Motor unit discharge rate modulation during isometric contractions to failure is intensity- and modality-dependent.

The physiological mechanisms determining the progressive decline in the maximal muscle torque production capacity during isometric contractions to task failure are known to depend on task demands. Task-specificity of the associated adjustments in motor unit discharge rate (MUDR), however, remains unclear. This study examined MUDR adjustments during different submaximal isometric knee extension tasks to failure. Participants performed a sustained and an intermittent task at 20% and 50% of maximal voluntary torque (MVT), respectively (Experiment 1). High-density surface EMG signals were recorded from vastus lateralis (VL) and medialis (VM) and decomposed into individual MU discharge timings, with the identified MUs tracked from recruitment to task failure. MUDR was quantified and normalised to intervals of 10% of contraction time (CT). MUDR of both muscles exhibited distinct modulation patterns in each task. During the 20% MVT sustained task, MUDR decreased until ∼50% CT, after which it gradually returned to baseline. Conversely, during the 50% MVT intermittent task, MUDR remained stable until ∼40-50% CT, after which it started to continually increase until task failure. To explore the effect of contraction intensity on the observed patterns, VL and VM MUDR was quantified during sustained contractions at 30% and 50% MVT (Experiment 2). During the 30% MVT sustained task, MUDR remained stable until ∼80-90% CT in both muscles, after which it continually increased until task failure. During the 50% MVT sustained task the increase in MUDR occurred earlier, after ∼70-80% CT. Our results suggest that adjustments in MUDR during submaximal isometric contractions to failure are contraction modality- and intensity-dependent. KEY POINTS: During prolonged muscle contractions a constant motor output can be maintained by recruitment of additional motor units and adjustments in their discharge rate. Whilst contraction-induced decrements in neuromuscular function are known to depend on task demands, task-specificity of motor unit discharge behaviour adjustments is still unclear. In this study, we tracked and compared discharge activity of several concurrently active motor units in the vastii muscles during different submaximal isometric knee extension tasks to failure, including intermittent vs. sustained contraction modalities performed in the same intensity domain (Experiment 1), and two sustained contractions performed at different intensities (Experiment 2). During each task, motor units modulated their discharge rate in a distinct, biphasic manner, with the modulation pattern depending on contraction intensity and modality. These results provide insight into motoneuronal adjustments during contraction tasks posing different demands on the neuromuscular system.

Exacerbated impairments in neuromuscular function when two bouts of team sport match simulations are separated by 48 h.

Intermittent team sports, involving high metabolic and mechanical demands, elicit prolonged impairments in neuromuscular function which persist for ∼48-72 h. Whether impairments in neuromuscular function are exacerbated when such exercise is repeated with incomplete recovery is unknown. This study assessed the neuromuscular, heart rate and metabolic responses to two bouts of ∼90 min modified team sport match simulations separated by 48 h in 12 competitive football players. Before and 2 min after both bouts, knee extensor isometric maximal voluntary contraction (MVC), contractile function (Qtw,pot ) and voluntary activation (VA) were measured. Heart rate (HR), sprint time, blood lactate and glucose were measured throughout both bouts. MVC was reduced relative to baseline at post-bout 1 (21 ± 12%; P = 0.003) and pre-bout 2 (14 ± 11%; P = 0.009), and was lower post-bout 2 (33 ± 14%; P < 0.001) relative to post-bout 1 (P = 0.036). Qtw,pot was reduced post-bout 1 (30 ± 11%; P < 0.001) and pre-bout 2 (9 ± 6%; P = 0.004), and was not different post-bout 2 (28 ± 8%; P < 0.001) relative to post-bout 1 (P = 0.872). VA was reduced post-bout 1 (8 ± 7%; P = 0.023), recovered pre-bout 2 (P = 0.133) and was lower post-bout 2 (16 ± 7%; P < 0.001) relative to post-bout 1 (P = 0.029). Total sprint time was longer, and HR, blood lactate and glucose were lower during bout 2 than bout 1 (P ≤ 0.021). Thus, impairments in neuromuscular function are exacerbated when high-intensity intermittent exercise is performed with incomplete recovery concurrent with accentuated reductions in VA. The lower blood lactate and glucose during the second bout might be due, at least in part, to reduced glycogen availability upon commencing exercise and consequently a greater reliance on glucose extraction. NEW FINDINGS: What is the central question of this study? There is limited evidence on whether impairments in neuromuscular function are exacerbated when prolonged high-intensity intermittent exercise is repeated with incomplete recovery: what are the neuromuscular consequences of performing two bouts of a modified team sport match simulations separated by 48 h? What is the main finding and its importance? Impairments in knee extensor force generating capacity are exacerbated concurrent with accentuated reductions in nervous system activation of muscle when prolonged high-intensity intermittent exercise is repeated with 48 h recovery.

