Force-generating Capacity Research Articles

Acute Changes in Hamstring Injury Risk Factors After a Session of High-Volume Maximal Sprinting Speed Efforts in Soccer Players.

Maximal sprinting speed (MSS) overexposure is associated with increased risk of injury. This study aimed to describe changes in sprint performance-related factors and hamstring strain injury (HSI) risk factors after a high-volume sprinting session in soccer players. A high-volume sprinting session can induce acute changes in several sprint performance-related factors (sprint time and mechanical properties) and HSI risk factors (posterior chain muscle strength, hamstring range of motion, and dynamic lumbo-pelvic control [LPC], measured as changes in anterior pelvic tilt [APT] during maximal speed sprinting). Prospective observational case series. Level 4. Fifteen active male amateur soccer players participated. Changes in sprint performance-related factors and HSI risk factors were examined for 72 hours after high-volume MSS efforts (H-VMSSE) using a soccer-contextualized multifactorial approach. Muscle damage proxy markers (hamstring perceived soreness and creatine kinase) were also examined. H-VMSSE induced decrements in sprint performance-related factors. Significant reductions in theoretical maximal horizontal velocity (P < 0.01; effect size [ES], -0.71) and performance (P = 0.02; ES, -0.59) were observed for 48 and 72 hours after H-VMSSE. Small but significant reductions in posterior chain muscle force-generating capacity were detected for 48 and 72 hours after H-VMSSE for the nondominant (P < 0.03; ES, -0.60) and dominant (P < 0.04; ES, -0.40) leg. Finally, players exhibited persistent small, albeit nonsignificant (P = 0.06; ES, 0.53), decreases in dynamic LPC (APT increases) for 72 hours after H-VMSSE. H-VMSSE induced declines in both sprint performance-related factors and HSI risk factors. Sprinting can alter a player's anatomic structure by increasing APT during the maximum speed phase of the sprint. A soccer-contextualized multifactorial approach might allow for the regulation of MSS dosage depending on individual HSI risk factor status, thereby serving as a tailored "vaccine" for sprinting needs.

P38α kinase governs muscle strength through PGC1α in mice.

Skeletal muscle, with its remarkable plasticity and dynamic adaptation, serves as a cornerstone of locomotion and metabolic homeostasis in the human body. Muscle tissue, with its extraordinary capacity for force generation and energy expenditure, plays a fundamental role in the movement, metabolism, and overall health. In this context, we sought to determine the role of p38α in mitochondrial metabolism since mitochondrial dynamics play a crucial role in the development of muscle-related diseases that result in muscle weakness. We conducted our study using male mice (MCK-cre, p38αMCK-KO and PGC1α MCK-KO) and mouse primary myoblasts. We analyzed mitochondrial metabolic, physiological parameters as well as proteomics, western blot, RNA-seq analysis from muscle samples. Our findings highlight the critical involvement of muscle p38α in the regulation of mitochondrial function, a key determinant of muscle strength. The absence of p38α triggers changes in mitochondrial dynamics through the activation of PGC1α, a central regulator of mitochondrial biogenesis. These results have substantial implications for understanding the complex interplay between p38α kinase, PGC1α activation, and mitochondrial content, thereby enhancing our knowledge in the control of muscle biology. This knowledge holds relevance for conditions associated with muscle weakness, where disruptions in these molecular pathways are frequently implicated in diminishing physical strength. Our research underscores the potential importance of targeting the p38α and PGC1α pathways within muscle, offering promising avenues for the advancement of innovative treatments. Such interventions hold the potential to improve the quality of life for individuals affected by muscle-related diseases.

