Motor unit modes in the calf muscles during a submaximal isometric contraction are changed by brief stretches.

The purpose of our study was to investigate the influence of a stretch intervention on the common modulation of discharge rate among motor units in the calf muscles during a submaximal isometric contraction. The current report comprises a computational analysis of a motor unit dataset that we published previously (Mazzo et al., 2021). Motor unit activity was recorded from the three main plantar flexor muscles while participants performed an isometric contraction at 10% of the maximal voluntary contraction force before and after each of two interventions. The interventions were a control task (standing balance) and static stretching of the plantar flexor muscles. A factorization analysis on the smoothed discharge rates of the motor units from all three muscles yielded three modes that were independent of the individual muscles. The composition of the modes was not changed by the standing-balance task, whereas the stretching exercise reduced the average correlation in the second mode and increased it in the third mode. A centroid analysis on the correlation values showed that most motor units were associated with two or three modes, which were presumed to indicate shared synaptic inputs. The percentage of motor units adjacent to the seven centroids changed after both interventions: Control intervention, mode 1 decreased and the shared mode 1 + 2 increased; stretch intervention, shared modes either decreased (1 + 2) or increased (1 + 3). These findings indicate that the neuromuscular adjustments during both interventions were sufficient to change the motor unit modes when the same task was performed after each intervention. KEY POINTS: Based on covariation of the discharge rates of motor units in the calf muscles during a submaximal isometric contraction, factor analysis was used to assign the correlated discharge trains to three motor unit modes. The motor unit modes were determined from the combined set of all identified motor units across the three muscles before and after each participant performed a control and a stretch intervention. The composition of the motor unit modes changed after the stretching exercise, but not after the control task (standing balance). A centroid analysis on the distribution of correlation values found that most motor units were associated with a shared centroid and this distribution, presumably reflecting shared synaptic input, changed after both interventions. Our results demonstrate how the distribution of multiple common synaptic inputs to the motor neurons innervating the plantar flexor muscles changes after a brief series of stretches.

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.

Control of motor output during steady submaximal contractions is modulated by contraction history.

The purpose of the study was to investigate the influence of contraction history on force steadiness and the associated EMG activity during submaximal isometric contractions performed with the dorsiflexor muscles. The key feature of the protocol was a triangular ramp contraction performed in the middle of a steady contraction at a lower target force. The target force during the ramp contraction was 20% MVC greater than that during the steady contraction. Thirty-seven healthy individuals (21 men and 16 women) performed the submaximal tasks with the ankle dorsiflexors. Electromyography (EMG) signals were recorded from tibialis anterior with a pair of surface electrodes. The coefficient of variation for force was significantly greater during the second steady contraction compared with the first one at each of the seven target forces (p < 0.015; d = 0.38-0.92). Although the average applied force during the steady contractions before and after the triangular contraction was the same (p = 0.563), the mean EMG amplitude for the steady contractions performed after the triangular contraction was significantly greater at each of the seven target forces (p < 0.0001; d = 0.44-0.68). Also, there were significant differences in mean EMG frequency between the steady contractions performed before and after the triangular contraction (p < 0.01; d = 0.13-0.82), except at 10 and 20% MVC force. The greater force fluctuations during a steady submaximal contraction after an intervening triangular contraction indicate a change in the discharge characteristics of the involved motor units.

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.

Voluntary muscle activation in people with multiple sclerosis is reduced across a wide range of forces following maximal effort-fatiguing contractions.