Acute effects of conventional versus wide-pulse neuromuscular electrical stimulation on quadriceps evoked torque and neuromuscular function.

PURPOSE: The effectiveness of a neuromuscular electrical stimulation (NMES) program is proportional to the level of evoked torque, which can be achieved with either conventional or wide-pulse stimulations. The aim of this study was to compare evoked torque, objective fatigability, and related peripheral and central alterations, as well as changes in central nervous system (CNS) excitability induced by an acute session of conventional versus wide-pulse NMES. METHODS: Seventeen young men underwent three 20-min NMES sessions: conventional (0.2 ms/50 Hz), wide-pulse at 50 Hz (1 ms/50 Hz), and wide-pulse at 100 Hz (1 ms/100 Hz). Neuromuscular measurements (i.e., maximal voluntary contraction, voluntary activation, evoked responses to femoral nerve stimulation, and CNS excitability) were performed on the right quadriceps femoris muscle before and after each NMES session. CNS excitability was measured using transcranial magnetic, thoracic, and transcutaneous spinal cord stimulations. RESULTS: The level of evoked torque was not significantly different between conventional and wide-pulse protocols applied at the maximal tolerable current intensity. All NMES protocols induced objective fatigability (~14% decrease in maximal voluntary contraction torque, p < 0.001) associated with peripheral (decrease in doublet torque and potentiated M-wave amplitude, p = 0.002 and p < 0.001, respectively) but not central (unchanged voluntary activation, p = 0.79) alterations. However, these acute changes did not differ between NMES protocols and none of the NMES protocols modified markers of CNS excitability. CONCLUSION: These results may allow to conjecture that chronic effects and treatment effectiveness could be comparable between conventional and wide-pulse NMES.

Cardiorespiratory Fitness and Neuromuscular Function of Mechanically Ventilated ICU COVID-19 Patients.

OBJECTIVES: The aim of the current study was to investigate the level of cardiorespiratory fitness and neuromuscular function of ICU survivors after COVID-19 and to examine whether these outcomes are related to ICU stay/mechanical ventilation duration. DESIGN: Prospective nonrandomized study. SETTING: Patients hospitalized in ICU for COVID-19 infection. PATIENTS: Sixty patients hospitalized in ICU (mean duration: 31.9 ± 18.2 d) were recruited 4-8 weeks post discharge from ICU. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients visited the laboratory on two separate occasions. The first visit was dedicated to quality of life questionnaire, cardiopulmonary exercise testing, whereas measurements of the knee extensors neuromuscular function were performed in the second visit. Maximal oxygen uptake (V o2 max) was 18.3 ± 4.5 mL·min -1 ·kg -1 , representing 49% ± 12% of predicted value, and was significantly correlated with ICU stay/mechanical ventilation (MV) duration ( R = -0.337 to -0.446; p < 0.01 to 0.001), as were maximal voluntary contraction and electrically evoked peak twitch. V o2 max (either predicted or in mL· min -1 ·kg -1 ) was also significantly correlated with key indices of pulmonary function such as predicted forced vital capacity or predicted forced expiratory volume in 1 second ( R = 0.430-0.465; p ≤ 0.001) and neuromuscular function. Both cardiorespiratory fitness and neuromuscular function were correlated with self-reported physical functioning and general health status. CONCLUSIONS: V o2 max was on average only slightly above the 18 mL·min -1 ·kg -1 , that is, the cut-off value known to induce difficulty in performing daily tasks. Overall, although low physical capacities at admission in ICU COVID-19 patients cannot be ruled out to explain the association between V o2 max or neuromuscular function and ICU stay/MV duration, altered cardiorespiratory fitness and neuromuscular function observed in the present study may not be specific to COVID-19 disease but seem applicable to all ICU/MV patients of similar duration.

Reductions in motoneuron excitability during sustained isometric contractions are dependent on stimulus and contraction intensity.