Knee joint pathology and efferent pathway dysfunction: Mapping muscle inhibition from motor cortex to muscle force

BackgroundDysfunction in efferent pathways after knee pathology is tied to long-term impairments in quadriceps and hamstrings muscle performance, daily function, and health-related quality of life. Understanding the underlying etiology is crucial for effective treatment and prevention of poor outcomes, such as post-traumatic osteoarthritis or joint replacement. ObjectivesTo synthesize recent evidence of efferent pathway dysfunction (i.e., motor cortex, motor units) among individuals with knee pathology. DesignCommentary. MethodWe summarize the current literature investigating the motor cortex, corticospinal tract, and motoneuron pool in individuals with three common knee pathologies: anterior cruciate ligament (ACL) injury, anterior knee pain (AKP), and knee osteoarthritis (OA). To offer a complete perspective, we draw from studies applying a range of neuroimaging and neurophysiologic techniques. ResultsAdaptations within the motor cortices, corticospinal tract, and motoneuron pool are present in those with knee pathology and underline impairments in quadriceps and hamstrings muscle function. Each pathology has evidence of altered motor system excitability and reduced volitional muscle activation and force-generating capacity, but few impairments were common across ACL injury, AKP, and OA studies. These findings underscore the central role of the motor cortex and motor unit behavior in the long-term outcomes of individuals with knee pathology. ConclusionsAdaptations in the efferent pathways underlie persistent muscle dysfunction across three common knee pathologies. This review provides an overview of these changes and summarizes key findings from neurophysiology and neuroimaging studies, offering direction for future research and clinical application in the rehabilitation of joint injuries.

Training for Elite Team-Pursuit Track Cyclists-Part II: A Comparison of Preparation Phases in Consecutive World-Record-Breaking Seasons.

To compare the training characteristics of an elite team pursuit cycling squad in the 3-month preparation phases prior to 2 successive world-record (WR) performances. Training data of 5 male track endurance cyclists (mean [SD]; age 23.4 [3.46]y; body mass 80.2 [2.74]kg; 4.5 [0.17]W·kg-1 at LT2; maximal aerobic power6.2 [0.27]W·kg-1; maximal oxygen uptake 65.9 [2.89]mL·kg-1·min-1) were analyzed with weekly total training volume by training type and heart rate, power output, and torque intensity distributions calculated with reference to the respective WRs' performance requirements. Athletes completed 805 (82.81) and 725 (68.40)min·wk-1 of training, respectively, in each season. In the second season, there was a 32% increase in total track volume, although track sessions were shorter (ie,greater frequency) in the second season. A pyramidal intensity distribution was consistent across both seasons, with 81% of training, on average, performed below LT1 power output each week, whereas 6% of training was performed above LT2. Athletes accumulated greater volume above WR team pursuit lead power (2.4% vs 0.9%) and torque (6.2% vs 3.2%) in 2019. In one athlete, mean single-leg-press peak rate of force development was 71% and 46% higher at mid- and late-phases, respectively, during the preparation period. These findings provide novel insights into the common and contrasting methods contributing to successive WR team pursuit performances. Greater accumulation of volume above race-specific power and torque (eg,team pursuit lead), as well as improved neuromuscular force-generating capacities, may be worthy of investigation for implementation in training programs.

Myosin-I synergizes with Arp2/3 complex to enhance the pushing forces of branched actin networks.

Class I myosins (myosin-Is) colocalize with Arp2/3 complex-nucleated actin networks at sites of membrane protrusion and invagination, but the mechanisms by which myosin-I motor activity coordinates with branched actin assembly to generate force are unknown. We mimicked the interplay of these proteins using the "comet tail" bead motility assay, where branched actin networks are nucleated by the Arp2/3 complex on the surface of beads coated with myosin-I and nucleation-promoting factor. We observed that myosin-I increased bead movement efficiency by thinning actin networks without affecting growth rates. Myosin-I triggered symmetry breaking and comet tail formation in dense networks resistant to spontaneous fracturing. Even with arrested actin assembly, myosin-I alone could break the network. Computational modeling recapitulated these observations, suggesting myosin-I acts as a repulsive force shaping the network's architecture and boosting its force-generating capacity. We propose that myosin-I leverages its power stroke to amplify the forces generated by Arp2/3 complex-nucleated actin networks.

Effects of Short-Term Treatment of Rabbit Extraocular Muscle With Ciliary Neurotrophic Factor.

