Addition Of Sarcomeres Research Articles

Multiscale hamstring muscle adaptations following 9 weeks of eccentric training.

Eccentric training, such as Nordic hamstring exercise (NHE) training, is commonly used as a preventive measure for hamstring strains. Eccentric training is believed to induce lengthening of muscle fascicles and to be associated with the addition of sarcomeres in series within muscle fibers. However, the difficulty in measuring sarcomere adaptation in human muscles has severely limited information about the precise mechanisms of adaptation. This study addressed this limitation by measuring the multiscale hamstring muscle adaptations in response to 9 weeks of NHE training and 3 weeks of detraining. Twelve participants completed 9 weeks of supervised NHE training, followed by a 3-week detraining period. We assessed biceps femoris long-head (BFlh) muscle fascicle length, sarcomere length, and serial sarcomere number in the central and distal regions of the muscle. Additionally, we measured muscle volume and eccentric strength at baseline, post-training, and post-detraining. NHE training over 9 weeks induced significant architectural and strength adaptations in the BFlh muscle. Fascicle length increased by 19% in the central muscle region and 33% in the distal muscle region. NHE also induced increases in serial sarcomere number (25% in the central region and 49% in the distal region). BFlh muscle volume increased by 8%, and knee flexion strength increased by 40% with training. Following 3 weeks of detraining, fascicle length decreased by 12% in the central region and 16% in the distal region along with reductions in serial sarcomere number. Nine weeks of NHE training produced substantial, region-specific increases in BFlh muscle fascicle length, muscle volume, and force generation. The direct measurement of sarcomere lengths revealed that the increased fascicle length was accompanied by the addition of sarcomeres in series within the muscle fascicles.

Muscle cofilin alters neuromuscular junction postsynaptic development to strengthen functional neurotransmission.

Cofilin, an actin-severing protein, plays key roles in muscle sarcomere addition and maintenance. Our previous work found that Drosophila cofilin (DmCFL) knockdown in muscle causes progressive deterioration of muscle structure and function and produces features seen in nemaline myopathy caused by cofilin mutations. We hypothesized that disruption of actin cytoskeleton dynamics by DmCFL knockdown would impact other aspects of muscle development, and, thus, conducted an RNA-sequencing analysis that unexpectedly revealed upregulated expression of numerous neuromuscular junction (NMJ) genes. We found that DmCFL is enriched in the muscle postsynaptic compartment and that DmCFL muscle knockdown causes F-actin disorganization in this subcellular domain prior to the sarcomere defects observed later in development. Despite NMJ gene expression changes, we found no significant changes in gross presynaptic Bruchpilot active zones or total postsynaptic glutamate receptor levels. However, DmCFL knockdown resulted in mislocalization of GluRIIA class glutamate receptors in more deteriorated muscles and strongly impaired NMJ transmission strength. These findings expand our understanding of the roles of cofilin in muscle to include NMJ structural development and suggest that NMJ defects may contribute to the pathophysiology of nemaline myopathy.

Age-related blunting of serial sarcomerogenesis and mechanical adaptations following 4 wk of maximal eccentric resistance training.

During aging, muscles undergo atrophy, which is partly accounted for by a loss of sarcomeres in series. Serial sarcomere number (SSN) is associated with aspects of muscle mechanical function including the force-length and force-velocity-power relationships; hence, the age-related loss of SSN contributes to declining performance. Training emphasizing eccentric contractions increases SSN in young healthy rodents; however, the ability for eccentric training to increase SSN in old age is unknown. Ten young (8 mo) and 11 old (32 mo) male Fisher344/BN rats completed 4 wk of unilateral eccentric plantar flexion training. Pre- and posttraining, the plantar flexors were assessed for the torque-frequency, passive torque-angle, and torque-velocity-power relationships. The soleus, lateral gastrocnemius (LG), and medial gastrocnemius (MG) were harvested for SSN assessment via laser diffraction, with the untrained leg used as a control. In the untrained leg/pretraining, old rats had lower SSN in the soleus, LG, and MG, lower maximum torque, power, and shortening velocity, and greater passive torque than young. Young showed increased soleus and MG SSN following training. In contrast, old had no change in soleus SSN and experienced SSN loss in the LG. Pre- to posttraining, young experienced an increase in maximum isometric torque, whereas old had reductions in maximum torque, shortening velocity, and power, and increased passive torque. Our results show that although young muscle has the ability to add sarcomeres in response to maximal eccentric training, this stimulus could be not only ineffective, but also detrimental to aged muscle leading to dysfunctional remodeling.NEW & NOTEWORTHY The loss of sarcomeres in series with age contributes to declining muscle performance. The present study investigated whether eccentric training could improve performance via serial sarcomere addition in old muscle, like in young muscle. Four weeks of maximal eccentric training induced serial sarcomere addition in the young rat plantar flexors and improved in vivo performance, however, led to dysfunctional remodeling accompanied by further impaired performance in old rats.

