Force-generating Capacity Research Articles

Postnatal Phrenic Motor Neuron and Diaphragm Maturation in the Mouse

In rats, there is a strong association between the expansion of phrenic motor neuron (PhMN) size (from ~21‐28 days postnatal), the emergence of mature diaphragm muscle (DIAm) myosin heavy chain (MyHC2X and MyHC2B) isoform expression, alongside the manifestation of mature morphological and functional properties. Despite mice models being de rigueur for developmental investigations, the postnatal development of mouse PhMN and DIAm properties have not been comprehensively characterized. Using wildtype C57 mice at ages P7, P14, P21, P28, and >3 months (maturity) we evaluated PhMN and DIAm physiologic properties. PhMNs were labelled via rhodamine phrenic nerve dip, processed for longitudinal cryosectioning (70 µm) and prepared for confocal imaging and PhMN assessment. Ex vivo DIAm strips were used for functional assessments of maximum specific force (Po) and fatigue. DIAm strips were also fresh‐frozen, with 8 µm cross‐sections immuno‐labelled for MyHCslow, MyHC2A, MyHC2X and MyHC2X and processed for fluorescent assessment. The number of PhMNs remained stable throughout postnatal life (~195), while PhMN surface area increased steadily, ~10% from P14 to P21, P21 to P28, and P28 to maturity, with overall ~30% increase from P14 to maturity. The biggest changes in number of primary dendrites occurred between P14 and P28 and between P28 and maturity, 25% decrease in primary dendrites between each group. DIAm maximum Po increased in two phases, 3.5‐fold from P7 to P14 and remained similar until P21. The second large increase was ~3‐fold from P21 to P28 and remained steady to maturity. The fatiguability of the DIAm increased with age in two phases, with fatigability being similar from P7 and P14 and increasing by ~20% at P21. Following, fatigability of the DIAm was similar from P21 to P28 and increased by ~35% at maturity. These major PhMN and DIAm changes coincide with the steady growth of PhMN and the emergence of MyHC2X and MyHC2B expression in DIAm from P14 to P21 onwards. The maturation of orderly PhMN recruitment likely depends on an interplay between PhMN size properties and network inputs to a refined dendritic tree. We show that DIAm muscle fiber maturation in mice hinges on the expression of MyHC2X and MyHC2B isoforms that is associated with an ~10 fold increase in DIAm force‐generation capacity.

Autophagy Impairment and Sarcopenia in Type‐Identified Muscle Fibers of Aging Extensor Digitorum Longus Muscle

Sarcopenia is the aging‐related loss of force‐generating capacity and atrophy of skeletal muscles and is a major contributor to morbidity and mortality in the elderly. The molecular mechanisms underlying sarcopenia remain to be elucidated. Skeletal muscles exhibit different rates of sarcopenia, generally reflecting their specific muscle fiber type composition. Muscles primarily composed of type IIx and/or IIb muscle fibers (i.e., extensor digitorum longus; EDLm) develop sarcopenia at a faster rate than other muscles. In the diaphragm, muscle fiber cross‐sectional area (CSA) is reduced in old age, predominantly in type IIx and/or IIb fibers. Autophagy is a multistep, catabolic process that targets dysfunctional cytoplasmatic structures including proteins and organelles for degradation and recycling. Autophagy is impaired in old age across several tissues, including motor neurons and skeletal muscle. Expression of core autophagy proteins can indicate changes in autophagy, e.g., LC3 reflects initiation/elongation steps and p62 clearance reflects degradation. We hypothesize that impaired autophagy is associated with the development of sarcopenia in type‐identified muscle fibers of the EDLm. Indeed, at 24‐months of age, the CSA of type I and IIa fibers was not reduced, whereas the CSA of type IIx and/or IIb fibers was ~25% smaller (p<0.01 in both cases), compared to 6‐month‐old mice. These findings are consistent with fiber type selective sarcopenia in the EDLm. Expression of LC3 and p62 in the EDLm of mice at 6‐ and 24‐ months of age was evaluated via immunofluorescence by quantification of the number of LC3 and p62 puncta per muscle fiber type. In type I and IIa fibers, the number of LC3 puncta increased by ~30% and of p62 increased three‐fold in 24‐ compared to 6‐month‐old mice (p<0.01 in both cases). In type IIx and/or IIb fibers, the number of LC3 puncta decreased by ~60% and p62 puncta increased by ~50% in 24‐ compared to 6‐month‐old mice (p<0.01 in both cases). Accordingly, compared to 6 month‐old mice, autophagic degradation is impaired across muscle fiber types in 24‐month old mice, but likely to a greater extent in type I and IIa fibers of old mice given the increase in both LC3 and p62. Autophagic initiation is primarily reduced in type IIx and/or IIb fibers in the EDL as indicated by the reduced LC3 expression. Taken together these findings indicate that fiber type selective sarcopenia may reflect differences in autophagy across muscle fiber types.

