High-threshold motor unit firing reflects force recovery following a bout of damaging eccentric exercise.
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ABSTRACT:
SUBMITTER: Macgregor LJ
PROVIDER: S-EPMC5890972 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Purpose: The neuromuscular mechanisms leading to impaired motor performance in the presence of mental fatigue remain unclear. It is also unknown if mental fatigue differentially impacts motor performance in males and females. The purpose of this study was to assess the impact of mental fatigue on force production and motor unit (MU) firing behavior in males and females. Methods: Nineteen participants performed 10-s isometric dorsiflexion (DF) contractions at 20 and 50% maximum voluntary contraction (MVC) before, during, and after completing 22 min of the psychomotor vigilance task (PVT), to induce mental fatigue. The DF force and indwelling MU firing behavior of the tibialis anterior (TA) was measured before and immediately following the PVT and within the first and final minutes of the PVT. Results: Force steadiness and motor unit firing rate (MUFR) variability did not change during or following the PVT at either contraction intensity (p ? 0.16). Overall, females had more variability than males in MUFR during the 20% MVCs (15.98 ± 2.19 vs. 13.64 ± 2.19%, p = 0.03), though no sex differences were identified during the 50% MVCs (p = 0.20). Mean MUFR decreased following mental fatigue in both sexes in the 20% MVC condition (14.79 ± 3.20 vs. 12.92 ± 2.53 Hz, p = 0.02), but only in males during the 50% MVC condition (18.65 ± 5.21 vs. 15.03 ± 2.60 Hz, p = 0.01). Conclusions: These results suggest possible sex and contraction intensity-specific neuromuscular changes in the presence of mental fatigue.
| S-EPMC7137823 | biostudies-literature
Project description:Background: Resting Motor threshold (rMT) is one of the measurement obtained by Transcranial Magnetic Stimulation (TMS) that reflects corticospinal excitability. As a functional marker of the corticospinal pathway, the question arises whether rMT is a suitable biomarker for predicting post-stroke upper limb function. To that aim, we conducted a systematic review of relevant studies that investigated the clinical significance of rMT in stroke survivors by using correlations between upper limb motor scores and rMT. Methods: Studies that reported correlations between upper limb motor function and rMT as a measure of corticospinal excitability in distal arm muscle were identified via a literature search in stroke patients. Two authors extracted the data using a home-made specific form. Subgroup analyses were carried out with patients classified with respect to time post-stroke onset (early vs. chronic stage) and stroke location (cortical, subcortical, or cortico-subcortical). Methodological quality of the study was also evaluated by a published checklist. Results: Eighteen studies with 22 groups (n = 508 stroke patients) were included in this systematic review. Mean methodological quality score was 14.75/24. rMT was often correlated with motor function or hand dexterity (n = 15/22, 68%), explaining on average 31% of the variance of the motor score. Moreover, the results did not seem impacted if patients were examined at the early or chronic stages of stroke. Two findings could not be properly interpreted: (i) the fact that the rMT is an independent predictor of motor function as several confounding factors are well-established, and, (ii) whether the stroke location impacts this prediction. Conclusion: Most of the studies found a correlation between rMT and upper limb motor function after stroke. However, it is still unclear if rMT is an independent predictor of upper limb motor function when taking into account for age, time post stroke onset and level of corticospinal tract damage as confounding factors. Clear-cut conclusions could not be drawn at that time but our results suggest that rMT could be a suitable candidate although future investigations are needed. Systematic Review Registration Number: (https://www.crd.york.ac.uk/prospero/): ID 114317.