The importance of serial sarcomere addition for muscle function and the impact of aging.

During natural aging, skeletal muscle experiences impairments in mechanical performance due, in part, to changes in muscle architecture and size, notably with a loss of muscle cross-sectional area. Another important factor that has received less attention is the shortening of fascicle length, potentially reflective of a decrease in serial sarcomere number (SSN). Interventions that promote the growth of new serial sarcomeres, such as chronic stretching and eccentric-biased resistance training, have been suggested as potential ways to mitigate age-related impairments in muscle function. While current research suggests it is possible to stimulate serial sarcomerogenesis in muscle in old age, the magnitude of sarcomerogenesis may be less than in young muscle. This blunted effect may be partly due to age-related impairments in the pathways regulating mechanotransduction, muscle gene expression, and protein synthesis, as some have been implicated in SSN adaptation. The purpose of this review was to investigate the impact of aging on the ability for serial sarcomerogenesis, and elucidate the molecular pathways that may limit serial sarcomerogenesis in old age. Age-related changes in mTOR, IGF-1, myostatin, and serum response factor signalling, MuRFs, and satellite cells may hinder serial sarcomerogenesis. In addition, our current understanding of SSN in older humans is limited by assumptions based on ultrasound-derived fascicle length. Future research should explore the effects of age-related changes in the identified pathways on the ability to stimulate serial sarcomerogenesis, and better estimate SSN adaptations to gain a deeper understanding of the adaptability of muscle in old age.

Biceps femoris long head sarcomere and fascicle length adaptations after three weeks of eccentric exercise training

Background: Eccentric exercise is widely used to increase muscle fascicle lengths and thus decrease the risk of muscle strain injuries. It is commonly assumed that increased sarcomere number drives this training adaptation and reduces risk of muscle strain, however this has yet to be experimentally tested. This study used a new microendoscopy technique to determine whether addition of sarcomeres can account for increases in fascicle length of the Biceps femoris long head (BFlh) after 3 weeks of eccentric exercise.

Stimuli for Adaptations in Muscle Length and the Length Range of Active Force Exertion-A Narrative Review.

Treatment strategies and training regimens, which induce longitudinal muscle growth and increase the muscles’ length range of active force exertion, are important to improve muscle function and to reduce muscle strain injuries in clinical populations and in athletes with limited muscle extensibility. Animal studies have shown several specific loading strategies resulting in longitudinal muscle fiber growth by addition of sarcomeres in series. Currently, such strategies are also applied to humans in order to induce similar adaptations. However, there is no clear scientific evidence that specific strategies result in longitudinal growth of human muscles. Therefore, the question remains what triggers longitudinal muscle growth in humans. The aim of this review was to identify strategies that induce longitudinal human muscle growth. For this purpose, literature was reviewed and summarized with regard to the following topics: (1) Key determinants of typical muscle length and the length range of active force exertion; (2) Information on typical muscle growth and the effects of mechanical loading on growth and adaptation of muscle and tendinous tissues in healthy animals and humans; (3) The current knowledge and research gaps on the regulation of longitudinal muscle growth; and (4) Potential strategies to induce longitudinal muscle growth. The following potential strategies and important aspects that may positively affect longitudinal muscle growth were deduced: (1) Muscle length at which the loading is performed seems to be decisive, i.e., greater elongations after active or passive mechanical loading at long muscle length are expected; (2) Concentric, isometric and eccentric exercises may induce longitudinal muscle growth by stimulating different muscular adaptations (i.e., increases in fiber cross-sectional area and/or fiber length). Mechanical loading intensity also plays an important role. All three training strategies may increase tendon stiffness, but whether and how these changes may influence muscle growth remains to be elucidated. (3) The approach to combine stretching with activation seems promising (e.g., static stretching and electrical stimulation, loaded inter-set stretching) and warrants further research. Finally, our work shows the need for detailed investigation of the mechanisms of growth of pennate muscles, as those may longitudinally grow by both trophy and addition of sarcomeres in series.