Cervicomedullary stimulation provides a means of assessing motoneuron excitability. Previous studies demonstrated that during low-intensity sustained contractions, small cervicomedullary evoked potentials (CMEPs) conditioned using transcranial magnetic stimulation (TMS-CMEPs) are reduced, whereas large TMS-CMEPs are less affected. As small TMS-CMEPs recruit motoneurons most active during low-intensity contractions whereas large TMS-CMEPs recruit a high proportion of motoneurons inactive during the task, these results suggest that reductions in motoneuron excitability could be dependent on repetitive activation. To further test this hypothesis, this study assessed changes in small and large TMS-CMEPs across low- and high-intensity contractions. Twelve participants performed a sustained isometric contraction of the elbow flexor for 4.5 min at the electromyography (EMG) level associated with 20% maximal voluntary contraction force (MVC; low intensity) and 70% MVC (high intensity). Small and large TMS-CMEPs with amplitudes of ∼15% and ∼50% Mmax at baseline, respectively, were delivered every minute throughout the tasks. Recovery measures were taken at 1-, 2.5- and 4-min postexercise. During the low-intensity trial, small TMS-CMEPs were reduced at 2-4 min (P ≤ 0.049) by up to -10% Mmax, whereas large TMS-CMEPs remained unchanged (P ≥ 0.16). During the high-intensity trial, small and large TMS-CMEPs were reduced at all time points (P < 0.01) by up to -14% and -33% Mmax, respectively, and remained below baseline during all recovery measures (P ≤ 0.02). TMS-CMEPs were unchanged relative to baseline during recovery following the low-intensity trial (P ≥ 0.24). These results provide novel insight into motoneuron excitability during and following sustained contractions at different intensities and suggest that contraction-induced reductions in motoneuron excitability depend on repetitive activation.NEW & NOTEWORTHY This study measured motoneuron excitability using cervicomedullary evoked potentials conditioned using transcranial magnetic stimulation (TMS-CMEPs) of both small and large amplitudes during sustained low- and high-intensity contractions of the elbow flexors. During the low-intensity task, only the small TMS-CMEP was reduced. During the high-intensity task, both small and large TMS-CMEPs were substantially reduced. These results indicate that repetitively active motoneurons are specifically reduced in excitability compared with less active motoneurons in the same pool.

Central fatigue aetiology in prolonged trail running races.

NEW FINDINGS: What is the central question of this study? Are spinal and/or supraspinal perturbations implicated in central fatigue induced in the plantar flexor muscles following prolonged trail running races? What is the main finding and its importance? The study confirmed the presence of central fatigue following various trail running distances from 40 to 170 km. The reduction in the V-wave in conjunction with the lack of change in the H-reflex suggests that a major component of this central fatigue may arise from supraspinal mechanisms in the plantar flexor muscles. ABSTRACT: Trail running races are known to induce considerable impairments in neuromuscular function of which central mechanisms are a substantial component. However, the loci of this central fatigue (i.e. supraspinal and/or spinal) is not well identified. The aim of this study was to better understand central fatigue aetiology induced in the plantar flexor muscles by various trail running distances from 40 to 170 km. Eighteen runners participated in the study and neuromuscular function of their plantar flexors was tested before (PRE) and after (POST) various races during the Ultra-Trail du Mont Blanc. Neuromuscular function was evaluated with voluntary and evoked contractions using electrical tibial nerve stimulation. H-reflex and V-wave responses were also measured during submaximal and maximal voluntary contraction, respectively. Reductions in maximal voluntary contraction torque (-29%; P < 0.001) and voluntary activation level (-12%; P < 0.001) were observed after trail running races. The V-wave was reduced in soleus (-35%; P = 0.003) and gastrocnemius medialis (-28%; P = 0.031), with no changes for the H-reflex in soleus (P = 0.577). The present study confirmed the presence of central fatigue following trail running exercise. The reduction in the V-wave in conjunction with the lack of change in the H-reflex suggests that a major component of this central fatigue may arise from supraspinal mechanisms.

Effect of race distance on performance fatigability in male trail and ultra-trail runners.

The etiology of changes in lower-limb neuromuscular function, especially to the central nervous system, may be affected by exercise duration. Direct evidence is lacking as few studies have directly compared different race distances. This study aimed to investigate the etiology of deficits in neuromuscular function following short versus long trail-running races. Thirty-two male trail runners completed one of five trail-running races as LONG (>100 km) or SHORT (<60 km). Pre- and post-race, maximal voluntary contraction (MVC) torque and evoked responses to electrical nerve stimulation during MVCs and at rest were used to assess voluntary activation and muscle contractile properties of knee-extensor (KE) and plantar-flexor (PF) muscles. Transcranial magnetic stimulation (TMS) was used to assess evoked responses and corticospinal excitability in maximal and submaximal KE contractions. Race distance correlated with KE MVC (ρ = -0.556) and twitch (ρ = -0.521) torque decreases (p ≤ .003). KE twitch torque decreased more in LONG (-28 ± 14%) than SHORT (-14 ± 10%, p = .005); however, KE MVC time × distance interaction was not significant (p = .073). No differences between LONG and SHORT for PF MVC or twitch torque were observed. Maximal voluntary activation decreased similarly in LONG and SHORT in both muscle groups (p ≥ .637). TMS-elicited silent period decreased in LONG (p = .021) but not SHORT (p = .912). Greater muscle contractile property impairment in longer races, not central perturbations, contributed to the correlation between KE MVC loss and race distance. Conversely, PF fatigability was unaffected by race distance.