| S-EPMC6281982 | biostudies-literature
Project description:Whole body vibration (WBV) has been suggested to elicit reflex muscle contractions but this has never been verified. We recorded from 32 single motor units (MU) in the vastus lateralis of 7 healthy subjects (34 ± 15.4 yr) during five 1-min bouts of WBV (30 Hz, 3 mm peak to peak), and the vibration waveform was also recorded. Recruitment thresholds were recorded from 38 MUs before and after WBV. The phase angle distribution of all MUs during WBV was nonuniform (P < 0.001) and displayed a prominent peak phase angle of firing. There was a strong linear relationship (r = -0.68, P < 0.001) between the change in recruitment threshold after WBV and average recruitment threshold; the lowest threshold MUs increased recruitment threshold (P = 0.008) while reductions were observed in the higher threshold units (P = 0.031). We investigated one possible cause of changed thresholds. Presynaptic inhibition in the soleus was measured in 8 healthy subjects (29 ± 4.6 yr). A total of 30 H-reflexes (stimulation intensity 30% Mmax) were recorded before and after WBV: 15 conditioned by prior stimulation (60 ms) of the antagonist and 15 unconditioned. There were no significant changes in the relationship between the conditioned and unconditioned responses. The consistent phase angle at which each MU fired during WBV indicates the presence of reflex muscle activity similar to the tonic vibration reflex. The varying response in high- and low-threshold MUs may be due to the different contributions of the mono- and polysynaptic pathways but not presynaptic inhibition.
| S-EPMC3289430 | biostudies-literature
Project description:Inexperienced vigorous exercise, including eccentric contraction (ECC), causes muscle pain and damage. Similar prior light exercise suppresses the development of muscle pain (repeated-bout effect), but the molecular mechanisms behind this are not sufficiently understood. In this study, the influence of a nondamaging preconditioning ECC load (Precon) on muscle pain-related molecules and satellite cell-activating factors was investigated at the mRNA expression level. Nine-week-old male Wistar rats (n=36) were divided into 2 groups: a group receiving only a damaging ECC (100 contractions) load (non-Precon) and a group receiving a nondamaging ECC (10 contractions) load 2 days before receiving the damaging ECC load (Precon). ECC was loaded on the left leg, and the right leg was regarded as the intact control (CTL). The medial head of the gastrocnemius muscle from all rats was excised 2 or 4 days after the damaging ECC loading, and the relative mRNA expression levels of muscle pain- and satellite cell-related molecules were quantitated using real-time RT PCR. Precon suppressed increases in MHC-embryonic and MHC-neonatal mRNA expressions. Enhancement of HGF, Pax7, MyoD, and myogenin mRNA expression was also suppressed, suggesting that Precon decreased the degree of muscle damage and no muscle regeneration or satellite cell activation occurred. Similarly, increases in mRNA expression of muscle pain-related molecules (BKB2 receptor, COX-2, and mPGEC-1) were also suppressed. This study clearly demonstrated that at the mRNA level, prior light ECC suppressed muscle damage induced by later damaging ECC and promoted recovery from muscle pain.
| S-EPMC6204166 | biostudies-literature
Project description:The current consensus in exercise physiology is that the repeated bout effect always appears after few eccentric exercise sessions. This is the first attempt to challenge this tenet, by exploiting specificity in muscle plasticity. More specifically, we examined whether the opposing adaptations in muscle induced after concentric and eccentric exercise can attenuate and/or remove the repeated bout effect. Seventeen young men were randomly assigned into one of the following groups: (1) the alternating eccentric-concentric exercise group; and (2) the eccentric-only exercise group. Both groups performed 8 weeks of resistance exercise using the knee extensors of both legs on an isokinetic dynamometer. The alternating eccentric-concentric exercise group performed an alternating exercise protocol, switching between eccentric-only and concentric-only exercise every 4 weeks, while the eccentric-only group performed eccentric exercise. Evaluation of muscle damage using physiological (isometric torque, delayed onset muscle soreness, and range of movement) and biochemical (creatine kinase) markers and inflammation (C-reactive protein) was performed at weeks 1, 5, and 10. Baseline isometric peak torque was also evaluated at week 14 after another cycle (4 weeks) of alternating or eccentric-only exercise training. In the alternating eccentric-concentric exercise group, the concentric exercise training performed prior to eccentric exercise reduced dramatically the repeated bout effect by reversing muscle back to its unaccustomed state. On the contrary, the eccentric-only exercise group exhibited a typical manifestation of the repeated bout effect. Interestingly, muscle strength was elevated similarly for both alternating and eccentric-only exercise groups after 13 weeks of training. The alternating eccentric-concentric exercise scheme, implemented in the present study, has for the first time successfully overcame the repeated bout effect. The similarity in muscle strength measurements following the two protocols is against the notion that inflammation plays an important role in exercise-induced adaptations in muscle.