Biceps femoris long head sarcomere and fascicle length adaptations after 3 weeks of eccentric exercise training

BackgroundEccentric exercise increases muscle fascicle lengths; however, the mechanisms behind this adaptation are still unknown. This study aimed to determine whether biceps femoris long head (BFlh) fascicle length increases in response to 3 weeks of eccentric exercise training are the result of an in-series addition of sarcomeres within the muscle fibers. MethodsTen recreationally active participants (age = 27 ± 3 years; mass = 70 ± 14 kg; height = 174 ± 9 cm; mean ± SD) completed 3 weeks of Nordic hamstring exercise (NHE) training on a custom exercise device that was instrumented with load cells. We collected in vivo sarcomere and muscle fascicle images of the BFlh in 2 regions (central and distal) by using microendoscopy and 3 dimension ultrasonography. We then estimated sarcomere length, sarcomere number, and fascicle length before and after the training intervention. ResultsEccentric knee flexion strength increased after the training (15%; p < 0.001; ηp2 = 0.75). Further, we found a significant increase in fascicle length (21%; p < 0.001; ηp2 = 0.81) and sarcomere length (17%; p < 0.001; ηp2 = 0.90) in the distal but not in the central portion of the muscle. The estimated number of sarcomeres in series did not change in either region. ConclusionFascicle length adaptations appear to be heterogeneous in the BFlh in response to 3 weeks of NHE training. An increase in sarcomere length, rather than the addition of sarcomeres in series, appears to underlie increases in fascicle length in the distal region of the BFlh. The mechanism driving regional increases in fascicle and sarcomere length remains unknown, but we speculate that it may be driven by regional changes in the passive tension of muscle or connective tissue adaptations.

Stretch-induced satellite cell deformation incontracturedmuscles in children with cerebral palsy

Satellite cells (SCs) are quiescent, adult skeletal muscle stem cells responsible for postnatal muscle growth and repair. Children with cerebral palsy (CP) have muscle contractures with reduced SC abundance, extracellular matrix abnormalities and reduced serial sarcomere number resulting in greatly increased in vivo sarcomere length, perhaps due to impaired sarcomere addition, compared to children with typical development (TD). Stretch is a strong activator of SCs that leads to addition of sarcomeres during bone-muscle growth. Mechanical loading and subsequent deformation of intracellular structures can lead to activation and proliferation, perhaps by cytoskeletal transmissions of extracellular mechanical signals to the nuclei. The primary aim of this study was to determine the effect of ex vivo stretch-induced sarcomere length change on SC deformation in children with CP and TD. Muscle biopsies were obtained from twelve children (7 CP, 5 TD) during surgery. Fiber bundles were labeled with fluorescent antibodies for Pax7 (SC), DRAQ5 (nuclei), and alpha-actinin (sarcomere protein). Fibers were stretched using a custom jig and imaged using confocal microscopy. SC nuclear length, height and aspect ratio underwent increased deformation with increasing sarcomere length (p < 0.05) in both groups. Slopes of association for SC nuclear length, aspect ratio and sarcomere lengths were similar between CP and TD. Our results indicate that SC in children with CP undergo similar deformation as TD across sarcomere lengths.

A thermodynamic transient cross-bridge model for prediction of contractility and remodelling of the ventricle

Cardiac hypertrophy is an adaption of the heart to a change in cardiovascular loading conditions. The current understanding is that progression may be stress or strain driven, but the multi-scale nature of the cellular remodelling processes have yet to be uncovered. In this study, we develop a model of the contractile left ventricle, with the active cell tension described by a thermodynamically motivated cross-bridge cycling model. Simulation of the transient recruitment of myosin results in correct patterns of ventricular pressure predicted over a cardiac cycle. We investigate how changes in tissue loading and associated deviations in transient force generation can drive restructuring of cellular myofibrils in the heart wall. Our thermodynamic framework predicts in-series sarcomere addition (eccentric remodelling) in response to volume overload, and sarcomere addition in parallel (concentric remodelling) in response to valve and signalling disfunction. This framework provides a significant advance in the current understanding of the fundamental sub-sarcomere level biomechanisms underlying cardiac remodelling. Simulations reveal that pathological tissue loading conditions can significantly alter actin-myosin cross-bridge cycling over the course of the cardiac cycle. The resultant variation in sarcomere stress pushes an imbalance between the internal free energy of the myofibril and that of unbound contractile proteins, initiating remodelling. The link between cross-bridge thermodynamics and myofibril remodelling proposed in this study may significantly advance current understanding of cardiac disease onset.