This Month in Anesthesiology

This Month in Anesthesiology

Early Restrictive Fluid Strategy Impairs the Diaphragm Force in Lambs with Acute Respiratory Distress Syndrome.

The effect of fluid management strategies in critical illness-associated diaphragm weakness are unknown. This study hypothesized that a liberal fluid strategy induces diaphragm muscle fiber edema, leading to reduction in diaphragmatic force generation in the early phase of experimental pediatric acute respiratory distress syndrome in lambs. Nineteen mechanically ventilated female lambs (2 to 6 weeks old) with experimental pediatric acute respiratory distress syndrome were randomized to either a strict restrictive fluid strategy with norepinephrine or a liberal fluid strategy. The fluid strategies were maintained throughout a 6-h period of mechanical ventilation. Transdiaphragmatic pressure was measured under different levels of positive end-expiratory pressure (between 5 and 20 cm H2O). Furthermore, diaphragmatic microcirculation, histology, inflammation, and oxidative stress were studied. Transdiaphragmatic pressures decreased more in the restrictive group (-9.6 cm H2O [95% CI, -14.4 to -4.8]) compared to the liberal group (-0.8 cm H2O [95% CI, -5.8 to 4.3]) during the application of 5 cm H2O positive end-expiratory pressure (P = 0.016) and during the application of 10 cm H2O positive end-expiratory pressure (-10.3 cm H2O [95% CI, -15.2 to -5.4] vs. -2.8 cm H2O [95% CI, -8.0 to 2.3]; P = 0.041). In addition, diaphragmatic microvessel density was decreased in the restrictive group compared to the liberal group (34.0 crossings [25th to 75th percentile, 22.0 to 42.0] vs. 46.0 [25th to 75th percentile, 43.5 to 54.0]; P = 0.015). The application of positive end-expiratory pressure itself decreased the diaphragmatic force generation in a dose-related way; increasing positive end-expiratory pressure from 5 to 20 cm H2O reduced transdiaphragmatic pressures with 27.3% (17.3 cm H2O [95% CI, 14.0 to 20.5] at positive end-expiratory pressure 5 cm H2O vs. 12.6 cm H2O [95% CI, 9.2 to 15.9] at positive end-expiratory pressure 20 cm H2O; P < 0.0001). The diaphragmatic histology, markers for inflammation, and oxidative stress were similar between the groups. Early fluid restriction decreases the force-generating capacity of the diaphragm and diaphragmatic microcirculation in the acute phase of pediatric acute respiratory distress syndrome. In addition, the application of positive end-expiratory pressure decreases the force-generating capacity of the diaphragm in a dose-related way. These observations provide new insights into the mechanisms of critical illness-associated diaphragm weakness.

Influenza A Virus-Driven Airway Inflammation may be Dissociated From Limb Muscle Atrophy in Cigarette Smoke-Exposed Mice.