Although multiple sclerosis (MS) is frequently associated with motor impairment, little is known about how muscle activation is affected with MS. The aim of this study was to use transcranial magnetic stimulation (TMS) and motor nerve stimulation to investigate voluntary muscle activation in people with MS across a range of contraction forces. Ten people with MS (39 ± 7 yr) and 10 healthy controls (40 ± 5 yr) performed elbow flexions at target contraction forces of 25%, 50%, 75%, 90%, and 100% maximal voluntary contraction (MVC) while electromyography (EMG) of the biceps brachii was recorded. Sustained elbow flexion MVCs were then performed until force declined to 60% of baseline MVC, where the target contraction forces were again examined but after the sustained MVC. Following the sustained MVC, there was a reduction in biceps EMG amplitude (P < 0.01) and motor cortical voluntary activation (P < 0.01) for the MS group across all contraction intensities. There was also an increase in the rate of torque development for motor nerve-resting twitches in the MS group following the sustained MVC (P = 0.03). Despite the MS group reporting higher fatigue severity scale scores (P < 0.01), disease duration was a better predictor of muscle activation for the MS group (r = -0.757, P = 0.01). These findings indicate that voluntary muscle activation is compromised in people with MS following maximal effort contractions, which may be associated with disease duration rather than self-reports of fatigue.NEW & NOTEWORTHY We use transcranial magnetic stimulation to demonstrate that people with relapsing-remitting multiple sclerosis (MS) have a reduced ability to activate muscles following maximal effort-fatiguing contractions. A reduced ability to activate the elbow flexor muscles after a fatiguing contraction was associated with disease duration and not self-reported levels of fatigue.

Voluntary torque production is unaffected by changes in local thermal sensation during normothermia and hyperthermia.

NEW FINDINGS: What is the central question of this study? Hyperthermia reduces the human capacity to produce muscular force, which is associated with decreased neural drive: does mitigating a reduction in neural drive by altering localised thermal sensation help to preserve voluntary force output? What is the main finding and its importance? Altering thermal sensation by cooling and heating the head independent of core temperature did not change neural drive or benefit voluntary force production. Head cooling did slow the rate of rise in core temperature during heating, which may have practical applications in passive settings. ABSTRACT: This study investigated altered local head and neck thermal sensation on maximal and rapid torque production during voluntary contractions. Nine participants completed four visits in two environmental conditions: at rectal temperatures ∼39.5°C in hot (HOT; ∼50°C, ∼39% relative humidity) and ∼37°C in thermoneutral (NEU; ∼22°C, ∼46% relative humidity) conditions. Local thermal sensation was manipulated by heating in thermoneutral conditions and cooling in hot conditions. Evoked twitches and octets were delivered at rest. Maximum voluntary torque (MVT), normalised surface electromyography (EMG) and voluntary activation (VA) were assessed during brief maximal isometric voluntary contractions of the knee extensors. Rate of torque development (RTD) and EMG were measured during rapid voluntary contractions. MVT (P = 0.463) and RTD (P = 0.061) were similar between environmental conditions despite reduced VA (-6%; P = 0.047) and EMG at MVT (-31%; P = 0.019). EMG in the rapid voluntary contractions was also lower in HOT versus NEU during the initial 100 ms (-24%; P = 0.035) and 150 ms (-26%; P = 0.035). Evoked twitch (+70%; P < 0.001) and octet (+27%; P < 0.001) RTD during the initial 50 ms were greater in the HOT compared to NEU conditions, in addition to a faster relaxation rate of the muscle (-33%; P < 0.001). In conclusion, hyperthermia reduced neural drive without affecting voluntary torque, likely due to the compensatory effects of improved intrinsic contractile function and faster contraction and relaxation rates of the knee extensors. Changes in local thermal perception of the head and neck whilst hyperthermic or normothermic did not affect voluntary torque.

Heat acclimation reduces the effects of whole-body hyperthermia on knee-extensor relaxation rate, but does not affect voluntary torque production.

PURPOSE: This study investigated the effects of acute hyperthermia and heat acclimation (HA) on maximal and rapid voluntary torque production, and their neuromuscular determinants. METHODS: Ten participants completed 10 days of isothermic HA (50 °C, 50% rh) and had their knee-extensor neuromuscular function assessed in normothermic and hyperthermic conditions, pre-, after 5 and after 10 days of HA. Electrically evoked twitch and octet (300 Hz) contractions were delivered at rest. Maximum voluntary torque (MVT), surface electromyography (EMG) normalised to maximal M-wave, and voluntary activation (VA) were assessed during brief maximal isometric voluntary contractions. Rate of torque development (RTD) and normalised EMG were measured during rapid voluntary contractions. RESULTS: Acute hyperthermia reduced neural drive (EMG at MVT and during rapid voluntary contractions; P < 0.05), increased evoked torques (P < 0.05), and shortened contraction and relaxation rates (P < 0.05). HA lowered resting rectal temperature and heart rate after 10 days (P < 0.05), and increased sweating rate after 5 and 10 days (P < 0.05), no differences were observed between 5 and 10 days. The hyperthermia-induced reduction in twitch half-relaxation was attenuated after 5 and 10 days of HA, but there were no other effects on neuromuscular function either in normothermic or hyperthermic conditions. CONCLUSION: HA-induced favourable adaptations to the heat after 5 and 10 days of exposure, but there was no measurable benefit on voluntary neuromuscular function in normothermic or hyperthermic conditions. HA did reduce the hyperthermic-induced reduction in twitch half-relaxation time, which may benefit twitch force summation and thus help preserve voluntary torque in hot environmental conditions.

