline. The mean firing rate reduction during PAP occurs despite a speeding of evoked contractile properties and thus firing rates are more strongly matched to alterations in torque, rather than contractile speed when modified by various contractile histories. The reductions in firing rates during PAP may mitigate the effects of PLFFD during voluntary contractions. These results demonstrate that firing rates are highly responsive to opposing influences on the contractile state and can make rapid compensatory rate adjustments dependent on the active state of the muscle.

COVID-19 and postural sway: a comparison of individuals with a SARS-CoV-2 history and healthy sedentary women.

PURPOSE: The aim of the study was to evaluate the effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on postural sway in subjects who have recently recovered from infection. MATERIALS AND METHODS: Fifty-six female individuals with a mild to moderate history of SARS-CoV-2 (n = 25, mean age; 21.13 ± 0.64 years) and healthy sedentary controls (n = 31, mean age; 20.09 ± 1.05 years) were included in the study. Postural sway tests were performed in double and single-leg stance on a force plate with eyes open before and after the neuromuscular fatigue test. The Wingate test was used to induce neuromuscular fatigue. To evaluate the change of the variables determined by the measurements of the groups over time and the group-time interactions, a two-way analysis of variance in repeated measures (mixed design repeated measures ANOVA) was used. RESULTS: It was found that the SARS-CoV-2 group showed increased total sway path, velocity, and area than those in the healthy group on double and single-leg (right-left) stance (p < 0.05). CONCLUSIONS: Even if SARS-CoV-2 group individuals have been reported in a mild to moderate outpatient COVID-19 process, they showed deterioration in postural control compared to healthy individuals. In addition, it was found that SARS-CoV-2 accelerated neuromuscular fatigue effects. This can cause more fatigue during activities than individuals who have not had SARS-CoV-2.

Neuromuscular and autonomic function is fully recovered within 24 h following a sprint interval training session.

BACKGROUND: Recovery is a key factor to promote adaptations and enhance performance. Sprint Interval Training (SIT) is known to be an effective approach to improve overall physical function and health. Although a 2-day rest period is given between SIT sessions, the time-course of recovery after SIT is unknown. PURPOSE: The aim of this study was to determine whether the neuromuscular and autonomic nervous systems would be impaired 24 and 48 h after an SIT session. METHODS: Twenty-five healthy subjects performed an 8 × 15 s all-out session on a braked cycle ergometer with 2 min of rest between repetitions. Isometric maximal voluntary contraction (iMVC) and evoked forces to electrical nerve stimulation during iMVC and at rest were used to assess muscle contractile properties and voluntary activation before (Pre), 1 (Post24h), and 2 (Post48h) days after the session. Two maximal 7 s sprints with two different loads were performed at those same time-points to evaluate the maximal theoretical force (F0), velocity (V0) and maximal power (Pmax) production during a dynamic exercise. Additionally, nocturnal heart rate variability (HRV) was assessed the previous and the three subsequent nights to the exercise bout. RESULTS: No significant impairments were observed for the iMVC or for the force evoked by electrical stimulation 1 day after the session. Similarly, F0, V0, and Pmax were unchanged at Post24h and Post48h. Furthermore, HRV did not reveal any temporal or frequential significant difference the nights following SIT compared to Pre. CONCLUSION: The results of this study show a full recovery of neuromuscular and autonomic functions a day after an all-out SIT session.

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

PURPOSE: The 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. METHODS: Fifteen 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. RESULTS: Early-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). CONCLUSION: These 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.

Mechanisms underlying altered neuromuscular function in people with DPN.

Diabetes alters numerous physiological functions and can lead to disastrous consequences in the long term. Neuromuscular function is particularly affected and is impacted early, offering an opportunity to detect the onset of diabetes-related dysfunctions and follow the advancement of the disease. The role of physical training for counteracting the deleterious effects of diabetes is well accepted but at the same time, it appears difficult to reliably assess the effects of exercise on functional capacity in patients with diabetic peripheral neuropathy (DPN). In this paper, we will review the specific characteristics of various neuromuscular dysfunctions associated with diabetes according to the DPN presence or not, and their changes over time. We present several propositions regarding the onset of neuromuscular alterations in people with diabetes compared to people with DPN. It appears that motor unit loss and neuromuscular transmission impairment are among the main mechanisms explaining the considerable degradation of neuromuscular function in the transition from a diabetic to neuropathic state. Rate of force development and contractile properties could start to decrease with the onset of preferential type II fiber atrophy, commonly reported in people with DPN. Finally, Mmax amplitude could decrease with neuromuscular fatigue only in people with DPN, reflecting the fatigue-related neuromuscular transmission impairment reported in people with DPN. In this review, we show that the different neuromuscular parameters are altered at different stages of diabetes, according to the presence of DPN or not. The precise evaluation of these parameters might participate in adapting the physical training prescription.