Limb muscle dysfunction is a hallmark of Chronic Obstructive Pulmonary Disease (COPD) which is further worsened following a viral-induced acute exacerbation of COPD (AECOPD). An amplified airway inflammation underlies the aggravated respiratory symptoms seen during AECOPD, however, its contributory role to limb muscle dysfunction is unclear. The present study examined the impact of influenza A virus (IAV)-induced exacerbation on hind limb muscle parameters. Airway inflammation was established in male BALB/c mice by exposure to cigarette smoke (CS) for 8 weeks. Exacerbation was then induced via inoculation with IAV, and various lung and muscle parameters were assessed on day 3 (peak of airway inflammation) and day 10 (resolution phase) post-infection. IAV infection exacerbated CS-induced airway inflammation as evidenced by further increases in immune cell counts within bronchoalveolar lavage fluid. Despite no significant impact on muscle mass, IAV exacerbation worsened the force-generating capacity of the tibialis anterior (TA) muscle. Protein oxidation and myogenic disruption was observed in the TA following CS exposure, however, IAV exacerbation did not augment these detrimental processes. To further explore the contributory role of airway inflammation on myogenic signaling, cultured myotubes were exposed to conditioned medium (CM) derived from bronchial epithelial cells stimulated with polyinosinic:polycytidylic acid and cigarette smoke extract (CSE). Despite an amplified inflammatory response in the lung epithelial cells, the CM derived from these cells did not potentiate myogenic disruption in the C2C12 myotubes. In conclusion, our data suggest that certain parameters of limb muscle dysfunction seen during viral-induced AECOPD may be independent of airway inflammation.

Deaccelerated Myogenesis and Autophagy in Genetically Induced Pulmonary Emphysema.

Patients with chronic obstructive pulmonary disease (COPD)-pulmonary emphysema often develop locomotor muscle dysfunction, which entails reduced muscle mass and force-generation capacity and is associated with worse outcomes, including higher mortality. Myogenesis contributes to adult muscle integrity during injury-repair cycles. Injurious events crucially occur in the skeletal muscles of patients with COPD in the setting of exacerbations and infections, which lead to acute decompensations for limited periods of time, after which patients typically fail to recover the baseline status they had before the acute event. Autophagy, which is dysregulated in muscles from patients with COPD, is a key regulator of muscle stem-satellite- cells activation and myogenesis, yet very little research has so far mechanistically investigated the role of autophagy dysregulation in COPD muscles. Using a genetically inducible interleukin-13-driven pulmonary emphysema model leading to muscle dysfunction, and confirmed with a second genetic animal model, we found a significant myogenic dysfunction associated with the reduced proliferative capacity of satellite cells. Transplantation experiments followed by lineage tracing suggest that an intrinsic defect in satellite cells, and not in the COPD environment, plays a dominant role in the observed myogenic dysfunction. RNA sequencing analysis and direct observation of COPD mice satellite cells suggest dysregulated autophagy. Moreover, while autophagy flux experiments with bafilomycin demonstrated deacceleration of autophagosome turnover in COPD mice satellite cells, spermidine-induced autophagy stimulation leads to a higher replication rate and myogenesis in these animals. Our data suggest that pulmonary emphysema causes disrupted myogenesis, which could be improved with stimulation of autophagy and satellite cells activation, leading to an attenuated muscle dysfunction.

Single skeletal muscle fiber mechanical properties: a muscle quality biomarker of human aging.

Skeletal muscle strength, mass, and function should be carefully monitored for signs of decline with advanced adult age. An understanding of the pathophysiology and severity of sarcopenia can be improved with the exploration of changes in muscle fiber properties. Furthermore, although functional decline with increase age is a well-known phenomenon, the mechanisms underlying this decline, and the features that characterize it, are complex and variable. The age-related decline of muscle function is a result of not only a decrease of muscle mass but also a decline in the intrinsic properties of muscle fibers that are independent of size. We believe it is important to understand changes in muscle quality (force adjusted for size), and not to focus solely on muscle mass, because muscle quality is closely related to measurements of function and could potentially predict clinical outcomes such as morbidity, disability, and mortality. Neurological and metabolic mechanisms contribute to muscle quality, but the intrinsic properties of muscle cells are central to the maintenance of force-generating capacity. Muscle quality can be evaluated with the assessment of morphological, physiological, and mechanical properties in single permeabilized or skinned fibers. This approach excludes the influence of the nervous system, tendons, and the extracellular matrix. In this review, we summarized the changes in active and passive mechanical properties at the single muscle cell level in older skeletal muscles. We argue that intrinsic mechanical changes in human single muscle fibers are useful biomarkers and indicators of muscle quality.