Lower motor unit discharge rates in gastrocnemius lateralis, but not in gastrocnemius medialis or soleus, in runners with Achilles tendinopathy: a pilot study.

OBJECTIVES: Deficits in muscle performance could be a consequence of a reduced ability of a motor neuron to increase the rate in which it discharges. This study aimed to investigate motor unit (MU) discharge properties of each triceps surae muscle (TS) and TS torque steadiness during submaximal intensities in runners with Achilles tendinopathy (AT). METHODS: We recruited runners with (n = 12) and without (n = 13) mid-portion AT. MU discharge rate was analysed for each of the TS muscles, using high-density surface electromyography during 10 and 20% isometric plantar flexor contractions. RESULTS: MU mean discharge rate was lower in the gastrocnemius lateralis (GL) in AT compared to controls. In AT, GL MU mean discharge rate did not increase as torque increased from 10% peak torque, 8.24 pps (95% CI 7.08 to 9.41) to 20%, 8.52 pps (7.41 to 9.63, p = 0.540); however, in controls, MU discharge rate increased as torque increased from 10%, 8.39 pps (7.25-9.53) to 20%, 10.07 pps (8.89-11.25, p < 0.001). There were no between-group difference in gastrocnemius medialis (GM) or soleus (SOL) MU discharge rates. We found no between-group differences in coefficient of variation of MU discharge rate in any of the TS muscles nor in TS torque steadiness. CONCLUSION: Our data demonstrate that runners with AT may have a lower neural drive to GL, failing to increase MU discharge rate to adjust for the increase in torque demand. Further research is needed to understand how interventions focussing on increasing neural drive to GL would affect muscle function in runners with AT.

Exertional dyspnoea in patients with mild-to-severe chronic obstructive pulmonary disease: neuromechanical mechanisms.

In patients with chronic obstructive pulmonary disease (COPD), exertional dyspnoea generally arises when there is imbalance between ventilatory demand and capacity, but the neurophysiological mechanisms are unclear. We therefore determined if disparity between elevated inspiratory neural drive (IND) and tidal volume (VT ) responses (neuromechanical dissociation) impacted dyspnoea intensity and quality during exercise, across the COPD severity spectrum. In this two-centre, cross-sectional observational study, 89 participants with COPD divided into tertiles of FEV1 %predicted (Tertile 1 = FEV1 = 87 ± 9%, Tertile 2 = 60 ± 9%, Tertile 3 = 32 ± 8%) and 18 non-smoking controls, completed a symptom-limited cardiopulmonary exercise test (CPET) with measurement of IND by diaphragm electromyography (EMGdi (%max)). The association between increasing dyspnoea intensity and EMGdi (%max) during CPET was strong (r = 0.730, P < 0.001) and not different between the four groups who showed marked heterogeneity in pulmonary gas exchange and mechanical abnormalities. Significant inspiratory constraints (tidal volume/inspiratory capacity (VT /IC) ≥ 70%) and onset of neuromechanical dissociation (EMGdi (%max):VT /IC > 0.75) occurred at progressively lower minute ventilation ( V ̇ E ${\dot{V}}_{{\rm{E}}}$ ) from Control to Tertile 3. Lower resting IC meant earlier onset of neuromechanical dissociation, heightened dyspnoea intensity and greater propensity (93% in Tertile 3) to select qualitative descriptors of 'unsatisfied inspiration'. We concluded that, regardless of marked variation in mechanical and pulmonary gas exchange abnormalities in our study sample, exertional dyspnoea intensity was linked to the magnitude of EMGdi (%max). Moreover, onset of critical inspiratory constraints and attendant neuromechanical dissociation amplified dyspnoea intensity at higher exercise intensities. Simple measurements of IC and breathing pattern during CPET provide useful insights into mechanisms of dyspnoea and exercise intolerance in individuals with COPD. KEY POINTS: Dyspnoea during exercise is a common and troublesome symptom reported by patients with chronic obstructive pulmonary disease (COPD) and is linked to an elevated inspiratory neural drive (IND). The precise mechanisms of elevated IND and dyspnoea across the continuum of airflow obstruction severity in COPD remains unclear. The present study sought to determine the mechanisms of elevated IND (by diaphragm EMG, EMGdi (%max)) and dyspnoea during cardiopulmonary exercise testing (CPET) across the continuum of COPD severity. There was a strong association between increasing dyspnoea intensity and EMGdi (%max) during CPET across the COPD continuum despite significant heterogeneity in underlying pulmonary gas exchange and respiratory mechanical impairments. Critical inspiratory constraints occurred at progressively lower ventilation during exercise with worsening severity of COPD. This was associated with the progressively lower resting inspiratory capacity with worsening disease severity. Earlier critical inspiratory constraint was associated with earlier neuromechanical dissociation and greater likelihood of reporting the sensation of 'unsatisfied inspiration'.

