Quantity and Distribution of Muscle Spindles in Animal and Human Muscles.

Muscle spindles have unique anatomical characteristics that can be directly affected by the surrounding tissues under physiological and pathological conditions. Understanding their spatial distribution and density in different muscles is imperative to unravel the complexity of motor function. In the present study, the distribution and number/density of muscle spindles in human and animal muscles were reviewed. We identified 56 articles focusing on muscle spindle distribution; 13 articles focused on human muscles and 43 focused on animal muscles. The results demonstrate that spindles are located at the nerve entry points and along distributed vessels and they relate to the intramuscular connective tissue. Muscles' deep layers and middle segments are the main topographic distribution areas. Eleven articles on humans and thirty-three articles on animals (totaling forty-four articles) focusing on muscle spindle quantity and density were identified. Hand and head muscles, such as the pronator teres/medial pterygoid muscle/masseter/flexor digitorum, were most commonly studied in the human studies. For animals, whole-body musculature was studied. The present study summarized the spindle quantity in 77 human and 189 animal muscles. We identified well-studied muscles and any as-yet unfound data. The current data fail to clarify the relationship between quantity/density and muscle characteristics. The intricate distribution of the muscle spindles and their density and quantity throughout the body present some unique patterns or correlations, according to the current data. However, it remains unclear whether muscles with fine motor control have more muscle spindles since the study standards are inconsistent and data on numerous muscles are missing. This study provides a comprehensive and exhaustive approach for clinicians and researchers to determine muscle spindle status.

The role of sarcopenic obesity for the prediction of prognosis of patients with gastrointestinal cancer.

BACKGROUND: Sarcopenic obesity (SO) in patients with gastrointestinal cancer is associated with a poor prognosis. We aimed to investigate the prognostic impact of SO in patients with gastrointestinal cancer, as well as the diagnostic cut-off value of SO in patients with gastrointestinal cancer among Chinese population. METHODS: We conducted a consecutive cohort study. Between January 2017 and January 2019, 289 patients diagnosed with gastrointestinal cancer were included in our study. Skeletal muscle area, total fat area, and subcutaneous fat area were measured by CT scan. All patients were followed up for 5 years. Receiver operating characteristic curves (ROC) were adopted to determine the cut-off values of visceral fat obesity for the prediction of sarcopenia. Based on the cut-off values, patients with sarcopenia combined with visceral fat obesity were divided into the SO group, and the others were divided into the non-sarcopenic obesity (NSO) group. Kaplan-Meier curves and univariate and multivariate Cox proportional hazard models were employed to explore the associations of body composition profiles with 5-year overall survival and disease-specific survival. RESULTS: Obtained from Youden's Index for ROC for the prediction of 5-year survival, skeletal muscle mass index (SMI) ≤40.02 cm2/m2 with VFA ≥ 126.30 cm2 in men and SMI ≤32.05 cm2/m2 with VFA ≥72.42 cm2 in women indicate a risk of poor prognosis in patients diagnosed with gastrointestinal cancer. Patients with SO had poorer 5-year overall survival (OS) than patients with NSO (6.74% vs. 82.84%, p < 0.001), and poorer 5-year DFS (6.74% vs. 81.82%, p < 0.001). In multivariate analysis, we found that the long-term mortality risk was approximately 13-fold higher among patients in the SO group compared to those with no conditions. CONCLUSIONS: Preoperative assessment of SO is useful not only for monitoring nutritional status but also for predicting 5-year OS in gastrointestinal cancer patients.

Skeletal Muscle Proteome Modifications following Antibiotic-Induced Microbial Disturbances in Cancer Cachexia.

Cancer cachexia is an involuntary loss of body weight, mostly of skeletal muscle. Previous research favors the existence of a microbiota-muscle crosstalk, so the aim of the study was to evaluate the impact of microbiota alterations induced by antibiotics on skeletal muscle proteins expression. Skeletal muscle proteome changes were investigated in control (CT) or C26 cachectic mice (C26) with or without antibiotic treatment (CT-ATB or C26-ATB, n = 8 per group). Muscle protein extracts were divided into a sarcoplasmic and myofibrillar fraction and then underwent label-free liquid chromatography separation, mass spectrometry analysis, Mascot protein identification, and METASCAPE platform data analysis. In C26 mice, the atrogen mafbx expression was 353% higher than CT mice and 42.3% higher than C26-ATB mice. No effect on the muscle protein synthesis was observed. Proteomic analyses revealed a strong effect of antibiotics on skeletal muscle proteome outside of cachexia, with adaptative processes involved in protein folding, growth, energy metabolism, and muscle contraction. In C26-ATB mice, proteome adaptations observed in CT-ATB mice were blunted. Differentially expressed proteins were involved in other processes like glucose metabolism, oxidative stress response, and proteolysis. This study confirms the existence of a microbiota-muscle axis, with a muscle response after antibiotics that varies depending on whether cachexia is present.

Development of a local controlled release system for therapeutic proteins in the treatment of skeletal muscle injuries and diseases.