Little is known about the effect of ciliary neurotrophic factor (CNTF) on extraocular muscles, but microarray studies suggested CNTF might play a role in the development and/or maintenance of strabismus. The effect of short-term treatment of adult rabbit extraocular muscle with injected CNTF was examined for its ability to alter muscle characteristics. Eight adult New Zealand white rabbits received an injection into one superior rectus muscle of 2 µg/100 µL CNTF on 3 consecutive days. One week after the first injection, the rabbits were euthanized, and the treated and contralateral superior rectus muscles were assessed for force generation capacity and contraction characteristics using an in vitro stimulation protocol and compared to naïve control superior rectus muscles. All muscles were analyzed to determine mean cross-sectional areas and expression of slow twitch myosin heavy chain isoform. Short-term treatment of rabbit superior rectus muscles with CNTF resulted in a significant decrease in muscle force generation, but only at the higher stimulation frequencies. Significantly decreased myofiber cross-sectional areas of the treated muscles correlated with the decreased generated force. In addition, there were significant changes to contractile properties of the treated muscles, as well as a decrease in the number of myofibers expressing slow twitch myosin heavy chain. We show that short-term treatment of a single rabbit superior rectus muscle results in decreased myofiber size, decreased force, and altered contractile characteristics. Further studies are needed to determine if it can play a role in improving alignment in animal models of strabismus.

Gearing in a hydrostatic skeleton: the tube feet of juvenile sea stars (Leptasterias sp.).

Hydrostatic skeletons, such as an elephant trunk or a squid tentacle, permit the transmission of mechanical work through a soft body. Despite the ubiquity of these structures among animals, we generally do not understand how differences in their morphology affect their ability to transmit muscular work. Therefore, the present study used mathematical modeling, morphometrics, and kinematics to understand the transmission of force and displacement in the tube feet of the juvenile six-rayed star (Leptasterias sp.). An inverse-dynamic analysis revealed that the forces generated by the feet during crawling primarily serve to overcome the submerged weight of the body. These forces were disproportionately generated by the feet at more proximal positions along each ray, which were used more frequently for crawling. Owing to a combination of mechanical advantage and muscle mass, these proximal feet exhibited a greater capacity for force generation than the distal feet. However, the higher displacement advantage of the more elongated distal feet offer a superior ability to extend the feet into the environment. Therefore, the morphology of tube feet demonstrates a gradient in gearing along each ray that compliments their role in behavior.

Motor domain phosphorylation increases nucleotide exchange and turns MYO6 into a faster and stronger motor

Myosin motors perform many fundamental functions in eukaryotic cells by providing force generation, transport or tethering capacity. Motor activity control within the cell involves on/off switches, however, few examples are known of how myosins regulate speed or processivity and fine-tune their activity to a specific cellular task. Here, we describe a phosphorylation event for myosins of class VI (MYO6) in the motor domain, which accelerates its ATPase activity leading to a 4-fold increase in motor speed determined by actin-gliding assays, single molecule mechanics and stopped flow kinetics. We demonstrate that the serine/threonine kinase DYRK2 phosphorylates MYO6 at S267 in vitro. Single-molecule optical-tweezers studies at low load reveal that S267-phosphorylation results in faster nucleotide-exchange kinetics without change in the working stroke of the motor. The selective increase in stiffness of the acto-MYO6 complex when proceeding load-dependently into the nucleotide-free rigor state demonstrates that S267-phosphorylation turns MYO6 into a stronger motor. Finally, molecular dynamic simulations of the nucleotide-free motor reveal an alternative interaction network within insert-1 upon phosphorylation, suggesting a molecular mechanism, which regulates insert-1 positioning, turning the S267-phosphorylated MYO6 into a faster motor.