Exercise-induced fatigue affects knee proprioceptive acuity and quadriceps neuromuscular function more in patients with ACL reconstruction or meniscus surgery than in healthy individuals.

PURPOSE: To observe how knee proprioceptive acuity and quadriceps neuromuscular function change during and after repeated isokinetic knee-extension exercise in patients with anterior cruciate ligament reconstruction (ACLR) or meniscus surgery. METHODS: Patients with ACLR or meniscus surgery and matched controls (n = 19 in each group) performed knee-flexion replication at 15° and 75°, and quadriceps peak torque (PT), central activation ratio (CAR) and rate of torque development (RTD) at baseline and immediately after every five sets of isokinetic knee-extension exercise (times 1-5). RESULTS: Compared to the baseline, the ACLR and control groups displayed errors in knee-flexion replication at 75° only at time 5 (115.9-155.6%; p ≤ 0.04, d ≥ 0.97), whereas the meniscus surgery group exhibited errors at all time points (142.5-265.6%; p ≤ 0.0003, d ≥ 1.4). Significant percentage reductions in quadriceps CAR were observed between times 4 and 5 in the ACLR group (-5.8%; p = 0.0002, d = 0.96), but not in the meniscus surgery (-1.4%; n.s.) and control (0.1%; n.s.) groups. Significant percentage reductions in quadriceps RTD were observed between times 4 and 5 in the ACLR (-24.2%; p = 0.007, d = 0.99) and meniscus surgery (-23.0%; p = 0.01, d = 0.85) groups, but not in the control group (-0.2%; n.s.). CONCLUSION: Patients with ACLR or meniscus surgery displayed a greater loss in knee proprioceptive acuity and quadriceps neuromuscular function during and after exercise than healthy individuals. Evidence-based interventions to enhance exercise-induced fatigue resistance should be implemented following ACLR or meniscus surgery, aiming to prevent proprioceptive and neuromuscular changes within the knee joint and quadriceps. LEVEL OF EVIDENCE: III.

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 ± 5 years; 180 ± 4 cm; 76 ± 10 kg) performed two consecutive intermittent isometric single-leg knee-extensor trials (60 maximal voluntary contractions; 3 s contraction, 2 s relaxation) interspersed with 5 min 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+ ] (ß 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 5 min 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.

Relationship between neuromuscular fatigue, muscle activation and the work done above the critical power during severe-intensity exercise.

NEW FINDINGS: What is the central question of this study? Does the work done above critical power (W') or muscle activation determine the degree of peripheral fatigue induced by cycling time trials performed in the severe-intensity domain? What is the main finding and its importance? Peripheral fatigue increased when power output and muscle activation increased, whereas W' did not change between the time trials. Therefore, no relationship was found between W' and exercise-induced peripheral fatigue such as previously postulated in the literature. In contrast, we found a significant association between EMG amplitude during exercise and exercise-induced reduction in the potentiated quadriceps twitch, suggesting that muscle activation plays a key role in determining peripheral fatigue during severe-intensity exercise. ABSTRACT: In order to determine the relationship between peripheral fatigue, muscle activation and the total work done above critical power (W'), 10 men and four women performed, on separated days, self-paced cycling time trials of 3, 6, 10 and 15 min. Exercise-induced quadriceps fatigue was quantified using pre- to postexercise (15 s to 15 min recovery) changes in maximal voluntary contraction (MVC) peak force, voluntary activation and potentiated twitch force (QT). Voluntary activation was measured using the interpolated twitch technique, and QT was evoked by electrical stimulations of the femoral nerve. Quadriceps muscle activation was determined using the root mean square of surface EMG of vastus lateralis (VLRMS ), vastus medialis (VMRMS ) and rectus femoris (RFRMS ). Critical power and W' were calculated from the power-duration relationship from the four time trials. Mean power output and mean VLRMS , VMRMS and RFRMS were greater during shorter compared with longer exercise periods (P < 0.05), whereas no significant between-trial change in W' was found. The magnitude of exercise-induced reductions in QT increased with the increase in power output (P < 0.001) and was associated with mean VLRMS, VMRMS and RFRMS (P < 0.001, r2  > 0.369) but not W' (P > 0.150, r2  < 0.044). Reduction in voluntary activation tended (P = 0.067) to be more pronounced with the lengthening in time trial duration, whereas no significant between-trial changes in MVC peak force were found. Our data suggest that peripheral fatigue is not related to the amount of work done above the critical power but rather to the level of muscle activation during exercise in the severe-intensity domain.