Less common synaptic input between muscles from the same group allows for more flexible coordination strategies during a fatiguing task.

This study aimed to determine whether neural drive is redistributed between muscles during a fatiguing isometric contraction, and if so, whether the initial level of common synaptic input between these muscles constrains this redistribution. We studied two muscle groups: triceps surae (14 participants) and quadriceps (15 participants). Participants performed a series of submaximal isometric contractions and a torque-matched contraction maintained until task failure. We used high-density surface electromyography to identify the behavior of 1,874 motor units from the soleus, gastrocnemius medialis (GM), gastrocnemius lateralis (GL), rectus femoris, vastus lateralis (VL), and vastus medialis (VM). We assessed the level of common drive between muscles in the absence of fatigue using a coherence analysis. We also assessed the redistribution of neural drive between muscles during the fatiguing contraction through the correlation between their cumulative spike trains (index of neural drive). The level of common drive between VL and VM was significantly higher than that observed for the other muscle pairs, including GL-GM. The level of common drive increased during the fatiguing contraction, but the differences between muscle pairs persisted. We also observed a strong positive correlation of neural drive between VL and VM during the fatiguing contraction (r = 0.82). This was not observed for the other muscle pairs, including GL-GM, which exhibited differential changes in neural drive. These results suggest that less common synaptic input between muscles allows for more flexible coordination strategies during a fatiguing task, i.e., differential changes in neural drive across muscles. The role of this flexibility on performance remains to be elucidated.NEW & NOTEWORTHY Redundancy of the neuromuscular system theoretically allows for a redistribution of the neural drive across muscles (i.e., between-muscle compensation) during a fatiguing contraction. Our results suggest that a high level of common input between muscles (e.g., vastus lateralis and medialis) represents a neural constraint making it less likely to redistribute the neural drive across these muscles. In this way, redistribution was only observed across muscles that share little common synaptic input (e.g., gastrocnemius lateralis and medialis).

People with multiple sclerosis have reduced TMS-evoked motor cortical output compared with healthy individuals during fatiguing submaximal contractions.