Chronic N-acetyl cysteine treatment does not improve respiratory system performance in the mdx mouse model of Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is characterised by respiratory muscle injury, inflammation, fibrosis and weakness, ultimately culminating in respiratory failure. The dystrophin-deficient mouse model of DMD (mdx) shows evidence of respiratory muscle remodelling and dysfunction contributing to impaired respiratory system performance. The antioxidant N-acetylcysteine (NAC) has been shown to exert anti-inflammatory and anti-fibrotic effects leading to improved respiratory muscle performance in a range of animal models of muscle dysfunction, including mdx mice, following short-term administration (2weeks). We sought to build on previous work by exploring the effects of chronic NAC administration (3months) on respiratory system performance in mdx mice. One-month-old male mdx mice were randomised to receive normal drinking water (n=30) or 1% NAC in the drinking water (n=30) for 3months. At 4months of age, we assessed breathing in conscious mice by plethysmography followed by ex vivo assessment of diaphragm force-generating capacity. Additionally, diaphragm histology was performed. In separate studies, in anaesthetised mice, respiratory electromyogram (EMG) activity and inspiratory pressure across a range of behaviours were determined, including assessment of peak inspiratory pressure-generating capacity. NAC treatment did not affect force-generating capacity of the mdx diaphragm. Collagen content and immune cell infiltration were unchanged in mdx + NAC compared with mdx diaphragms. Additionally, there was no significant effect of NAC on breathing, ventilatory responsiveness, inspiratory EMG activity or inspiratory pressure across the range of behaviours from basal conditions to peak system performance. We conclude that chronic NAC treatment has no apparent beneficial effects on respiratory system performance in the mdx mouse model of DMD suggesting limited potential of NAC treatment alone for human DMD.

Load Dependency of Ventricular Pump Function: Impact on the Non-Invasive Evaluation of the Severity and the Prognostic Relevance of Myocardial Dysfunction.

Ventricular pump function, which is determined by myocyte contractility, preload and afterload, and, additionally, also significantly influenced by heart rhythm, synchrony of intraventricular contraction and ventricular interdependence, explains the difficulties in establishing the contribution of myocardial contractile dysfunction to the development and progression of heart failure. Estimating myocardial contractility is one of the most difficult challenges because the most commonly used clinical measurements of cardiac performance cannot differentiate contractility changes from alterations in ventricular loading conditions. Under both physiological and pathological conditions, there is also a permanent complex interaction between myocardial contractility, ventricular anatomy and hemodynamic loading conditions. All this explains why no single parameter can alone reveal the real picture of ventricular dysfunction. Over time there has been increasing recognition that a load-independent contractility parameter cannot truly exist, because loading itself changes the myofilament force-generating capacity. Because the use of a single parameter is inadequate, it is necessary to perform multiparametric evaluations and also apply integrative approaches using parameter combinations which include details about ventricular loading conditions. This is particularly important for evaluating the highly afterload-sensitive right ventricular function. In this regard, the existence of certain reluctance particularly to the implementation of non-invasively obtainable parameter combinations in the routine clinical praxis should be reconsidered in the future. Among the non-invasive approaches used to evaluate ventricular function in connection with its current loading conditions, assessment of the relationship between ventricular contraction (e.g., myocardial displacement or deformation) and pressure overload, or the relationship between ejection volume (or ejection velocity) and pressure overload, as well as the relationship between ventricular dilation and pressure overload, were found useful for therapeutic decision-making. In the future, it will be unavoidable to take the load dependency of ventricular function much more into consideration. A solid basis for achieving this goal will be obtainable by intensifying the clinical research necessary to provide more evidence for the practical importance of this largely unsolved problem.

Effect of muscle length on maximum evoked torque, discomfort, contraction fatigue, and strength adaptations during electrical stimulation in adult populations: A systematic review.