Inclusion of image-based in vivo experimental data into the Hill-type muscle model affects the estimation of individual force-sharing strategies during walking

The study of muscle coordination requires knowledge of the force produced by individual muscles, which can be estimated using Hill-type models. Predicted forces from Hill-type models are sensitive to the muscle’s maximal force-generating capacity (Fmax), however, to our knowledge, no study has investigated the effect of different Fmax personalization methods on predicted muscle forces. The aim of this study was to determine the influence of two personalization methods on predicted force-sharing strategies between the human gastrocnemii during walking. Twelve participants performed a walking protocol where we estimated muscle activation using surface electromyography and fascicle length, velocity, and pennation angle using B-mode ultrasound to inform the Hill-type model. Fmax was determined using either a scaling method or experimental method. The scaling method used anthropometric scaling to determine both muscle volume and fiber length, which were used to estimate the Fmax of the gastrocnemius medialis and lateralis. The experimental method used muscle volume and fascicle length obtained from magnetic resonance imaging and diffusion tensor imaging, respectively. We found that the scaling and the experimental method predicted similar gastrocnemii force-sharing strategies at the group level (mean over the participants). However, substantial differences between methods in predicted force-sharing strategies was apparent for some participants revealing the limited ability of the scaling method to predict force-sharing strategies at the level of individual participants. Further personalization of muscle models using in vivo experimental data from imaging techniques is therefore likely important when using force predictions to inform the diagnosis and management of neurological and orthopedic conditions.

Amyotrophic lateral sclerosis and delayed onset muscle soreness in light of the impaired blink and stretch reflexes - watch out for Piezo2.

Amyotrophic lateral sclerosis (ALS) is a fatal, multisystem neurodegenerative disease that causes the death of motoneurons (MNs) progressively and eventually leads to paralysis. In contrast, delayed onset muscle soreness (DOMS) is defined as delayed onset soreness, muscle stiffness, loss of force-generating capacity, reduced joint range of motion, and decreased proprioceptive function. Sensory deficits and impaired proprioception are common symptoms of both ALS and DOMS, as impairment at the proprioceptive sensory terminals in the muscle spindle is theorized to occur in both. The important clinical distinction is that extraocular muscles (EOM) are relatively spared in ALS, in contrast to limb skeletal muscles; however, the blink reflex goes through a gradual impairment in a later stage of disease progression. Noteworthy is, that, the stretch of EOM induces the blink reflex. The current authors suggest that the impairment of proprioceptive sensory nerve terminals in the EOM muscle spindles are partially responsible for lower blink reflex, beyond central origin, and implies the critical role of Piezo2 ion channels and Wnt-PIP2 signaling in this pathomechanism. The proposed microinjury of Piezo2 on muscle spindle proprioceptive terminals could provide an explanation for the painless dying-back noncontact injury mechanism theory of ALS.

The Reliability and Magnitude of Time-Dependent Force-Time Characteristics During the Isometric Midthigh Pull Are Affected by Both Testing Protocol and Analysis Choices.

Guppy, SN, Kotani, Y, Brady, CJ, Connolly, S, Comfort, P, and Haff, GG. Title: The reliability and magnitude of time-dependent force-time characteristics during the isometric mid-thigh pull are impacted by both testing protocol and analysis choices. J Strength Cond Res 36(5): 1191-1199, 2022-This study aimed to investigate whether the use of short-duration (SHORT) isometric midthigh pull (IMTP) trials resulted in greater reliability and magnitude of time-dependent force-time characteristics than traditionally performed IMTP trials (TRAD). Fourteen subjects with >6 months' training experience with the power clean volunteered to take part in the study. Subjects performed five ∼1-second IMTP trials (SHORT) and five 5-second IMTP trials (TRAD). SHORT resulted in substantially more reliable rate of force development (RFD) measures (intraclass correlation coefficient [ICC] = 0.97-0.99; coefficient of variation [CV] = 2.6-7.0%), particularly during time bands from force-onset to 150 ms, compared with TRAD when trials were selected for analysis based on peak force (ICC = 0.66-0.83; CV = 14.1-38.5%). Selecting TRAD trials based on RFD0-200 resulted in similar reliability compared with SHORT of those same epochs (ICC = 0.97-0.99; CV = 2.5-7.8%). Furthermore, SHORT resulted in significantly greater force at specific time points, RFD, and impulse compared with TRAD trials (p = 0.001-0.033; g = -0.16 to -0.66). Based on these results, strength and conditioning professionals should use specific testing protocols (i.e., TRAD and SHORT) depending on the component of an athlete's force-generating capacity that they wish to assess and remain aware of the effect analysis choices they have on the reliability of IMTP force-time characteristics.