People with multiple sclerosis (PwMS) typically experience greater levels of exercise-induced fatigue compared with healthy individuals. Therefore, this study examined performance fatigability in PwMS when executing a prolonged submaximal contraction. Nine PwMS (38 ± 7 yr, 6 females) and nine healthy controls (35 ± 6 yr, 4 females) performed an elbow flexion at 15% maximal voluntary contraction (MVC) for 26 min. MVCs were performed every 2 min during, and following, the contraction to determine if maximal force was impaired by the low-intensity contraction. Single-pulse transcranial magnetic stimulation (TMS) was delivered to the primary motor cortex with a circular coil during each MVC and during the submaximal contraction. Superimposed and resting twitches were calculated from elbow flexion torque, whereas motor-evoked potentials were calculated from biceps brachii electromyography. Ratings of perceived exertion (RPE) were obtained before each MVC. During the fatiguing contraction protocol, the MS group exhibited a reduced MVC torque compared with the healthy control group (P = 0.044), which aligned with group differences in biceps brachii EMG activity (P = 0.022) and superimposed twitch amplitude (P = 0.016). Fatigue-related decrements in MVC torque (P = 0.044) and biceps brachii EMG activity (P = 0.043) demonstrated in the MS group persisted throughout recovery. However, MS did not affect the RPE during the fatigue task. These findings suggest that PwMS may have greater levels of performance fatigability due to decreased voluntary drive from the motor cortex, which is not associated with greater ratings of perceived exertion.NEW & NOTEWORTHY By combining TMS and motor nerve stimulation during a low-intensity exercise task, we were able to uncover the contribution that different levels of the CNS have during fatiguing exercise in PwMS. Our findings are novel and revealed that PwMS experienced decreased voluntary drive from the motor cortex during a low-intensity sustained fatiguing task that was associated with heightened levels of performance fatigability.

Association between effective neural drive to the triceps surae and fluctuations in plantar-flexion torque during submaximal isometric contractions.

NEW FINDINGS: What is the central question of this study? What is the association between the fluctuations in various estimates of effective neural drive to the triceps surae muscles and fluctuations in net plantar-flexion torque during steady submaximal contractions? What is the main finding and its importance? The fluctuations in estimates of effective neural drive to the triceps surae were moderately correlated with fluctuations in net torque at light and moderate plantar-flexion torques. Significant variability was observed in the association between neural drive and torque across participants, trials, short epochs of individual contractions and varying motor unit number. ABSTRACT: The influence of effective neural drive on low-frequency fluctuations in torque during steady contractions can be estimated from the cumulative spike train (CST) or first principal component (FPC) of smoothed motor unit discharge rates obtained with high-density electromyography. However, the association between these estimates of total neural drive to synergist muscles and the fluctuations in net torque has not been investigated. We exposed the variability and compared the correlations between estimates of effective neural drive to the triceps surae muscles and fluctuations in plantar-flexion torque during steady contractions at 10% and 35% of maximal voluntary contraction (MVC) torque. Both neural drive estimates were moderately correlated with torque (CST, 0.55 ± 0.14; FPC, 0.58 ± 0.16) and highly correlated with one another (0.81 ± 0.1) during the 30-s steady contractions. There was substantial variability in cross-correlation values across participants, trials, and the 1- and 5-s epochs of single contractions. Moreover, epoch duration significantly influenced cross-correlation values. Motor unit number was weakly associated with cross-correlation strength at 35% MVC (marginal R2 0.09-0.11; all P < 2.2 × 10-5 ), but not at 10% MVC (all P > 0.37). Approximately, one-fifth of the variance in the coefficient of variation (CV) for torque was explained by CV for the CST estimate of the neural drive (P = 6.6 × 10-13 , R2  = 0.21). Estimates of total neural drive to the synergistic triceps surae muscles obtained by pooling motor unit discharge times were moderately correlated with fluctuations in net plantar-flexion torque.

Compensatory responses to increased mechanical abnormalities in COPD during sleep.