Neuromuscular electrical stimulation (NMES) can improve physical function in different populations. NMES-related outcomes may be influenced by muscle length (i.e., joint angle), a modulator of the force generation capacity of muscle fibers. Nevertheless, to date, there is no comprehensive synthesis of the available scientific evidence regarding the optimal joint angle for maximizing the effectiveness of NMES. We performed a systematic review to investigate the effect of muscle length on NMES-induced torque, discomfort, contraction fatigue, and strength training adaptations in healthy and clinical adult populations (PROSPERO: CRD42022332965). We conducted searches across seven electronic databases: PUBMED, Web of Science, EMBASE, PEDro, BIREME, SCIELO, and Cochrane, over the period from June 2022 to October 2023, without restricting the publication year. We included cross-sectional and longitudinal studies that used NMES as an intervention or assessment tool for comparing muscle lengths in adult populations. We excluded studies on vocalization, respiratory, or pelvic floor muscles. Data extraction was performed via a standardized form to gather information on participants, interventions, and outcomes. Risk of bias was assessed using the Revised Cochrane risk-of-bias tool for cross-over trials and the Physiotherapy Evidence Database scale. Out of the 1185 articles retrieved through our search strategy, we included 36 studies in our analysis, that included 448 healthy young participants (age: 19-40 years) in order to investigate maximum evoked torque (n = 268), contraction fatigability (n = 87), discomfort (n = 82), and muscle strengthening (n = 22), as well as six participants with spinal cord injuries, and 15 healthy older participants. Meta-analyses were possible for comparing maximal evoked torque according to quadriceps muscle length through knee joint angle. At optimal muscle length 50° - 70° of knee flexion, where 0° is full extension), there was greater evoked torque during nerve stimulation compared to very short (0 - 30°) (p<0.001, CI 95%: -2.03, -1.15 for muscle belly stimulation, and -3.54, -1.16 for femoral nerve stimulation), short (31° - 49°) (p = 0.007, CI 95%: -1.58, -0.25), and long (71° - 90°) (p<0.001, CI 95%: 0.29, 1.02) muscle lengths. At long muscle lengths, NMES evoked greater torque than very short (p<0.001, CI 95%: -2.50, -0.67) and short (p = 0.04, CI 95%: -2.22, -0.06) lengths. The shortest quadriceps length generated the highest perceived discomfort for a given current amplitude. The amount of contraction fatigability was greater when muscle length allowed greater torque generation in the pre-fatigue condition. Strength gains were greater for a protocol at the optimal muscle length than for short muscle length. The quality of evidence was very high for most comparisons for evoked torque. However, further studies are necessary to achieve certainty for the other outcomes. Optimal muscle length should be considered the primary choice during NMES interventions, as it promotes higher levels of force production and may facilitate the preservation/gain in muscle force and mass, with reduced discomfort. However, a longer than optimal muscle length may also be used, due to possible muscle lengthening at high evoked tension. Thorough understanding of these physiological principles is imperative for the appropriate prescription of NMES for healthy and clinical populations.

EMG-Constrained and Ultrasound-Informed Muscle-Tendon Parameter Estimation in Post-Stroke Hemiparesis.

Secondary morphological and mechanical property changes in the muscle-tendon unit at the ankle joint are often observed in post-stroke individuals. These changes may alter the force generation capacity and affect daily activities such as locomotion. This work aimed to estimate subject-specific muscle-tendon parameters in individuals after stroke by solving the muscle redundancy problem using direct collocation optimal control methods based on experimental electromyography (EMG) signals and measured muscle fiber length. Subject-specific muscle-tendon parameters of the gastrocnemius, soleus, and tibialis anterior were estimated in seven post-stroke individuals and seven healthy controls. We found that the maximum isometric force, tendon stiffness and optimal fiber length in the post-stroke group were considerably lower than in the control group. We also computed the root mean square error between estimated and experimental values of muscle excitation and fiber length. The musculoskeletal model with estimated subject-specific muscle tendon parameters (from the muscle redundancy solver), yielded better muscle excitation and fiber length estimations than did scaled generic parameters. Our findings also showed that the muscle redundancy solver can estimate muscle-tendon parameters that produce force behavior in better accordance with the experimentally-measured value. These muscle-tendon parameters in the post-stroke individuals were physiologically meaningful and may shed light on treatment and/or rehabilitation planning.

Indices of exercise induced muscle damage following low load resistance exercise with blood flow restriction in untrained males.

There is conflicting evidence regarding the presence and magnitude of exercise-induced muscle damage (EIMD) following low-load resistance training with blood flow restriction (LL+BFR), which may be related to the protocol implemented or exercise volume. Therefore, the purpose of this investigation was to examine the effects of a 75 repetition (BFR-75) (1×30, 3×15) and four sets to volitional failure (BFR-4x) protocols on indices of EIMD among untrained men. Twelve males with no history of lower-body resistance training during the previous six months volunteered for this investigation. One leg was randomly assigned to BFR-75, and the other to BFR-4x. Participants performed isokinetic, unilateral, concentric-eccentric, leg extension muscle actions at 30% of maximal strength with BFR. Indices of EIMD (limb circumference, perceived muscle soreness, pain pressure threshold [PPT], passive range of motion, and maximal strength [MVIC]) were recorded before exercise and 0, 24, 48, 72, and 96-hours post-exercise for each protocol. There were no significant changes (P>0.05) in limb circumference, PPT, passive range of motion, or MVIC. For both BFR-75 and BFR-4x, perceived muscle soreness increased (P<0.001) similarly 24- (2.5±1.7 AU) and 48-hours (1.9±1.7 AU) post-exercise. There was an increase in muscle soreness 24-48 hours post-exercise for both conditions, which may be due to metabolic stress, but this did not affect the force-generating capacity of the muscle (MVIC), suggesting minimal EIMD. The conflicting evidence of EIMD following LL+BFR may be related to differences in restriction time or overall exercise time.