The effect of hypertonic saline evoked muscle pain on neurophysiological changes and exercise performance in the contralateral limb.

Non-local muscle pain may impair endurance performance through neurophysiological mechanisms, but these are relatively unknown. This study examined the effects of muscle pain on neuromuscular and neurophysiological responses in the contralateral limb. On separate visits, nine participants completed an isometric time to task failure (TTF) using the right knee extensors after intramuscular injection of isotonic saline (CTRL) or hypertonic saline (HYP) into the left vastus lateralis. Measures of neuromuscular fatigue were taken before, during and after the TTF using transcranial magnetic stimulation (TMS) and peripheral nerve stimulation. Mean pain intensity was greater in the left leg in HYP (3.3 ± 1.9) compared to CTRL (0.4 ± 0.7; P < 0.001) which was combined with a reduced TTF by 9.8% in HYP (4.54 ± 0.56 min) compared to CTRL (5.07 ± 0.77 min; P = 0.005). Maximum voluntary force was not different between conditions (all P > 0.05). Voluntary activation was lower in HYP compared to CTRL (P = 0.022). No difference was identified between conditions for doublet amplitude (P > 0.05). Furthermore, no difference in MEP·Mmax-1 or the TMS silent period between conditions was observed (all P > 0.05). Non-local pain impairs endurance performance of the contralateral limb. This impairment in performance is likely due to the faster attainment of the sensory tolerance limit from a greater amount of sensory feedback originating from the non-exercising, but painful, left leg.

Muscular heat shock protein response and muscle damage after semi-professional football match.

PURPOSE: A typical football match leads to neuromuscular fatigue and physical performance impairments up to 72-96 h post-match. While muscle damage is thought to be a major factor, damage on the ultrastructural level has never been documented. The purpose of this study was to investigate post-match cellular muscle damage by quantifying the heat shock protein (HSP) response as a proxy for protein damage. METHODS: Muscle biopsies, blood samples, countermovement jumps, and perception of muscle soreness were obtained from twelve semi-professional football players 1, 24, 48, and 72 h after a 90-min football match. Muscle biopsies were analyzed for αB-crystallin and HSP70 in the cytosolic and cytoskeletal sub-cellular fractions by Western blotting. Fiber type-specific αB-crystallin and HSP70 staining intensity, and tenascin-C immunoreactivity were analyzed with immunohistochemistry. Blood samples were analyzed for creatine kinase and myoglobin. RESULTS: Within 24 h post-match, a 2.7- and 9.9-fold increase in creatine kinase and myoglobin were observed, countermovement jump performance decreased by -9.7% and muscle soreness increased by 0.68 units. αB-crystallin and HSP70 accumulated in cytoskeletal structures evident by a 3.6- and 1.8-fold increase in the cytoskeletal fraction and a parallel decrease in the cytosolic fraction. In type I and II fibers, αB-crystallin staining intensity increased by 15%-41% and remained elevated at 72 h post-match. Lastly, the percentage of fibers with granular staining of αB-crystallin increased 2.2-fold. CONCLUSIONS: Football match play induced a muscular HSP stress response 1-72 h post-match. Specifically, the accumulation of HSPs in cytoskeletal structures and the granular staining of αB-crystallin suggests occurrence of ultrastructural damage. The damage, indicated by the HSP response, might be one reason for the typically 72 h decrease in force-generating capacity after football matches.

Relationship between perceived and neuromuscular fatigue in COPD patients with chronic respiratory failure with long-term oxygen therapy: a cross-sectional study.