The knowns and unknowns of neural adaptations to resistance training.

The initial increases in force production with resistance training are thought to be primarily underpinned by neural adaptations. This notion is firmly supported by evidence displaying motor unit adaptations following resistance training; however, the precise locus of neural adaptation remains elusive. The purpose of this review is to clarify and critically discuss the literature concerning the site(s) of putative neural adaptations to short-term resistance training. The proliferation of studies employing non-invasive stimulation techniques to investigate evoked responses have yielded variable results, but generally support the notion that resistance training alters intracortical inhibition. Nevertheless, methodological inconsistencies and the limitations of techniques, e.g. limited relation to behavioural outcomes and the inability to measure volitional muscle activity, preclude firm conclusions. Much of the literature has focused on the corticospinal tract; however, preliminary research in non-human primates suggests reticulospinal tract is a potential substrate for neural adaptations to resistance training, though human data is lacking due to methodological constraints. Recent advances in technology have provided substantial evidence of adaptations within a large motor unit population following resistance training. However, their activity represents the transformation of afferent and efferent inputs, making it challenging to establish the source of adaptation. Whilst much has been learned about the nature of neural adaptations to resistance training, the puzzle remains to be solved. Additional analyses of motoneuron firing during different training regimes or coupling with other methodologies (e.g., electroencephalography) may facilitate the estimation of the site(s) of neural adaptations to resistance training in the future.

Task-specific strength increases after lower-limb compound resistance training occurred in the absence of corticospinal changes in vastus lateralis.

NEW FINDINGS: What is the central question of the study? Are corticospinal responses to acute and short-term squat resistance training task-specific? What is the main finding and its importance? A single bout of resistance training increased spinal excitability, but no changes in corticospinal responses were noted following 4 weeks of squat training despite task-specific increases in strength. The present data suggest that processes along the corticospinal pathway of the knee extensors play a limited role in the task-specific increase in strength following resistance training. ABSTRACT: Neural adaptations subserving strength increases have been shown to be task-specific, but responses and adaptation to lower-limb compound exercises such as the squat are commonly assessed in a single-limb isometric task. This two-part study assessed neuromuscular responses to an acute bout (Study A) and 4 weeks (Study B) of squat resistance training at 80% of one-repetition-maximum, with measures taken during a task-specific isometric squat (IS) and non-specific isometric knee extension (KE). Eighteen healthy volunteers (25 ± 5 years) were randomised into either a training (n = 10) or a control (n = 8) group. Neural responses were evoked at the intracortical, corticospinal and spinal levels, and muscle thickness was assessed using ultrasound. The results of Study A showed that the acute bout of squat resistance training decreased maximum voluntary contraction (MVC) for up to 45 min post-exercise (-23%, P < 0.001). From 15-45 min post-exercise, spinally evoked responses were increased in both tasks (P = 0.008); however, no other evoked responses were affected (P ≥ 0.240). Study B demonstrated that following short-term resistance training, participants improved their one repetition maximum squat (+35%, P < 0.001), which was reflected by a task-specific increase in IS MVC (+49%, P = 0.001), but not KE (+1%, P = 0.882). However, no training-induced changes were observed in muscle thickness (P = 0.468) or any evoked responses (P = 0.141). Adjustments in spinal motoneuronal excitability are evident after acute resistance training. After a period of short-term training, there were no changes in the responses to central nervous system stimulation, which suggests that alterations in corticospinal properties of the vastus lateralis might not contribute to increases in strength.

Sex differences in fatigability and recovery relative to the intensity-duration relationship.