Neuromodulatory Contribution to Muscle Force Production after Short-Term Unloading and Active Recovery.

Prior evidence has shown that neural factors contribute to the loss of muscle force after skeletal muscle disuse. However, little is known about the specific neural mechanisms altered by disuse. Persistent inward current (PIC) is an intrinsic property of motoneurons responsible for prolonging and amplifying the synaptic input, proportionally to the level of neuromodulation, thus influencing motoneuron discharge rate and force production. Here, we hypothesized that short-term unilateral lower limb suspension (ULLS) would reduce the neuromodulatory input associated with PIC, contributing to the reduction of force generation capacity. In addition, we tested whether physical exercise would restore the force generation capacity by reestablishing the initial level of neuromodulatory input. In 12 young adults, we assessed maximal voluntary contraction pre- and post-10 d of ULLS and after 21 d of active recovery (AR) based on resistance exercise. PIC was estimated from high-density surface electromyograms of the vastus lateralis muscle as the delta frequency (Δ F ) of paired motor units calculated during isometric ramped contractions. The values of Δ F were reduced after 10 d of ULLS (-33%, P < 0.001), but were fully reestablished after the AR (+29.4%, P < 0.001). The changes in estimated PIC values were correlated ( r = 0.63, P = 0.004) with the reduction in maximal voluntary contraction after ULLS (-29%, P = 0.002) and its recovery after the AR (+28.5%, P = 0.003). Our findings suggest that PIC estimates are reduced by muscle disuse and may contribute to the loss of force production and its recovery with exercise. Overall, this is the first study demonstrating that, in addition to peripheral neuromuscular changes, central neuromodulation is a major contributor to the loss of force generation capacity after disuse, and can be recovered after resistance exercise.

Advanced Age Impairs the Neuromuscular Control of Peak Inspiratory Performance in Mice

Respiratory muscle wasting is known to occur in ageing adults resulting in a decreased capacity for force production and an associated reduction in high-threshold respiratory performance. Dysfunction of the respiratory musculature in this manner may contribute to an increased susceptibility to respiratory complications frequently observed in older populations. The objective of the current study was to characterise the respiratory phenotype during advanced age to assess the impact of sarcopenia on the neuromuscular control of respiratory performance. Male wild type (BL10) mice were studied at 6-months and 24-months, representing young and old age cohorts, respectively. In anaesthetised animals, inspiratory pressure and contemporaneous obligatory and accessory respiratory muscle electromyography (EMG) activities were measured during baseline and sustained tracheal occlusion (n = 9 young; n = 8 old). Diaphragm muscle contractile performance was assessed ex-vivo via tissue bath preparations (n = 8 young; n = 8 old). Furthermore, diaphragm and limb muscle tissues were harvested and snap frozen for subsequent structural and molecular analyses which will assess potential differences in cross-sectional area and relative fibre type composition. Peak inspiratory pressure was significantly reduced in 24-month-old compared to 6-month-old mice (P &lt; 0.0001). Associated EMG activity was significantly lower (P &lt; 0.05) in obligatory (external intercostal; parasternal) and accessory (cleidomastoid; scalene; trapezius; sternomastoid; sternohyoid) muscles of breathing in the old group compared to the young. Diaphragm EMG amplitude was not different between the groups. No differences were observed in the force-generating capacity of the diaphragm between young and old cohorts. Our preliminary results suggest an impairment in the neuromuscular control of the respiratory system during peak performance which apparently precedes the age-related decline in diaphragm muscle force generating capacity. Our further histological and molecular analyses will provide additional insight into the nature of this respiratory phenotype in advanced age. This work was funded by the Department of Physiology, UCC. B.T. Murphy is funded by an Irish Research Council Doctoral Scholarship. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Specificity of early motor unit adaptations with resistive exercise training.