The effect of small changes in rate of force development on muscle fascicle velocity and motor unit discharge behaviour

When rate of force development is increased, neural drive increases. There is presently no accepted explanation for this effect. We propose and experimentally test the theory that a small increase in rate of force development increases medial gastrocnemius fascicle shortening velocity, reducing the muscle’s force-generating capacity, leading to active motor units being recruited at lower forces and with increased discharge frequencies. Participants produced plantar flexion torques at three different rates of force development (slow: 2% MVC/s, medium: 10% MVC/s, fast: 20% MVC/s). Ultrasound imaging showed that increased rate of force development was related to higher fascicle shortening velocity (0.4 ± 0.2 mm/s, 2.0 ± 0.9 mm/s, 4.1 ± 1.9 mm/s in slow, medium, fast, respectively). In separate experiments, medial gastrocnemius motor unit recruitment thresholds and discharge frequencies were measured using fine-wire electromyography (EMG), together with surface EMG. Recruitment thresholds were lower in the fast (12.8 ± 9.2% MVC) and medium (14.5 ± 9.9% MVC) conditions compared to the slow (18.2 ± 8.9% MVC) condition. The initial discharge frequency was lower in the slow (5.8 ± 3.1 Hz) than the fast (6.7 ± 1.4 Hz), but not than the medium (6.4 ± 2.4 Hz) condition. The surface EMG was greater in the fast (mean RMS: 0.029 ± 0.017 mV) compared to the slow condition (0.019 ± 0.013 mV). We propose that the increase in muscle fascicle shortening velocity reduces the force-generating capacity of the muscle, therefore requiring greater neural drive to generate the same forces.

Variability of in vivo Sarcomere Length Measures in the Upper Limb Obtained With Second Harmonic Generation Microendoscopy.

The lengths of a muscle’s sarcomeres are a primary determinant of its ability to contract and produce force. In addition, sarcomere length is a critical parameter that is required to make meaningful comparisons of both the force-generating and excursion capacities of different muscles. Until recently, in vivo sarcomere length data have been limited to invasive or intraoperative measurement techniques. With the advent of second harmonic generation microendoscopy, minimally invasive measures of sarcomere length can be made for the first time. This imaging technique expands our ability to study muscle adaptation due to changes in stimulus, use, or disease. However, due to past inability to measure sarcomeres outside of surgery or biopsy, little is known about the natural, anatomical variability in sarcomere length in living human subjects. To develop robust experimental protocols that ensure data provide accurate representations of a muscle’s sarcomere lengths, we sought to quantify experimental uncertainty associated with in vivo measures of sarcomere lengths. Specifically, we assessed the variability in sarcomere length measured (1) within a single image, along a muscle fiber, (2) across images captured within a single trial, across trials, and across days, as well as (3) across locations in the muscle using second harmonic generation in two upper limb muscles with different muscle architectures, functions, and sizes. Across all of our measures of variability we estimate that the magnitude of the uncertainty for in vivo sarcomere length is on the order of ∼0.25 μm. In the two upper limb muscles studied we found larger variability in sarcomere lengths within a single insertion than across locations. We also developed custom code to make measures of sarcomere length variability across a single fiber and determined that this codes’ accuracy is an order of magnitude smaller than our measurement uncertainty due to sarcomere variability. Together, our findings provide guidance for the development of robust experimental design and analysis of in vivo sarcomere lengths in the upper limb.