PURPOSE: To assess whether night-time increases in mechanical loading negatively impact respiratory muscle function in COPD and whether compensatory increases in inspiratory neural drive (IND) are adequate to stabilize ventilatory output and arterial oxygen saturation, especially during sleep when wakefulness drive is withdrawn. METHODS: 21 patients with moderate-to-severe COPD and 20 age-/sex-matched healthy controls (CTRL) participated in a prospective, cross-sectional, one-night study to assess the impact of COPD on serial awake, supine inspiratory capacity (IC) measurements and continuous dynamic respiratory muscle function (esophageal manometry) and IND (diaphragm electromyography, EMGdi) in supine sleep. RESULTS: Supine inspiratory effort and EMGdi were consistently twice as high in COPD versus CTRL (p < 0.05). Despite overnight increases in awake total airways resistance and dynamic lung hyperinflation in COPD (p < 0.05; not in CTRL), elevated awake EMGdi and respiratory effort were unaltered in COPD overnight. At sleep onset (non-rapid eye movement sleep, N2), EMGdi was decreased versus wakefulness in COPD (- 43 ± 36%; p < 0.05) while unaffected in CTRL (p = 0.11); however, respiratory effort and arterial oxygen saturation (SpO2) were unchanged. Similarly, in rapid eye movement (stage R), sleep EMGdi was decreased (- 38 ± 32%, p < 0.05) versus wakefulness in COPD, with preserved respiratory effort and minor (2%) reduction in SpO2. CONCLUSIONS: Despite progressive mechanical loading overnight and marked decreases in wakefulness drive, inspiratory effort and SpO2 were well maintained during sleep in COPD. Preserved high inspiratory effort during sleep, despite reduced EMGdi, suggests continued (or increased) efferent activation of extra-diaphragmatic muscles, even in stage R sleep. CLINICAL TRIAL INFORMATION: The COPD data reported herein were secondary data (Placebo arm only) obtained through the following Clinical Trial: "Effect of Aclidinium/Formoterol on Nighttime Lung Function and Morning Symptoms in Chronic Obstructive Pulmonary Disease" ( https://clinicaltrials.gov/ct2/show/NCT02429765 ; NCT02429765).

Maximal intended velocity enhances strength training-induced neuromuscular stimulation in older adults.

The age-related attenuation in neuromuscular function can be mitigated with strength training. Current recommendations for untrained and elderly recommend performing the strength training with a controlled movement velocity (CON). However, applying maximal intended velocity (MIV) in the concentric phase of movement may augment neuromuscular stimulation and potentially enhance training adaptations. Thus, applying rate of electromyography (EMG) rise (RER) recordings, we examined the acute early phase neuromuscular response to these two contraction types in quadriceps femoris during leg extension, along with actual movement velocity, in 12 older (76 ± 6 years) and 12 young men (23 ± 2 years). Results revealed that older adults had a lower one repetition maximum (1RM) than young (33 ± 9 kg vs. 50 ± 9 kg; p = 0.001) and lower actual velocity across relative intensities of ~ 10%, 30%, 50%, 70% and 90% of 1RM for CON and MIV (all p < 0.05). Older adults also had consistently reduced RER compared to young during both conditions (old: 1043-1810 µV; young: 1844-3015 µV; all p < 0.05). However, RER was higher in contractions with MIV compared to CON for both age groups, and across all intensities (98-674%, all p < 0.05). In conclusion, despite decreased maximal strength and attenuated neuromuscular response with advancing age, our results document an augmented neuromuscular activation when repetitions are performed with MIV in the concentric phase of movement.

Changes in neural drive to calf muscles during steady submaximal contractions after repeated static stretches.

KEY POINTS: Repeated static-stretching interventions consistently increase the range of motion about a joint and decrease total joint stiffness, but findings on the changes in muscle and connective-tissue properties are mixed. The influence of these stretch-induced changes on muscle function at submaximal forces is unknown. To address this gap in knowledge, the changes in neural drive to the plantar flexor muscles after a static-stretch intervention were estimated. Neural drive to the plantar flexor muscles during a low-force contraction increased after repeated static stretches. These findings suggest that adjustments in motor unit activity are necessary at low forces to accommodate reductions in the force-generating and transmission capabilities of the muscle-tendon unit after repeated static stretches of the calf muscles. ABSTRACT: Static stretching decreases stiffness about a joint, but its influence on muscle-tendon unit function and muscle activation is unclear. We investigated the influence of three static stretches on changes in neural drive to the plantar flexor muscles, both after a stretch intervention and after a set of maximal voluntary contractions (MVCs). Estimates of neural drive were obtained during submaximal isometric contractions by decomposing high-density electromyographic signals into the activity of individual motor units from medial gastrocnemius, lateral gastrocnemius and soleus. Motor units were matched across contractions and an estimate of neural drive to the plantar flexors was calculated by normalizing the cumulative spike train to the number of active motor units (normalized neural drive). Mean discharge rate increased after the stretch intervention during the 10% MVC task for all recorded motor units and those matched across conditions (all, P = 0.0046; matched only, P = 0.002), recruitment threshold decreased for motor units matched across contractions (P = 0.022), and discharge rate at recruitment was elevated (P = 0.004). Similarly, the estimate of normalized neural drive was significantly greater after the stretch intervention at 10% MVC torque (P = 0.029), but not at 35% MVC torque. The adjustments in motor unit activity required to complete the 10% MVC task after stretch may have been partially attenuated by a set of plantar flexor MVCs. The increase in neural drive required to produce low plantar-flexion torques after repeated static stretches of the calf muscles suggests stretch-induced changes in muscle and connective tissue properties.