After exposure of the human body to resistive exercise, the force-generation capacity of the trained muscles increases significantly. Despite decades of research, the neural and muscular stimuli that initiate these changes in muscle force are not yet fully understood. The study of these adaptations is further complicated by the fact that the changes may be partly specific to the training task. For example, short-term strength training does not always influence the neural drive to muscles during the early phase (<100ms) of force development in rapid isometric contractions. Here we discuss some of the studies that have investigated neuromuscular adaptations underlying changes in maximal force and rate of force development produced by different strength training interventions, with a focus on changes observed at the level of spinal motor neurons. We discuss the different motor unit adjustments needed to increase force or speed, and the specificity of some of the adaptations elicited by differences in the training tasks.

Neuromuscular consequences of spinal cord injury: New mechanistic insights and clinical considerations.

The spinal cord facilitates communication between the brain and the body, containing intrinsic systems that work with lower motor neurons (LMNs) to manage movement. Spinal cord injuries (SCIs) can lead to partial paralysis and dysfunctions in muscles below the injury. While traditionally this paralysis has been attributed to disruptions in the corticospinal tract, a growing body of work demonstrates LMN damage is a factor. Motor units, comprising the LMN and the muscle fibers with which they connect, are essential for voluntary movement. Our understanding of their changes post-SCI is still emerging, but the health of motor units is vital, especially when considering innovative SCI treatments like nerve transfer surgery. This review seeks to collate current literature on how SCI impact motor units and explore neuromuscular clinical implications and treatment avenues. SCI reduced motor unit number estimates, and surviving motor units had impaired signal transmission at the neuromuscular junction, force-generating capacity, and excitability, which have the potential to recover chronically, yet the underlaying mechanisms are unclear. Furthermore, electrodiagnostic evaluations can aid in assessing the health lower and upper motor neurons, identify suitable targets for nerve transfer surgeries, and detect patients with time sensitive injuries. Lastly, many electrodiagnostic abnormalities occur in both chronic and acute SCI, yet factors contributing to these abnormalities are unknown. Future studies are required to determine how motor units adapt following SCI and the clinical implications of these adaptations.

Reduction and recovery of self-sustained muscle activity after fatiguing plantar flexor contractions.

Persistent inward calcium and sodium currents (PICs) are crucial for initiation and maintenance of motoneuron firing, and thus muscular force. However, there is a lack of data describing the effects of fatiguing exercise on PIC activity in humans. We simultaneously applied tendon vibration and neuromuscular electrical stimulation (VibStim) before and after fatiguing exercise. VibStim induces self-sustained muscle activity that is proposed to result from PIC activation. Twelve men performed 5-s maximal isometric plantar flexor contractions (MVC) with 5-s rests until joint torque was reduced to 70%MVC. VibStim trials consisted of five 2-s trains of neuromuscular electrical stimulation (20 Hz, evoking 10% MVC) of triceps surae with simultaneous Achilles tendon vibration (115 Hz) without voluntary muscle activation. VibStim was applied before (PRE), immediately (POST), 5-min (POST-5), and 10-min (POST-10) after exercise completion. Sustained torque (Tsust) and soleus electromyogram amplitudes (EMG) measured 3 s after VibStim were reduced (Tsust: -59.0%, p<0.001; soleus EMG: -38.4%, p<0.001) but largely recovered by POST-5, and changes in MVC and Tsust were correlated across the four time points (r=0.69; p<0.001). After normalisation to values obtained at the end of the vibration phase to control for changes in fibre-specific force and EMG signal characteristics, decreases in Tsust (-42.9%) and soleus EMG (-22.6%) remained significant and were each correlated with loss and recovery of MVC (r=0.41 and 0.46, respectively). The parallel changes observed in evoked self-sustained muscle activity and force generation capacity provide motivation for future examinations on the potential influence of fatigue-induced PIC changes on motoneuron output.