KEY POINTS: Females demonstrate greater fatigue resistance than males during contractions at intensities relative to maximum force. However, previous studies have not accounted for the influence of metabolic thresholds on fatigability. This study is the first to test whether sex differences in fatigability exist when exercise intensity is normalised relative to a metabolic threshold: the critical intensity derived from assessment of the intensity-duration relationship during intermittent, isometric knee extensor contractions. We show that critical intensity in females occurred at a higher percentage of maximum force compared to males. Furthermore, females demonstrated greater fatigue resistance at exercise intensities above and below this metabolic threshold. Our data suggest that the sex difference was mediated by lesser deoxygenation of the knee extensors during exercise. These data highlight the importance of accounting for metabolic thresholds when comparing fatigability between sexes, whilst emphasising the notion that male data are not generalisable to female populations. ABSTRACT: Females are less fatigable than males during isometric exercise at intensities relative to maximal voluntary contraction (MVC); however, whether a sex difference in fatigability exists when exercise is prescribed relative to a critical intensity is unknown. This study established the intensity-duration relationship, and compared fatigability and recovery between sexes following intermittent isometric contractions normalised to critical intensity. Twenty participants (10 females) completed four intermittent isometric knee extension trials to task failure to determine critical intensity and the curvature constant (W'), followed by fatiguing tasks at +10% and -10% relative to critical intensity. Neuromuscular assessments were completed at baseline and for 45 min post-exercise. Non-invasive neurostimulation, near-infrared spectroscopy, and non-invasive haemodynamic monitoring were used to elucidate the physiological mechanisms responsible for sex differences. Females demonstrated a greater critical intensity relative to MVC than males (25 ± 3 vs. 21 ± 2% MVC, P = 0.003), with no sex difference for W' (18,206 ± 6331 vs. 18,756 ± 5762 N s, P = 0.850). Time to task failure was greater for females (62.37 ± 17.25 vs. 30.43 ± 12.75 min, P < 0.001) during the +10% trial, and contractile function recovered faster post-exercise (P = 0.034). During the -10% trial females experienced less contractile dysfunction (P = 0.011). Throughout the +10% trial, females demonstrated lesser decreases in deoxyhaemoglobin (P = 0.007) and an attenuated exercise pressor reflex. These data show that a sex difference in fatigability exists even when exercise is matched for critical intensity. We propose that greater oxygen availability during exercise permits females to sustain a higher relative intensity than males, and is an explanatory factor for the sex difference in fatigability during intermittent, isometric contractions.

Electrical stimulation of human corticospinal axons at the level of the lumbar spinal segments.

Electrical stimulation over the mastoids or thoracic spinous processes has been used to assess subcortical contribution to corticospinal excitability, but responses are difficult to evoke in the resting lower limbs or are limited to only a few muscle groups. This might be mitigated by delivering the stimuli lower on the spinal column, where the descending tracts contain a greater relative density of motoneurons projecting to lower limb muscles. We investigated activation of the corticospinal axons innervating tibialis anterior (TA) and rectus femoris (RF) by applying a single electrical stimulus over the first lumbar spinous process (LS). LS was paired with transcranial magnetic stimulation (TMS) at interstimulus intervals (ISIs) of -16 (TMS before LS) to 14 ms (LS before TMS). The relationship between muscle contraction strength (10%-100% maximal) and the amplitude of single-pulse TMS and LS responses was also investigated. Compared to the responses to TMS alone, responses to paired stimulation were significantly occluded in both muscles for ISIs ≥-8 ms (p ≤ 0.035), consistent with collision of descending volleys from TMS with antidromic volleys originating from LS. This suggests that TMS and LS activate some of the same corticospinal axons. Additionally, the amplitude of TMS and LS responses increased with increasing contraction strengths with no change in onset latency, suggesting responses to LS are evoked transsynaptically and have a monosynaptic component. Taken together, these experiments provide evidence that LS is an alternative method that could be used to discern segmental changes in the corticospinal tract when targeting lower limb muscles.

Myths and Methodologies: How loud is the story told by the transcranial magnetic stimulation-evoked silent period?