| S-EPMC4760450 | biostudies-other
Project description:We investigate firing threshold manifolds in a mathematical model of an excitable neuron. The model analyzed investigates the phenomenon of post-inhibitory rebound spiking due to propofol anesthesia and is adapted from McCarthy et al. (SIAM J. Appl. Dyn. Syst. 11(4):1674-1697, 2012). Propofol modulates the decay time-scale of an inhibitory GABAa synaptic current. Interestingly, this system gives rise to rebound spiking within a specific range of propofol doses. Using techniques from geometric singular perturbation theory, we identify geometric structures, known as canards of folded saddle-type, which form the firing threshold manifolds. We find that the position and orientation of the canard separatrix is propofol dependent. Thus, the speeds of relevant slow synaptic processes are encoded within this geometric structure. We show that this behavior cannot be understood using a static, inhibitory current step protocol, which can provide a single threshold for rebound spiking but cannot explain the observed cessation of spiking for higher propofol doses. We then compare the analyses of dynamic and static synaptic inhibition, showing how the firing threshold manifolds of each relate, and why a current step approach is unable to fully capture the behavior of this model.
| S-EPMC3819701 | biostudies-literature
Project description:Weakness, one of the key characteristics of sarcopenia, is a significant risk factor for functional limitations and disability in older adults. It has long been suspected that reductions in motor unit firing rates (MUFRs) are one of the mechanistic causes of age-related weakness. However, prior work has not investigated the extent to which MUFR is associated with clinically meaningful weakness in older adults. Forty-three community-dwelling older adults (mean: 75.4 ± 7.4 years; 46.5% female) and 24 young adults (mean: 22.0 ± 1.8 years; 58.3% female) performed torque matching tasks at varying submaximal intensities with their non-dominant leg extensors. Decomposed surface electromyographic recordings were used to quantify MUFRs from the vastus lateralis muscle. Computational modeling was subsequently used to independently predict how slowed MUFRs would negatively impact strength in older adults. Bivariate correlations between MUFRs and indices of lean mass, voluntary activation, and physical function/mobility were also assessed in older adults. Weak older adults (n = 14) exhibited an approximate 1.5 and 3 Hz reduction in MUFR relative to non-weak older adults (n = 29) at 50% and 80% MVC, respectively. Older adults also exhibited an approximate 3 Hz reduction in MUFR relative to young adults at 80% MVC only. Our model predicted that a 3 Hz reduction in MUFR results in a strength decrement of 11-26%. Additionally, significant correlations were found between slower MUFRs and poorer neuromuscular quality, voluntary activation, chair rise time performance, and stair climb power (r's = 0.31 to 0.43). These findings provide evidence that slowed MUFRs are mechanistically linked with clinically meaningful leg extensor weakness in older adults.
| S-EPMC10791983 | biostudies-literature
Project description:While neural changes are thought to be responsible for early increases in strength following resistance training (RT), the exact changes in motor unit (MU) firing properties remain unclear. This review aims to synthesize the available evidence on the effect of RT on MU firing properties. MEDLINE (OVID interface), EMBASE (OVID interface), Web of Science (all databases), Cochrane Library, EBSCO CINAHL Plus, PubMed, and EBSCO SportDiscus were searched from inception until June 2021. Randomized controlled trials and non-randomized studies of interventions that compared RT to no intervention (control) were included. Two reviewers independently extracted data from each trial, assessed the risk of bias and rated the cumulative quality of evidence. Motor unit discharge rate (MUDR), motor unit recruitment threshold (MURT), motor unit discharge rate variability (MUDRV), MU discharge rate at recruitment vs. recruitment threshold relationship, and MU discharge rate vs. recruitment threshold relationship were assessed. Seven trials including 167 participants met the inclusion criteria. Meta-analysis (four studies) revealed that MUDR did not change significantly (P = 0.43), but with considerable heterogeneity likely to be present (I 2 = 91). Low to moderate evidence supports changes in MUDRV, MUDR at recruitment vs. recruitment threshold relationship, and the MUDR vs. recruitment threshold relationship. Overall, this systematic review revealed that there is a lack of high-quality evidence for the effect of RT on MU firing properties. Heterogeneity across studies undermines the quality of the evidence for multiple outcomes and affects the conclusions that can be drawn.