Pelvic pain in Maigne\u2019s syndrome\u2014a multi-segmental approach

BackgroundMaigne’s syndrome is a poorly understood condition that affects the thoracolumbar junction. The symptoms can range from pain in the low back, pelvis, hip, lower abdomen, and groin. These symptoms can have bio-mechanical and neurophysiological attributions due to the complexity of spinal mechanics. Thoraco-lumbar junction (T12-L1) is a transitional zone with a higher degree of mean angular motion and a mean translation motion than T10-T11 and T11-T12. This higher degree of translational and rotation mobility predisposes these segments to a higher degree of stress, making them more prone to biomechanical faults such as dysfunctions and positional faults. These altered static and dynamic mechanics can create a cascade of problems along the biomechanical chain. The co-existence of thoracolumbar junction problems with pelvic pain and dysfunctions strengthens the idea of regional interdependence.Case presentationThe patient is a 44-year-old Caucasian male who reported pain in the low back with symptoms radiating to the right hip, iliac region, lower abdomen, and gluteal region. The patient tested positive for Sacroiliac joint dysfunction with both Laslett’s cluster testing and palpatory sacroiliac examination. In addition, the segmental examination showed restriction in thoracolumbar junction with positive skin rolling test and hypomobility in manual segmental testing. Thus, the manual therapy treatment targeted the thoracolumbar junction and sacroiliac joint to address the underlying biomechanical dysfunctions.ConclusionsThe manual therapy targeting both sacroiliac and thoracolumbar spine can improve pelvic and thoracic spine mobility. In addition, therapeutic exercises can focus on enhancing anterior and posterior chain force generation capacity. This combined approach helped improve functional outcomes with a significant decrease in the Modified Oswestry Disability index and significant improvement on Visual analog scale.

Evaluation of Diaphragm Thickness and Stiffness Using Ultrasound and Shear-Wave Elastography.

The purposes of this study are to measure the thickness and stiffness of diaphragm in association with the respiratory cyclus and to assess the reproducibility of these measurements. Forty individuals who are volunteered for participating diaphragm evaluation were included in the study. Two radiologists with 14 and 15 years of experiences in abdominal ultrasound performed all examinations independently. Furthermore, 8 chronic obstructive pulmonary disease (COPD) patients were examined by only the first radiologist. Gray scale and shear-wave elastography imaging of only the right hemidiaphragm of all participants were performed. Thickness and stiffness of diaphragm were measured at the peak inspiration and end expiration phases. Intraclass correlation coefficients test was used to assess the interobserver agreement. The thickness and stiffness of diaphragm significantly increased with inspiration (P < 0.001). The mean ± SD stiffness of diaphragm in peak inspiration and end expiration phases was 51.84 ± 16.83 kPa and 38.49 ± 9.42 kPa, respectively, for the first radiologist and 49.61 ± 13.83 kPa and 37.52 ± 10.71 kPa, respectively, for the second radiologist. Intraclass correlation coefficient values for diaphragm stiffness were 0.667 and 0.736 in peak inspiration and end expiration phases, respectively. In COPD patients, there was no significant difference between stiffness measurements of respiratory phases. In conclusion, the current study revealed that diaphragm thickness and stiffness increase at inspiration, and these measurements are slightly more reproducible at the end of expiration. However, diaphragm stiffness changes between respiratory phases may not be valid for COPD patients, and this may be related to loss of force-generating capacity of diaphragm in COPD patients.

Towards Soft Wearable Strain Sensors for Muscle Activity Monitoring

The force-generating capacity of skeletal muscle is an important metric in the evaluation and diagnosis of musculoskeletal health. Measuring changes in muscle force exertion is essential for tracking the progress of athletes during training, for evaluating patients’ recovery after muscle injury, and also for assisting the diagnosis of conditions such as muscular dystrophy, multiple sclerosis, or Parkinson’s disease. Traditional hardware for strength evaluation requires technical training for operation, generates discrete time points for muscle assessment, and is implemented in controlled settings. The ability to continuously monitor muscle force without restricting the range of motion or adapting the exercise protocol to suit specific hardware would allow for a richer dataset that can help unlock critical features of muscle health and strength evaluation. In this paper, we employ wearable, ultra-sensitive soft strain sensors for tracking changes in muscle deformation during contractions. We demonstrate the sensors’ sensitivity to isometric contractions, as well as the sensors’ capacity to track changes in peak torque over the course of an isokinetic fatiguing protocol for the knee extensors. The wearable soft system was able to efficiently estimate peak joint torque reduction caused by muscle fatigue (mean NRMSE = 0.15±0.03).