Cofilin Loss in Drosophila Muscles Contributes to Muscle Weakness through Defective Sarcomerogenesis during Muscle Growth

SUMMARYSarcomeres, the fundamental contractile units of muscles, are conserved structures composed of actin thin filaments and myosin thick filaments. How sarcomeres are formed and maintained is not well understood. Here, we show that knockdown of Drosophila cofilin (DmCFL), an actin depolymerizing factor, disrupts both sarcomere structure and muscle function. The loss of DmCFL also results in the formation of sarcomeric protein aggregates and impairs sarcomere addition during growth. The activation of the proteasome delays muscle deterioration in our model. Furthermore, we investigate how a point mutation in CFL2 that causes nemaline myopathy (NM) in humans affects CFL function and leads to the muscle phenotypes observed in vivo. Our data provide significant insights to the role of CFLs during sarcomere formation, as well as mechanistic implications for disease progression in NM patients.

CORR Insights®: Does a Reduced Number of Muscle Stem Cells Impair the Addition of Sarcomeres and Recovery from a Skeletal Muscle Contracture? A Transgenic Mouse Model.

CORR Insights®: Does a Reduced Number of Muscle Stem Cells Impair the Addition of Sarcomeres and Recovery from a Skeletal Muscle Contracture? A Transgenic Mouse Model.

Does a Reduced Number of Muscle Stem Cells Impair the Addition of Sarcomeres and Recovery from a Skeletal Muscle Contracture? A Transgenic Mouse Model.

Children with cerebral palsy have impaired muscle growth and muscular contractures that limit their ROM. Contractures have a decreased number of serial sarcomeres and overstretched lengths, suggesting an association with a reduced ability to add the serial sarcomeres required for normal postnatal growth. Contractures also show a markedly reduced number of satellite cells-the muscle stem cells that are indispensable for postnatal muscle growth, repair, and regeneration. The potential role of the reduced number of muscle stem cells in impaired sarcomere addition leading to contractures must be evaluated. (1) Does a reduced satellite cell number impair the addition of serial sarcomeres during recovery from an immobilization-induced contracture? (2) Is the severity of contracture due to the decreased number of serial sarcomeres or increased collagen content? The hindlimbs of satellite cell-specific Cre-inducible mice (Pax7; Rosa26; n = 10) were maintained in plantarflexion with plaster casts for 2 weeks so that the soleus was chronically shortened and the number of its serial sarcomeres was reduced by approximately 20%. Subsequently, mice were treated with either tamoxifen to reduce the number of satellite cells or a vehicle (an injection and handling control). The transgenic mouse model with satellite cell ablation combined with a casting model to reduce serial sarcomere number recreates two features observed in muscular contractures in children with cerebral palsy. After 30 days, the casts were removed, the mice ankles were in plantarflexion, and the mice's ability to recover its ankle ROM by cage remobilization for 30 days were evaluated. We quantified the number of serial sarcomeres, myofiber area, and collagen content of the soleus muscle as well as maximal ankle dorsiflexion at the end of the recovery period. Mice with reduced satellite cell numbers did not regain normal ankle ROM in dorsiflexion; that is, the muscles remained in plantarflexion contracture (-16° ± 13° versus 31° ± 39° for the control group, -47 [95% confidence interval -89 to -5]; p = 0.03). Serial sarcomere number of the soleus was lower on the casted side than the contralateral side of the mice with a reduced number of satellite cells (2214 ± 333 versus 2543 ± 206, -329 [95% CI -650 to -9]; p = 0.04) but not different in the control group (2644 ± 194 versus 2729 ± 249, -85 [95% CI -406 to 236]; p = 0.97). The degree of contracture was strongly associated with the number of sarcomeres and myofiber area (r =0.80; P < 0.01) rather than collagen content. No differences were seen between groups in terms of collagen content and the fraction of muscle area. We found that a reduced number of muscle stem cells in a transgenic mouse model impaired the muscle's ability to add sarcomeres in series and thus to recover from an immobilization-induced contracture. The results of our study in transgenic mouse muscle suggests there may be a mechanistic relationship between a reduced number of satellite cells and a reduced number of serial sarcomeres. Contracture development, secondary to impaired sarcomere addition in muscles in children with cerebral palsy may be due to a reduced number of muscle stem cells.