PURPOSE: To evaluate perceived fatigue (PF) and neuromuscular fatigue (NMF) in patients with COPD and chronic respiratory failure (CRF) on long-term oxygen therapy (CRF-COPD group), and the relationships between PF, NMF, patient's characteristics, comparing severe patients with COPD to patients without CRF (COPD group). METHODS: This cross-sectional study compared 19 CRF-COPD patients with 10 COPD patients attending a rehabilitation program. PF was determined by Fatigue Severity Scale (FSS), while dyspnea by the Barthel Dyspnea Index (BDI). We assessed quadriceps NMF via electrical nerve stimulation during and following a Maximal Voluntary Contraction (MVC) detecting changes after a Constant Workload Cycling Test (CWCT) at 80% of the peak power output at exhaustion. RESULTS: CRF-COPD patients showed higher PF (+ 1.79 of FSS score, p = 0.0052) and dyspnea (+ 21.03 of BDI score, p = 0.0023) than COPD patients. After the fatiguing task and normalization for the total work, there was a similar decrease in the MVC (CRF-COPD -1.5 ± 2.4 vs COPD -1.1 ± 1.2% baseline kJ-1, p = 0.5819), in the potentiated resting twitch force (CRF-COPD -2.8 ± 4.7 vs COPD -2.0 ± 3.3% baseline kJ-1, p = 0.7481) and in the maximal voluntary activation (CRF-COPD -0.1 ± 3.9 vs COPD -0.9 ± 1.2 -2.0 ± 3.3% baseline kJ-1, p = 0.4354). FSS and BDI were closely related (R = 0.5735, p = 0.0011), while no correlation between PF and NMF was found. CONCLUSION: Patients with CRF-COPD develop higher levels of perceived fatigue and dyspnea than patients with COPD; while neuromuscular fatigue is similar, suggesting a mismatch between symptoms and neuromuscular dysfunction.

The effect of elevated muscle pain on neuromuscular fatigue during exercise.

PURPOSE: Muscle pain can impair exercise performance but the mechanisms for this are unknown. This study examined the effects of muscle pain on neuromuscular fatigue during an endurance task. METHODS: On separate visits, twelve participants completed an isometric time-to-task failure (TTF) exercise of the right knee extensors at ~ 20% of maximum force following an intramuscular injection of isotonic saline (CTRL) or hypertonic saline (HYP) into the vastus lateralis. Measures of neuromuscular fatigue were taken before, during and after the TTF using transcranial magnetic stimulation (TMS) and peripheral nerve stimulation. RESULTS: The mean pain intensity was 57 ± 10 in HYP compared to 38 ± 18 in CTRL (P < 0.001). TTF was reduced in HYP (4.36 ± 0.88 min) compared to CTRL (5.20 ± 0.39 min) (P = 0.003). Maximum voluntary force was 12% lower at minute 1 (P = 0.003) and 11% lower at minute 2 in HYP (P = 0.013) compared to CTRL. Voluntary activation was 4% lower at minute 1 in HYP compared to CTRL (P = 0.006) but not at any other time point (all P > 0.05). The TMS silent period was 9% longer at 100 s during the TTF in HYP compared to CTRL (P = 0.026). CONCLUSION: Muscle pain reduces exercise performance through the excacerbation of neuromuscular fatigue that is central in origin. This appears to be from inhibitory feedback from group III/IV nociceptors which acts to reduce central motor output.

What Is the Most Sensitive Test to Identify Fatigue through the Analysis of Neuromuscular Status in Male Elite Futsal Players?

The present study aimed to determine which of the neuromuscular status (NMS) monitoring tests (1: Counter-movement jump, CMJ; 2: back squat with additional load) is the most sensitive and effective for evaluating the state of fatigue in futsal players during the preseason. Seventeen professional futsal players were recruited for this study (age: 23.07 ± 6.76 years; height: 1.75 ± 0.06 m; body mass: 75.47 ± 7.47 kg; playing experience in elite: 5.38 ± 2.03 years). All of them were evaluated during the preseason phase in two tests (CMJ and back squat with additional load) before and after each training session (pre- vs. post-test). A jump platform was used to extract jump height during CMJ, while a linear position transducer was used to extract mean velocity (MV) and mean propulsive velocity (MPV) during the back squat exercise. Significant differences were obtained for intra-subject analysis for MV and MPV in loaded back squat exercise (p < 0.001), finding lower values during the post-test. In conclusion, the monitoring of NMS through the back squat provides greater sensitivity and objectivity in comparison with CMJ, due to a more direct neuromuscular extrapolation to the physical demands of futsal.