An examination of a potential organized motor unit firing rate and recruitment scheme of an antagonist muscle during isometric contractions.

The primary purpose of the present study is to determine if an organized control scheme exists for the antagonist muscle during steady isometric torque. A secondary focus is to better understand how firing rates of the antagonist muscle change from a moderate- to higher-contraction intensity. Fourteen subjects performed two submaximal isometric trapezoid muscle actions of the forearm flexors that included a linearly increasing, steady force at both 40% and 70% maximum voluntary contraction, and linearly decreasing segments. Surface electromyographic signals of the biceps and triceps brachii were collected and decomposed into constituent motor unit action potential trains. Motor unit firing rate versus recruitment threshold, motor unit action potential amplitude versus recruitment threshold, and motor unit firing rate versus action potential amplitude relationships of the biceps brachii (agonist) and triceps brachii (antagonist) muscles were analyzed. Moderate- to-strong relationships (|r| ≥ 0.69) were present for the agonist and antagonist muscles for each relationship with no differences between muscles (P = 0.716, 0.428, 0.182). The y-intercepts of the motor unit firing rate versus recruitment threshold relationship of the antagonist did not increase from 40% to 70% maximal voluntary contractions (P = 0.96), unlike for the agonist (P = 0.009). The antagonist muscle exhibits a similar motor unit control scheme to the agonist. Unlike the agonist, however, the firing rates of the antagonist did not increase with increasing intensity. Future research should investigate how antagonist firing rates adapt to resistance training and changes in antagonist firing rates in the absence of peripheral feedback.NEW & NOTEWORTHY This is the first study to explore a potential motor unit control scheme and quantify changes in firing rates with increasing intensity of an antagonist muscle during isometric contractions. We demonstrate that the antagonist muscle possesses an organized motor unit firing rate and recruitment scheme similar to the agonist muscle during isometric forearm flexion, but unlike the agonist muscle, there was no significant increase in firing rates from a moderate- to higher-intensity isometric contraction.

Maximal strength training-induced increase in efferent neural drive is not reflected in relative protein expression of SERCA.

INTRODUCTION: Maximal strength training (MST), performed with heavy loads (~ 90% of one repetition maximum; 1RM) and few repetitions, yields large improvements in efferent neural drive, skeletal muscle force production, and skeletal muscle efficiency. However, it is elusive whether neural adaptations following such high intensity strength training may be accompanied by alterations in energy-demanding muscular factors. METHODS: Sixteen healthy young males (24 ± 4 years) were randomized to MST 3 times per week for 8 weeks (n = 8), or a control group (CG; n = 8). Measurements included 1RM and rate of force development (RFD), and evoked potentials recordings (V-wave and H-reflex normalized to M-wave (M) in the soleus muscle) applied to assess efferent neural drive to maximally contracting skeletal muscle. Biopsies were obtained from vastus lateralis and analyzed by western blots and real-time PCR to investigate the relative protein expression and mRNA expression of Sarcoplasmic Reticulum Ca2+ ATPase (SERCA) 1 and SERCA2. RESULTS: Significant improvements in 1RM (17 ± 9%; p < 0.001) and early (0-100 ms), late (0-200 ms) and maximal RFD (31-53%; p < 0.01) were observed after MST, accompanied by increased maximal Vmax/Msup-ratio (9 ± 14%; p = 0.046), with no change in H-reflex to M-wave ratio. No changes were observed in the CG. No pre- to post-training differences were found in mRNA or protein expressions of SERCA1 and SERCA2 in either group. CONCLUSION: MST increased efferent neural drive to maximally contracting skeletal muscle, causing improved force production. No change was observed in SERCA expression, indicating that responses to high intensity strength training may predominantly be governed by neural adaptations.