Cell shape determines gene expression: cardiomyocyte morphotypic transcriptomes

Cardiomyocytes undergo considerable changes in cell shape. These can be due to hemodynamic constraints, including changes in preload and afterload conditions, or to mutations in genes important for cardiac function. These changes instigate significant changes in cellular architecture and lead to the addition of sarcomeres, at the same time or at a later stage. However, it is currently unknown whether changes in cell shape on their own affect gene expression and the aim of this study was to fill that gap in our knowledge. We developed a single-cell morphotyping strategy, followed by single-cell RNA sequencing, to determine the effects of altered cell shape in gene expression. This enabled us to profile the transcriptomes of individual cardiomyocytes of defined geometrical morphotypes and characterize them as either normal or pathological conditions. We observed that deviations from normal cell shapes were associated with significant downregulation of gene expression and deactivation of specific pathways, like oxidative phosphorylation, protein kinase A, and cardiac beta-adrenergic signaling pathways. In addition, we observed that genes involved in apoptosis of cardiomyocytes and necrosis were upregulated in square-like pathological shapes. Mechano-sensory pathways, including integrin and Src kinase mediated signaling, appear to be involved in the regulation of shape-dependent gene expression. Our study demonstrates that cell shape per se affects the regulation of the transcriptome in cardiac myocytes, an effect with possible implications for cardiovascular disease.

Model of Anisotropic Reverse Cardiac Growth in Mechanical Dyssynchrony

Based on recent single-cell experiments showing that longitudinal myocyte stretch produces both parallel and serial addition of sarcomeres, we developed an anisotropic growth constitutive model with elastic myofiber stretch as the growth stimuli to simulate long-term changes in biventricular geometry associated with alterations in cardiac electromechanics. The constitutive model is developed based on the volumetric growth framework. In the model, local growth evolutions of the myocyte’s longitudinal and transverse directions are driven by the deviations of maximum elastic myofiber stretch over a cardiac cycle from its corresponding local homeostatic set point, but with different sensitivities. Local homeostatic set point is determined from a simulation with normal activation pattern. The growth constitutive model is coupled to an electromechanics model and calibrated based on both global and local ventricular geometrical changes associated with chronic left ventricular free wall pacing found in previous animal experiments. We show that the coupled electromechanics-growth model can quantitatively reproduce the following: (1) Thinning and thickening of the ventricular wall respectively at early and late activated regions and (2) Global left ventricular dilation as measured in experiments. These findings reinforce the role of elastic myofiber stretch as a growth stimulant at both cellular level and tissue-level.

Multiscale characterization of heart failure

Dilated cardiomyopathy is a progressive irreversible disease associated with contractile dysfunction and heart failure. During dilated cardiomyopathy, elevated diastolic wall strains trigger mechanotransduction pathways that initiate the addition of sarcomeres in series and an overall increase in myocyte length. At the whole organ level, this results in a chronic dilation of the ventricles, an increase in end diastolic and end systolic volumes, and a decrease in ejection fraction. However, how exactly changes in sarcomere number translate into changes in myocyte morphology, and how these cellular changes translate into ventricular dilation remains incompletely understood. Here we combined a chronic animal study, continuum growth modeling, and machine learning to quantify correlations between sarcomere dynamics, myocyte morphology, and ventricular dilation. In an eight-week long volume overload study of six pigs, we found that the average sarcomere number increased by +3.8%/week, from 47 to 62, resulting in a myocyte lengthening of +3.3%/week, from 85 to 108 μm, while the sarcomere length and myocyte width remained unchanged. At the same time, the average end diastolic volume increased by +6.0%/week. Using continuum growth modeling and Bayesian inference, we correlated alterations on the subcellular, cellular, and organ scales and found that the serial sarcomere number explained 88% of myocyte lengthening, which, in turn, explained 54% of cardiac dilation. Our results demonstrate that sarcomere number and myocyte length are closely correlated and constitute the major determinants of dilated heart failure. We anticipate our study to be a starting point for more sophisticated multiscale models of heart failure. Our study suggests that altering sarcomere turnover-and with it myocyte morphology and ventricular dimensions-could be a potential therapeutic target to attenuate or reverse the progression of heart failure. Statement of SignificanceHeart failure is a significant global health problem that affects more than 25 million people worldwide and increases in prevalence as the population ages. Heart failure has been studied excessively at various scales; yet, there is no compelling concept to connect knowledge from the subcellular, cellular, and organ level across the scales. Here we combined a chronic animal study, continuum growth modeling, and machine learning to quantify correlations between sarcomere dynamics, myocyte morphology, and ventricular dilation. We found that the serial sarcomere number explained 88% of myocyte lengthening, which, in turn, explained 54% of cardiac dilation. Our results show that sarcomere number and myocyte length are closely correlated and constitute the major determinants of dilated heart failure. This suggests that altering the sarcomere turnover—and with it myocyte morphology and ventricular dimensions–could be a potential therapeutic target to attenuate or reverse heart failure.