Clubfoot patients show more anterior-posterior displacement during one-leg-standing and less ankle power and plantarflexor moment during one-leg-hopping than typically developing children

BackgroundClubfoot patients show good-to-excellent foot correction after the Ponseti method. Nevertheless, underlying functional problems that limit motor abilities such as one-leg-standing and one-leg-hopping still persist. These restrictions have been proposed to arise due to problems with maintaining balance and the limited force-generating capacity of clubfoot patients. More insight is needed to understand the underlying limiting factors to improve overall motor ability in clubfoot patients. Research questionThe aim of this study was to determine the differences between clubfoot patients and typically developing children (TDC) in force and balance parameters during walking, one-leg-standing and hopping. MethodsThree-dimensional motion analysis was performed in 19 TDC and 16 idiopathic Ponseti-treated clubfoot patients between 5–9 years old. Kinematic and kinetic parameters were calculated during walking and one-leg-hopping. To describe the balance parameters, center of pressure (CoP) data was assessed during walking, one-leg-hopping and one-leg-standing. Mean group values were calculated and compared using nonparametric statistical tests. A general linear model with repeated measures was used to determine which activity showed the largest group differences. ResultsClubfoot patients showed lower peak plantarflexor moment and peak ankle power absorption and generation during one-leg-hopping compared to TDC. Furthermore, clubfoot patients showed a lower hop length and velocity than TDC. The difference in peak plantarflexor moment and ankle power between the study groups was larger during one-leg-hopping than during walking. Finally, clubfoot patients showed a higher anterior-posterior CoP range during one-leg-standing. SignificanceDeviations in force parameters seemed to limit one-leg-hopping in clubfoot patients, and impaired anterior-posterior static balance was thought to be the underlying cause of problems with one-leg-standing. Furthermore, one-leg-hopping was more sensitive to distinguish between clubfoot patients and TDC than walking. Individualized physiotherapy targeting static balance and force parameters, with extra emphasis on including eccentric contractions, might improve the overall motor abilities of clubfoot patients.

Assessment of inter-individual variability in hamstring muscle recovery after a sport-specific sprint training in women and men.

Background: Hamstring muscles are most affected by multiple sprint-based sports as a result of muscle strain during sprinting, leading to reduced performance and increased risk of injury. Therefore, the purpose of the study was to assess inter-individual variability in hamstrings recovery after a sport-specific repeated-sprint training (RST), through sprint-specific markers of muscle recovery and associated muscle damage biomarkers in women and men. Methods: Healthy females (n = 14) and males (n = 15) underwent 10 repeated 40-m sprints with a 3-min rest pause between each repetition. Force-generating capacity (FGC) by the 90° hip :20° knee test and range of motion Jurdan test, together with serum biomarkers [sarcomeric mitochondrial creatine kinase (sMtCK), oxidative stress, irisin] were tested at baseline and 24-, 48- and 72-h post-exercise through a repeated measures design. Participants were classified according to FGC loss into high responders (HR) and low responders (LR). Results: 21 individuals (10 females, 11 males) were classified as HR (FGC loss >20% and recovery >48h), while 8 individuals (4 females, 4 males) were classified as LR. HR individuals showed unrecovered maximal voluntary isometric contraction (MVIC) torque until 72h post-training (p = 0.003, np 2 = 0.170), whereas only HR males showed decreased range of motion (p = 0.026, np 2 = 0.116). HR individuals also showed increased sMtCK (p = 0.016, np 2 = 0.128), oxidative stress (p = 0.038, np 2 = 0.106) and irisin (p = 0.019, np 2 = 0.123). Conclusion: There is inter-individual variability in the muscular response to a sport-specific RST, identifiable by MVIC torque assessment. The findings support that the 90° hip :20° knee test is a powerful indirect test to screen hamstrings recovery in both women and men, in a cost-effective way. However, the Jurdan test might not be able to monitor hamstrings recovery in sportswomen after RST. Decreases in muscle capacity are linked to damage to muscle sarcolemma and mitochondria until 72h post-exercise. Overall, 72h will not be adequate time to restore hamstrings structure and function after a sport-specific RST in both female and male responders.