Myological variation in the hindlimb of three raptorial birds in relation to foraging behavior

Raptors share a common predatory lifestyle, but are different in food preferences and hunting behavior. The grip force and talons' grasping capabilities are fundamentally crucial for subduing and killing their prey to feed, but the abilities and differences to generate force are less known. In this study, the entire pelvic muscles were dissected with the muscle mass and fibre length measured and physiological cross-sectional area counted in the Common Kestrel (Falco tinnunculus), Eurasian Sparrowhawk (Accipiter nisus), and Long-eared Owl (Asio otus). Statistical tests were performed to explore the possible differences in architectural parameters among species. These species were same in distributing the greatest proportion of muscle mass to the shank region and the digital flexor functional group, allocating more than 60% muscle mass in relation to total single leg muscle mass to the same seven individual muscles including flexor digitorum longus (FDL), flexor hallucis longus (FHL), and tibialis cranialis (TC) which are three major muscles responsible for talon closure. Interspecies differentiations were most present in the shank and tarsus instead of other regions of the leg, which might reflect their difference in hunting mode and foot use. Greater force-generation capacity of FHL and some anatomical features suggest that digits 1 and 2 work together as an efficiently vise-like set, playing more critical role than digits 3–4 in foraging of diurnal raptors but to a different degree. In accordance with zygodactyl foot morphology, each digit of the Long-eared Owl plays a subequal role when hunting, evidenced by anatomical and architectural features. Because of its unique insertion to the base of the pygostyle, the striking numerical difference in the development of M. caudofemoralis was possibly related to raptors’ flight behavior and feeding ecology. Concluded from anatomical and architectural aspects, the similarities and differences of the hindlimb musculature were correlated to common predatory lifestyle and different foraging behaviors in three raptor species. These results illustrated the underlying myological basis for the functional capacities of the leg muscles and may provide additional information useful in further biomechanical investigation and computer simulation.

Quantity versus quality: Age-related differences in muscle volume, intramuscular fat, and mechanical properties in the triceps surae.

With aging comes reductions in the quality and size of skeletal muscle. These changes influence the force-generating capacity of skeletal muscle and contribute to movement deficits that accompany aging. Although declines in strength remain a significant barrier to mobility in older adults, the association between age-related changes in muscle structure and function remain unresolved. In this study, we compared age-related differences in (i) muscle volume and architecture, (ii) the quantity and distribution of intramuscular fat, and (iii) muscle shear modulus (an index of stiffness) in the triceps surae in 21 younger (24.6±4.3years) and 15 older (70.4±2.4years) healthy adults. Additionally, we explored the relationship between muscle volume, architecture, intramuscular fat and ankle plantar flexion strength in young and older adults. Magnetic resonance imaging was used to determine muscle volume and intramuscular fat content. B-mode ultrasound was used to quantify muscle architecture, shear-wave elastography was used to measure shear modulus, and ankle strength was measured during maximal isometric plantar flexion contractions. We found that older adults displayed higher levels of intramuscular fat yet similar muscle volumes in the medial (MG) and lateral gastrocnemius (LG) and soleus, compared to younger adults. These age-related higher levels of intramuscular fat were associated with lower muscle shear modulus in the LG and MG. We also found that muscle physiological cross-sectional area (PCSA) that accounted for age-associated differences in intramuscular fat showed a modest increase in its association with ankle strength compared to PCSA that did not account for fat content. This highlights that skeletal muscle fat infiltration plays a role in age-related strength deficits, but does not fully explain the age-related loss in muscle strength, suggesting that other factors play a more significant role.

Whole-limb scaling of muscle mass and force-generating capacity in amniotes.