Multiscale Characterization of Heart Failure

Dilated cardiomyopathy is a progressive irreversible disease associated with contractile dysfunction and heart failure. During dilated cardiomyopathy, elevated diastolic wall strains trigger mechanotransduction pathways that initiate the addition of sarcomeres in series and an overall increase in myocyte length. At the whole organ level, this results in a chronic dilation of the ventricles, an increase in end diastolic and end systolic volumes, and a decrease in ejection fraction. However, how exactly changes in sarcomere number translate into changes in myocyte morphology, and how these cellular changes translate into ventricular dilation remains incompletely understood. Here we combined a chronic animal study, continuum growth modeling, and machine learning to quantify correlations between sarcomere dynamics, myocyte morphology, and ventricular dilation. In an eight-week long volume overload study of n=6 pigs, we found that the average sarcomere number increased by 3.8%/week, from 47 to 62, resulting in a myocyte lengthening of 3.3%/week, from 85 to 108um, while the sarcomere length and myocyte width remained unchanged. At the same time, the average end diastolic volume increased by 6.0%/week. Using continuum growth modeling and Bayesian inference, we correlated alterations on the subcellular, cellular, and organ scales and found that the serial sarcomere number explained 88% of myocyte lengthening, which, in turn, explained 54% of cardiac dilation. Our results demonstrate that sarcomere number and myocyte length are closely correlated and constitute the major determinants of dilated heart failure. We anticipate our study to be a starting point for more sophisticated multiscale models of heart failure. Our study suggests that altering sarcomere turnover -- and with it myocyte morphology and ventricular dimensions -- could be a potential therapeutic target to attenuate or reverse the progression of heart failure.

Titin-based mechanosensing modulates muscle hypertrophy.

BackgroundTitin is an elastic sarcomeric filament that has been proposed to play a key role in mechanosensing and trophicity of muscle. However, evidence for this proposal is scarce due to the lack of appropriate experimental models to directly test the role of titin in mechanosensing.MethodsWe used unilateral diaphragm denervation (UDD) in mice, an in vivo model in which the denervated hemidiaphragm is passively stretched by the contralateral, innervated hemidiaphragm and hypertrophy rapidly occurs.ResultsIn wildtype mice, the denervated hemidiaphragm mass increased 48 ± 3% after 6 days of UDD, due to the addition of both sarcomeres in series and in parallel. To test whether titin stiffness modulates the hypertrophy response, RBM20ΔRRM and TtnΔIAjxn mouse models were used, with decreased and increased titin stiffness, respectively. RBM20ΔRRM mice (reduced stiffness) showed a 20 ± 6% attenuated hypertrophy response, whereas the TtnΔIAjxn mice (increased stiffness) showed an 18 ± 8% exaggerated response after UDD. Thus, muscle hypertrophy scales with titin stiffness. Protein expression analysis revealed that titin‐binding proteins implicated previously in muscle trophicity were induced during UDD, MARP1 & 2, FHL1, and MuRF1.ConclusionsTitin functions as a mechanosensor that regulates muscle trophicity.

Relationship of medial gastrocnemius relative fascicle excursion and ankle joint power and work performance during gait in typically developing children: A cross-sectional study.