NEW FINDINGS: What is the topic of this review? The origin, interpretation and methodological constraints of the silent period induced by transcranial magnetic stimulation are reviewed. What advances does it highlight? The silent period is generated by both cortical and spinal mechanisms. Therefore, it seems inappropriate to preface silent period with 'cortical' unless additional measures are taken. Owing to many confounding variables, a standardized approach to the silent period measurement cannot be suggested. Rather, recommendations of best practice are provided based on the available evidence and the context of the research question. ABSTRACT: Transcranial magnetic stimulation (TMS) of the motor cortex evokes a response in the muscle that can be recorded via electromyography (EMG). One component of this response, when elicited during a voluntary contraction, is a period of EMG silence, termed the silent period (SP), which follows a motor evoked potential (MEP). Modulation of SP duration was long thought to reflect the degree of intracortical inhibition. However, the evidence presented in this review suggests that both cortical and spinal mechanisms contribute to generation of the SP, which makes prefacing SP with 'cortical' misleading. Further investigations with multi-methodological approaches, such as TMS-EEG coupling or interaction of TMS with neuroactive drugs, are needed to make such inferences with greater confidence. A multitude of methodological factors can influence the SP and thus confound the interpretation of this measure; namely, background muscle activity, instructions given to the participant, stimulus intensity and the size of the MEP preceding the SP, and the approach to analysis. A systematic understanding of how the confounding factors influence the interpretation of SP is lacking, which makes standardization of the methodology difficult to conceptualize. Instead, the methodology should be guided through the lens of the research question and the population studied, ensuring greater reproducibility, repeatability and comparability of data sets. Recommendations are provided for the best practice within a given context of the experimental design.

Corticospinal excitability of tibialis anterior and soleus differs during passive ankle movement.

The purpose of this study was to assess corticospinal excitability of soleus (SOL) and tibialis anterior (TA) at a segmental level during passive ankle movement. Four experimental components were performed to assess the effects of passive ankle movement and muscle length on corticospinal excitability (MEP/Mmax) at different muscle lengths, subcortical excitability at the level of lumbar spinal segments (LEP/Mmax), intracortical inhibition (SICI) and facilitation (ICF), and H-reflex in SOL and TA. In addition, the degree of fascicle length changes between SOL and TA was assessed in a subpopulation during passive ankle movement. Fascicles shortened and lengthened with joint movement during passive shortening and lengthening of SOL and TA to a similar degree (p < 0.001). Resting motor threshold was greater in SOL compared to TA (p ≤ 0.014). MEP/Mmax was facilitated in TA during passive shortening relative to the static position (p ≤ 0.023) and passive lengthening (p ≤ 0.001), but remained similar during passive ankle movement in SOL (p ≥ 0.497), regardless of muscle length at the point of stimulus (p = 0.922). LEP/Mmax (SOL: p = 0.075, TA: p = 0.071), SICI (SOL: p = 0.427, TA: p = 0.540), and ICF (SOL: p = 0.177, TA: p = 0.777) remained similar during passive ankle movement. H-reflex was not different across conditions in TA (p = 0.258), but was reduced during passive lengthening compared to shortening in SOL (p = 0.048). These results suggest a differential modulation of corticospinal excitability between plantar and dorsiflexors during passive movement. The corticospinal behaviour observed might be mediated by an increase in corticospinal drive as a result of reduced afferent input during muscle shortening and appears to be flexor-biased.

Motor cortical and corticospinal function differ during an isometric squat compared with isometric knee extension.

NEW FINDINGS: What is the central question of this study? In order to discern information about testing modalities when assessing neuroplastic responses to squat resistance training, the present study investigated whether corticospinal and intracortical function was different between a joint-angle-matched isometric squat and isometric knee extension. What is the main finding and its importance? The present data show poor agreement of corticospinal and intracortical function between the isometric squat and isometric knee extension. The data reinforce the notion that task specificity is of the utmost importance for assessing neuroplasticity. ABSTRACT: It has been suggested that task-specific changes in neurophysiological function (neuroplasticity) should be assessed using testing modalities that replicate the characteristics of the intervention. The squat is a commonly prescribed resistance exercise that has been shown to elicit changes in CNS function. However, previous studies have assessed squat-induced neuroplasticity using isometric knee extension, potentially confounding the results. The aim of the present study was to assess the agreement between corticospinal and intracortical activity relating to the knee extensors during isometric knee extension compared with an isometric squat task. Eleven males completed a neurophysiological assessment in an isometric squat (IS) and knee-extension (KE) task matched for joint angles (hip, knee and ankle). Single- and paired-pulse transcranial magnetic stimulation was delivered during isometric contractions at a range of intensities to assess short-interval cortical inhibition (SICI) and corticospinal excitability. Group mean values for SICI (70 ± 14 versus 63 ± 12% of unconditioned motor evoked potential during IS and KE, respectively) and corticospinal excitability (mean differences 2-5% of the maximal compound muscle action potential at 25, 50, 75 and 100% maximal voluntary contraction between the IS and KE) were not different between the two tasks (P > 0.05) in the vastus lateralis. However, limits of agreement were wide, with poor-to-moderate average intraclass correlation coefficients (ICCs) (SICI, ICC3,1  = 0.15; corticospinal excitability, average ICC3,1 range = 0.0-0.63), indicating disparate corticospinal and intracortical activity between the IS and KE. These data highlight the importance of task specificity when assessing the modulation of corticospinal excitability and SICI in response to interventions resulting in neuroplastic changes.