Skeletal muscle mass, architecture and force-generating capacity are well known to scale with body size in animals, both throughout ontogeny and across species. Investigations of limb muscle scaling in terrestrial amniotes typically focus on individual muscles within select clades, but here this question was examined at the level of the whole limb across amniotes generally. In particular, the present study explored how muscle mass, force-generating capacity (measured by physiological cross-sectional area) and internal architecture (fascicle length) scales in the fore- and hindlimbs of extant mammals, non-avian saurians (‘reptiles’) and bipeds (birds and humans). Sixty species spanning almost five orders of magnitude in body mass were investigated, comprising previously published architectural data and new data obtained via dissections of the opossum Didelphis virginiana and the tegu lizard Salvator merianae. Phylogenetic generalized least squares was used to determine allometric scaling slopes (exponents) and intercepts, to assess whether patterns previously reported for individual muscles or functional groups were retained at the level of the whole limb, and to test whether mammals, reptiles and bipeds followed different allometric trajectories. In general, patterns of scaling observed in individual muscles were also observed in the whole limb. Reptiles generally have proportionately lower muscle mass and force-generating capacity compared to mammals, especially at larger body size, and bipeds exhibit strong to extreme positive allometry in the distal hindlimb. Remarkably, when muscle mass was accounted for in analyses of muscle force-generating capacity, reptiles, mammals and bipeds almost ubiquitously followed a single common scaling pattern, implying that differences in whole-limb force-generating capacity are principally driven by differences in muscle mass, not internal architecture. In addition to providing a novel perspective on skeletal muscle allometry in animals, the new dataset assembled was used to generate pan-amniote statistical relationships that can be used to predict muscle mass or force-generating capacity in extinct amniotes, helping to inform future reconstructions of musculoskeletal function in the fossil record.

Intrinsic contractile dysfunction in a surgical model of muscle hypertrophy

Synergistic ablation (SA) is widely used to induce muscle hypertrophy in rodent studies. However, it has been demonstrated that SA-induced compensatory hypertrophy induces increases in maximum isometric force that are smaller in magnitude than the increase in muscle cross-sectional area, suggesting a reduction in the specific force production due to intrinsic contractile dysfunction in the hypertrophied fibers. Here, by using the mechanical skinned fibers, we investigated the mechanisms behind the reduction in specific force in the compensatory hypertrophied muscles. Rats had unilateral surgical ablation of the gastrocnemius and soleus muscles to induce the compensatory hypertrophy in the plantaris muscles. Two wk after surgery, the mean fiber diameter was increased by 19% in the SA group compared with the contralateral control (CNT) group. In contrast, compared with the CNT group, both the depolarization-induced force (-51%) and the Ca2+-activated maximum specific force (-32%) were markedly reduced in skinned fibers from the SA group. These deleterious functional alterations were accompanied by decreases in the amount of DHPRα1, RYR, junctophilin 1, and SH3 and cysteine-rich domain 3 (STAC3) in SA muscles. Thus, these data clearly show that SA induces not only an increase in skeletal muscle fiber hypertrophy but also leads to a reduction in the intrinsic contractile dysfunction due to the excitation-contraction uncoupling and impaired force-generating capacity.

The force-generation capacity of the tibialis anterior muscle at different muscle\u2013tendon lengths depends on its motor unit contractile properties

PurposeMuscle–tendon length can influence central and peripheral motor unit (MU) characteristics, but their interplay is unknown. This study aims to explain the effect of muscle length on MU firing and contractile properties by applying deconvolution of high-density surface EMG (HDEMG), and torque signals on the same MUs followed at different lengths during voluntary contractions.MethodsFourteen participants performed isometric ankle dorsiflexion at 10% and 20% of the maximal voluntary torque (MVC) at short, optimal, and long muscle lengths (90°, 110°, and 130° ankle angles, respectively). HDEMG signals were recorded from the tibialis anterior, and MUs were tracked by cross-correlation of MU action potentials across ankle angles and torques. Torque twitch profiles were estimated using model-based deconvolution of the torque signal based on composite MU spike trains.ResultsMean discharge rate of matched motor units was similar across all muscle lengths (P = 0.975). Interestingly, the increase in mean discharge rate of MUs matched from 10 to 20% MVC force levels at the same ankle angle was smaller at 110° compared with the other two ankle positions (P = 0.003), and the phenomenon was explained by a greater increase in twitch torque at 110° compared to the shortened and lengthened positions (P = 0.002). This result was confirmed by the deconvolution of electrically evoked contractions at different stimulation frequencies and muscle–tendon lengths.ConclusionHigher variations in MU twitch torque at optimal muscle lengths likely explain the greater force-generation capacity of muscles in this position.