| S-EPMC8918924 | biostudies-literature
Project description:Neuromuscular physiology is a vibrant research field that has recently seen exciting advances. Previous publications have focused on thorough analyses of particular aspects of neuromuscular physiology, yet an integration of the various novel findings into a single, comprehensive model is missing. In this article, we provide a unified description of a comprehensive mathematical model of surface electromyographic (EMG) measurements and the corresponding force signal in skeletal muscles, both consolidating and extending the results of previous studies regarding various components of the neuromuscular system. The model comprises motor unit (MU) pool organization, recruitment and rate coding, intracellular action potential generation and the resulting EMG measurements, as well as the generated muscular force during voluntary isometric contractions. Mathematically, it consists of a large number of linear PDEs, ODEs, and various stochastic nonlinear relationships, some of which are solved analytically, others numerically. A parameterization of the electrical and mechanical components of the model is proposed that ensures a physiologically meaningful EMG-force relation in the simulated signals, in particular taking the continuous, size-dependent distribution of MU parameters into account. Moreover, a novel nonlinear transformation of the common drive model input is proposed, which ensures that the model force output equals the desired target force. On a physiological level, this corresponds to adjusting the rate coding model to the force generating capabilities of the simulated muscle, while from a control theoretic point of view, this step is equivalent to an exact linearizing transformation of the controlled neuromuscular system. Finally, an alternative analytical formulation of the EMG model is proposed, which renders the physiological meaning of the model more clear and facilitates a mathematical proof that muscle fibers in this model at no point in time represent a net current source or sink. A consistent description of a complete physiological model as presented here, including thorough justification of model component choices, will facilitate the use of these advanced models in future research. Results of a numerical simulation highlight the model's capability to reproduce many physiological effects observed in experimental measurements, and to produce realistic synthetic data that are useful for the validation of signal processing algorithms.
| S-EPMC6418040 | biostudies-literature
Project description:Spinal muscular atrophy (SMA) is a childhood motor neuron disease caused by anomalies in the SMN1 gene. Although therapeutics have been approved for the treatment of SMA, there is a therapeutic time window, after which efficacy is reduced. Hallmarks of motor unit pathology in SMA include loss of motor-neurons and neuromuscular junction (NMJs). Following an increase in Smn levels, it is unclear how much damage can be repaired and the degree to which normal connections are re-established. Here, we perform a detailed analysis of motor unit pathology before and after restoration of Smn levels. Using a Smn-inducible mouse model of SMA, we show that genetic restoration of Smn results in a dramatic reduction in NMJ pathology, with restoration of innervation patterns, preservation of axon and endplate number and normalized expression of P53-associated transcripts. Notably, presynaptic swelling and elevated Pmaip levels remained. We analysed the effect of either early or delayed treated of an antisense oligonucleotide (ASO) targeting SMN2 on a range of differentially vulnerable muscles. Following ASO administration, the majority of endplates appeared fully occupied. However, there was an underlying loss of axons and endplates, which was more prevalent following a delay in treatment. There was an increase in average motor unit size following both early and delayed treatment. Together this work demonstrates the remarkably regenerative capacity of the motor neuron following Smn restoration, but highlights that recovery is incomplete. This work suggests that there is an opportunity to enhance neuromuscular junction recovery following administration of Smn-enhancing therapeutics.
| S-EPMC9476628 | biostudies-literature