The Effect of Maturation on Performance During Repeated Sprints With Self-Selected Versus Standardized Recovery Intervals in Youth Footballers.

PURPOSE: The purpose of this experiment was to assess performance during repeated sprints utilizing self-selected recovery intervals in youth football (soccer) players at different stages of maturation. METHODS: Quota sampling method was used to recruit 14 prepeak height velocity (PHV) and 14 post-PHV participants for the study (N = 28; age = 13 [0.9] y, stature = 162.5 [10.8] cm, mass = 50.2 [12.7] kg). Players performed repeated sprints comprising 10 × 30 m efforts under 2 experimental conditions: using 30-second and self-selected recovery intervals. Magnitude of effects for within- and between-group differences were reported using effect size (ES) statistics ± 90% confidence intervals and percentage differences. RESULTS: The decline in sprint performance was likely lower in the pre-PHV compared with the post-PHV group during the standardized recovery trial (between-group difference = 37%; ES = 0.41 ± 0.51), and likely lower in the post-PHV group during the self-selected recovery trial (between-group difference = 50%; ES = 0.45 ± 0.54). Mean recovery duration was likely shorter in the pre-PHV compared with the post-PHV group during the self-selected recovery trial (between-group difference = 26.1%; ES = 0.47 ± 0.45). CONCLUSION: This is the first study to show that during repeated sprints with self-selected recovery, pre-PHV children have an impaired ability to accurately interpret physical capabilities in the context of the task compared with post-PHV adolescents.

Eccentric Exercise-Induced Muscle Damage Reduces Gross Efficiency.

INTRODUCTION: The effect of eccentric exercise-induced muscle damage (EIMD) on cycling efficiency is unknown. The aim of the present study was to assess the effect of EIMD on gross and delta efficiency and the cardiopulmonary responses to cycle ergometry. METHODS: Twenty-one recreational athletes performed cycling at 70%, 90% and 110% of the gas exchange threshold (GET) under control conditions (Control) and 24 h following an eccentric damaging protocol (Damage). Knee extensor isometric maximal voluntary contraction (MVC), potentiated twitch (Qtw,pot) and voluntary activation (VA) were assessed before Control and Damage. Gross and delta efficiency were assessed using indirect calorimetry, and cardiopulmonary responses were measured at each power output. Electromyography root-mean-square (EMGRMS) during cycling was also determined. RESULTS: MVC was 25 ± 18% lower for Damage than Control (p < 0.001). Gross efficiency was lower for Damage than Control (p < 0.001) by 0.55 ± 0.79%, 0.59 ± 0.73% and 0.60 ± 0.87% for 70%, 90% and 110% GET, respectively. Delta efficiency was unchanged between conditions (p = 0.513). Concurrently, cycling EMGRMS was higher for Damage than Control (p = 0.004). An intensity-dependent increase in breath frequency and V̇E/V̇CO2 was found, which were higher for Damage only at 110% GET (p ≤ 0.019). CONCLUSIONS: Thus, gross efficiency is reduced following EIMD. The concurrently higher EMGRMS suggests that increases in muscle activation in the presence of EIMD might have contributed to reduced gross efficiency. The lack of change in delta efficiency might relate to its poor reliability hindering the ability to detect change. The findings also show that EIMD-associated hyperventilation is dependent on exercise intensity, which might relate to increases in central command with EIMD.

Reliability of Corticospinal and Motoneuronal Excitability Evaluation During Unfatiguing and Fatiguing Cycling Exercise.