Mechanisms of Exertional Dyspnea in Patients with Mild COPD and a Low Resting DLCO.

Patients with mild chronic obstructive pulmonary disease (COPD) and lower resting diffusing capacity for carbon monoxide (DLCO) often report troublesome dyspnea during exercise although the mechanisms are not clear. We postulated that in such individuals, exertional dyspnea is linked to relatively high inspiratory neural drive (IND) due, in part, to the effects of reduced ventilatory efficiency. This cross-sectional study included 28 patients with GOLD I COPD stratified into two groups with (n = 15) and without (n = 13) DLCO less than the lower limit of normal (

Muscle activation during leg-press exercise with or without eccentric overload.

PURPOSE: This study sought to investigate the electromyographic activity of the vastus lateralis (VL) muscle during concentric-eccentric exercise using a new concept leg press machine enabling a preset overloading in the eccentric phase. METHODS: Ten young males familiar with resistive exercise were recruited for this study. Tests were performed on a Leg-press Biostrength® (Technogym S.p.A., Italy). The load was set to 70% and 80% of one-repetition maximum (1-RM). The participants performed 2 sets of 6 repetitions at each relative load with (ECC +) and without (ISOW) an eccentric overload equivalent to 150% of the concentric load. A metronome was employed to maintain the selected cadence. Sets were separated by a 5-min rest. Surface electromyography (EMG) of VL was recorded and integrated (iEMG). RESULTS: Results showed a higher iEMG in ECC + with respect to ISOW at both intensities (+ 29% for 70% 1-RM, p < 0.01 and + 31% for 80% 1-RM, p < 0.001). No statistically significant differences were detected between concentric and eccentric phase in both ECC + conditions. CONCLUSIONS: Training with a 150% eccentric overload provides a ~ 30% greater motor unit recruitment of the VL muscle in leg press exercise. Moreover, the results show that the eccentric overloading provided by the Biostrength® machine enables training at the same level of neural activation of the concentric phase. Hence, the derecruitment of motor units, normally observed during the eccentric phase when using conventional training machines, was overcome using the Biostrength® machine; this observation seems particularly important for maximizing neuromuscular responses to strength training.

You are as fast as your motor neurons: speed of recruitment and maximal discharge of motor neurons determine the maximal rate of force development in humans.

KEY POINTS: We propose and validate a method for accurately identifying the activity of populations of motor neurons during contractions at maximal rate of force development in humans. The behaviour of the motor neuron pool during rapid voluntary contractions in humans is presented. We show with this approach that the motor neuron recruitment speed and maximal motor unit discharge rate largely explains the individual ability in generating rapid force contractions. The results also indicate that the synaptic inputs received by the motor neurons before force is generated dictate human potential to generate force rapidly. This is the first characterization of the discharge behaviour of a representative sample of human motor neurons during rapid contractions. ABSTRACT: During rapid contractions, motor neurons are recruited in a short burst and begin to discharge at high frequencies (up to >200 Hz). In the present study, we investigated the behaviour of relatively large populations of motor neurons during rapid (explosive) contractions in humans, applying a new approach to accurately identify motor neuron activity simultaneous to measuring the rate of force development. The activity of spinal motor neurons was assessed by high-density electromyographic decomposition from the tibialis anterior muscle of 20 men during isometric explosive contractions. The speed of motor neuron recruitment and the instantaneous motor unit discharge rate were analysed as a function of the impulse (the time-force integral) and the maximal rate of force development. The peak of motor unit discharge rate occurred before force generation and discharge rates decreased thereafter. The maximal motor unit discharge rate was associated with the explosive force variables, at the whole population level (r2  = 0.71 ± 0.12; P < 0.001). Moreover, the peak motor unit discharge and maximal rate of force variables were correlated with an estimate of the supraspinal drive, which was measured as the speed of motor unit recruitment before the generation of afferent feedback (P < 0.05). We show for the first time the full association between the effective neural drive to the muscle and human maximal rate of force development. The results obtained in the present study indicate that the variability in the maximal contractile explosive force of the human tibialis anterior muscle is determined by the neural activation preceding force generation.