Muscle fascicles lengthen in response to chronic passive stretch through in-series sarcomere addition in order to maintain an optimum sarcomere length. In turn, the muscles’ force generating capacity, maximum excursion, and contraction velocity is enhanced. Thus, longer fascicles suggest a greater capacity to develop joint power and work. However, static fascicle length measurements may not be taking sarcomere length differences into account. Thus, we considered relative fascicle excursions through passive ankle dorsiflexion may better correlate with the capacity to generate joint power and work than fascicle length. Therefore, the aim of the present study was to determine if medial gastrocnemius relative fascicle excursions correlate with ankle joint power and work generation during gait in typically developing children. A sample of typically developing children (n = 10) were recruited for this study and data analysis was carried out on 20 legs. Medial gastrocnemius relative fascicle excursion from resting joint angle to maximum dorsiflexion was estimated from trigonometric relations of medial gastrocnemius pennation angle and thickness obtained from B-mode real-time ultrasonography. Furthermore, a three-dimensional motion capture system was used to obtain ankle joint work and power during the stance phase of gait. Significant correlations were found between relative fascicle excursion and peak power absorption (–) r(14) = −0.61, P = .012 accounting for 31% variability, positive work r(18) = 0.56, P = .021 accounting for 31% variability, and late stance positive work r(15) = 0.51, P = .037 accounting for 26% variability. The large unexplained variance may be attributed to mechanics of neighboring structures (e.g., soleus or Achilles tendon mechanics) and proximal joint kinetics which may also contribute to ankle joint power and work performance, and were not taken into account. Further studies are encouraged to provide greater insight on the relationship between relative fascicle excursions and joint function.

Reduced skeletal muscle satellite cell number alters muscle morphology after chronic stretch but allows limited serial sarcomere addition

Muscles add sarcomeres in response to stretch, presumably to maintain optimal sarcomere length. Clinical evidence from patients with cerebral palsy, who have both decreased serial sarcomere number and reduced satellite cells (SCs), suggests a hypothesis that SCs may be involved in sarcomere addition. A transgenic Pax7-DTA mouse model underwent conditional SC depletion, and their soleii were then stretch-immobilized to assess the capacity for sarcomere addition. Muscle architecture, morphology, and extracellular matrix (ECM) changes were also evaluated. Mice in the SC-reduced group achieved normal serial sarcomere addition in response to stretch. However, muscle fiber cross-sectional area was significantly smaller and was associated with hypertrophic ECM changes, consistent with fibrosis. While a reduced SC population does not hinder serial sarcomere addition, SCs play a role in muscle adaptation to chronic stretch that involves maintenance of both fiber cross-sectional area and ECM structure. Muscle Nerve 55: 384-392, 2017.

Chronic Adaptations to Eccentric Training: A Systematic Review.

Resistance training is an integral component of physical preparation for athletes. A growing body of evidence indicates that eccentric strength training methods induce novel stimuli for neuromuscular adaptations. The purpose of this systematic review was to determine the effects of eccentric training in comparison to concentric-only or traditional (i.e. constrained by concentric strength) resistance training. Searches were performed using the electronic databases MEDLINE via EBSCO, PubMed and SPORTDiscus via EBSCO. Full journal articles investigating the long-term (≥4weeks) effects of eccentric training in healthy (absence of injury or illness during the 4weeks preceding the training intervention), adult (17-35years), human participants were selected for the systematic review. A total of 40 studies conformed to these criteria. Eccentric training elicits greater improvements in muscle strength, although in a largely mode-specific manner. Superior enhancements in power and stretch-shortening cycle (SSC) function have also been reported. Eccentric training is at least as effective as other modalities in increasing muscle cross-sectional area (CSA), while the pattern of hypertrophy appears nuanced and increased CSA may occur longitudinally within muscle (i.e. the addition of sarcomeres in series). There appears to be a preferential increase in the size of type II muscle fibres and the potential to exert a unique effect upon fibre type transitions. Qualitative and quantitative changes in tendon tissue that may be related to the magnitude of strain imposed have also been reported with eccentric training. Eccentric training is a potent stimulus for enhancements in muscle mechanical function, and muscle-tendon unit (MTU) morphological and architectural adaptations. The inclusion of eccentric loads not constrained by concentric strength appears to be superior to traditional resistance training in improving variables associated with strength, power and speed performance.