INTRODUCTION: Central nervous system excitability depends on the task performed, muscle group solicited, and contraction type. However, little is known on corticospinal and motoneuronal excitability measured during locomotor exercise. This study aimed at determining the reliability of motor-evoked potentials (MEP) and thoracic motor-evoked potentials (TMEP) in dynamic mode during unfatiguing and fatiguing cycling exercise. METHODS: Twenty-two participants completed four visits. Visit 1 comprised familiarization and a maximal incremental test to determine maximal power output (Wmax). The remaining visits encompassed unfatiguing evaluations, which included 8 brief bouts of moderate (50% Wmax) and high intensity cycling (80% Wmax). In each bout, a set of two TMEPs, five MEPs and one M-max were obtained. Subsequently, a fatiguing exercise to exhaustion at 80% Wmax was performed, with four sets of measurements 3 min through the exercise and 4 additional sets at exhaustion, both measured at 50% Wmax. RESULTS: Intraclass correlation coefficients (ICCs) for 5, 10, 15 and 20 MEP·Mmax-1 revealed excellent reliability at both intensities and during fatiguing exercise (ICC ≥ 0.92). TMEP·Mmax-1 showed ICCs ≥0.82 for moderate and high intensity, and it was not affected by fatigability. Overall standard error of measurement was 0.090 [0.083, 0.097] for MEP·Mmax-1 and 0.114 [0.105, 0.125] for TMEP·Mmax-1. A systematic bias associated to the number of stimulations, especially at high intensity, suggested the evaluation itself may be influenced by fatigability. A mean reduction of 8% was detected in TMEP·Mmax-1 at exhaustion. CONCLUSIONS: Motoneuronal and corticospinal excitability measured in dynamic mode presented good to excellent reliability in unfatiguing and fatiguing exercise. Further studies inducing greater fatigability must be conducted to assess the sensitivity of central nervous system excitability during cycling.

Persistent inward currents in tibialis anterior motoneurons can be reliably estimated within the same session.

The response of spinal motoneurons to synaptic input greatly depends on the activation of persistent inward currents (PICs), the contribution of which can be estimated through the paired motor unit technique. Yet, the intra-session test-retest reliability of this measurement remains to be fully established. Twenty males performed isometric triangular dorsiflexion contractions to 20 and 50 % of maximal torque at baseline and after a 15-min resting period. High-density electromyographic signals (HD-EMG) of the tibialis anterior were recorded with a 64-electrode matrix. HD-EMG signals were decomposed, and motor units tracked across time points to estimate the contribution of PICs to motoneuron firing through quantification of motor unit recruitment-derecruitment hysteresis (ΔF). A good intraclass correlation coefficient (ICC = 0.75 [0.63, 0.83]) and a large repeated measures correlation coefficient (rrm = 0.65 [0.49, 0.77]; p < 0.001) were found between ΔF values obtained at both time points for 20 % MVC ramps. For 50 % MVC ramps, a good ICC (0.77 [0.65, 0.85]) and a very large repeated measures correlation coefficient (rrm = 0.73 [0.63, 0.80]; p < 0.001) were observed. Our data suggest that ΔF scores can be reliably investigated in tibialis anterior motor units during both low- and moderate-intensity contractions within a single experimental session.

Factors Associated with Fatigue in COVID-19 ICU Survivors.

PURPOSE: Approximately 30% of people infected with COVID-19 require hospitalization and 20% of them are admitted to an intensive care unit (ICU). Most of these patients experience symptoms of fatigue weeks post-ICU, so understanding the factors associated with fatigue in this population is crucial. METHODS: Fifty-nine patients [38-78 yr] hospitalized in ICU for COVID-19 infection for 32 [6-80] days including 23 [3-57] days of mechanical ventilation, visited the laboratory on two separate occasions. The first visit occurred 52 ± 15 days after discharge and was dedicated to questionnaires, blood sampling and cardiopulmonary exercise testing, while measurements of the knee extensors neuromuscular function and performance fatigability were performed in the second visit 7 ± 2 days later. RESULTS: Using the FACIT-F questionnaire, 56% of patients were classified as fatigued. Fatigued patients had worse lung function score than non- fatigued (i.e. 2.9 ± 0.8 L vs 3.6 ± 0.8 L; 2.4 ± 0.7 l vs 3.0 ± 0.7 L for forced vital capacity and forced expiratory volume in one second, respectively) and forced vital capacity was identified as a predictor of being fatigued. Maximal voluntary activation was lower in fatigued patients than non-fatigued patients (82 ± 14% vs 91 ± 3%) and was the only neuromuscular variable that discriminated between fatigued and non-fatigued patients. Patient-reported outcomes also showed differences between fatigued and non-fatigued patients for sleep, physical activity, depression and quality of life (p < 0.05). CONCLUSIONS: COVID-19 survivors showed altered respiratory function 4 to 8 weeks after discharge, that was further deteriorated in fatigued patients. Fatigue was also associated with lower voluntary activation and patient-reported impairments (i.e. sleep satisfaction, quality of life or depressive state). The present study reinforces the importance of exercise intervention and rehabilitation to counteract cardiorespiratory and neuromuscular impairments of COVID-19 patients admitted in ICU, especially individuals experiencing fatigue.