The present study aims to develop and characterize a controlled-release delivery system for protein therapeutics in skeletal muscle regeneration following an acute injury. The therapeutic protein, a membrane-GPI anchored protein called Cripto, was immobilized in an injectable hydrogel delivery vehicle for local administration and sustained release. The hydrogel was made of poly(ethylene glycol)-fibrinogen (PEG-Fibrinogen, PF), in the form of injectable microspheres. The PF microspheres exhibited a spherical morphology with an average diameter of approximately 100 micrometers, and the Cripto protein was uniformly entrapped within them. The release rate of Cripto from the PF microspheres was controlled by tuning the crosslinking density of the hydrogel, which was varied by changing the concentration of poly(ethylene glycol) diacrylate (PEG-DA) crosslinker. In vitro experiments confirmed a sustained-release profile of Cripto from the PF microspheres for up to 27 days. The released Cripto was biologically active and promoted the in vitro proliferation of mouse myoblasts. The therapeutic effect of PF-mediated delivery of Cripto in vivo was tested in a cardiotoxin (CTX)-induced muscle injury model in mice. The Cripto caused an increase in the in vivo expression of the myogenic markers Pax7, the differentiation makers eMHC and Desmin, higher numbers of centro-nucleated myofibers and greater areas of regenerated muscle tissue. Collectively, these results establish the PF microspheres as a potential delivery system for the localized, sustained release of therapeutic proteins toward the accelerated repair of damaged muscle tissue following acute injuries.

Bioimpedance analysis for identifying new indicators of exercise-induced muscle damage.

A noninvasive, immediate, and convenient method for assessing muscle tissue status during exercise-induced muscle damage (EIMD) has not been established. This study was designed to assess and determine parameters suitable for measuring EIMD after eccentric exercise, using multi-frequency bioimpedance analysis (BIA). Thirty-five young male participants performed dumbbell exercises with their left arm, and their BIA parameters were measured at various time points up to 168 h post exercise using a multi-frequency BIA device. At all-time points, intra and extracellular water content was greater in the left arm than in the right arm, whereas the impedance, reactance, resistance, and phase angle were lower in the left arm than in the right arm. Established EIMD indices, such as maximal isometric voluntary contraction, were measured and used in correlational analyses. Only reactance was correlated with biomarkers, indicating muscle damage (r = - 0.56 to - 0.49). Furthermore, reactance was found to correlate well with indirect indicators of EIMD, suggesting that it may be a suitable marker for evaluating EIMD. However, the relationship with the limited evaluation indices employed in this study is constrained. Future studies should investigate the correlation between reactance and direct damage indicators, such as structural damage, observed in biopsies.

[Physical Activity and Obesity - Underlying Mechanisms, Practical Actions]. / Körperliche Aktivierung bei Adipositas ­ Zugrunde liegende Mechanismen, praktische Massnahmen.

INTRODUCTION: Individuals with obesity who undergo surgical or pharmacological therapies achieve good results in terms of weight and cardiometabolic risk reduction. It is not uncommon for those affected to equate the extent of weight loss achieved, with long-term treatment success. What is overlooked is that, in addition to obesity, significant weight loss also carries a risk of sarcopenia. Sarcopenic obesity and sarcopenia, in turn, increase the risk of cardiometabolic diseases. Physical activity has the potential to counteract cardiometabolic disease risk caused by obesity and sarcopenia. The underlying mechanism is contained in the endocrine organ skeletal muscle. The production and release of myokines in particular counteracts sarcopenic obesity and its complications. Physical activity is required to initiate myokine production. Endurance and strength training proves to be an effective training combination. In order to achieve a sustainable cardiometabolic risk reduction, the objectives and timing of physical activity should therefore be divided into two phases, a preparatory phase and an actual weight loss phase.

Revisiting the role of trimetazidine for peripheral artery disease: a systematic review with meta-analysis.

OBJECTIVE: To examine the impact of trimetazidine on skeletal muscle function in patients suffering from peripheral artery disease. METHODS: The systematic review was conducted from July 20 to November 22, 2022, in line with the Preferred Reporting Items for Systematic Review and Meta-Analysis and comprised search for interventional studies on MEDLINE, ProQuest, Scopus and ScienceDirect databases using key words "peripheral artery disease" and "trimetazidine" or their synonyms. The cut-off date for the search was July 21, 2022. Clinical parameters, including Ankle-Brachial Index, Maximum Walking Distance, Maximum Walking Time and Pain Onset Time, were analysed both narratively and quantitatively whenever possible. RESULTS: Of the 587 studies initially identified, 12(2%) were shortlisted. Of them, 2(16.7%) qualified for detailed analysis, comprising 172 patients with intermittent claudication. There was no significant difference between the examined groups' Ankle-Brachial Index values at baseline and post-intervention (p=0.83). Maximum Walking Distance improvement was significantly higher (p=0.0006) in trimetazidine group compared to control group. Maximum Walking Time MWT and Pain Onset Time were significantly different between control and trimetazidine groups (p<0.05). CONCLUSIONS: Trimetazidine's anti-ischaemic effect in peripheral artery disease patients improved Maximum Walking Distance, while it had no significant influence on Ankle-Brachial Index. Well-designed studies addressing the issue are needed.

Tumor necrosis factor α deficiency promotes myogenesis and muscle regeneration.

Tumor necrosis factor α (TNFα) exhibits diverse biological functions; however, its regulatory roles in myogenesis are not fully understood. In the present study, we explored the function of TNFα in myoblast proliferation, differentiation, migration, and myotube fusion in primary myoblasts and C2C12 cells. To this end, we constructed TNFα muscle-conditional knockout ( TNFα-CKO) mice and compared them with flox mice to assess the effects of TNFα knockout on skeletal muscles. Results indicated that TNFα-CKO mice displayed phenotypes such as accelerated muscle development, enhanced regenerative capacity, and improved exercise endurance compared to flox mice, with no significant differences observed in major visceral organs or skeletal structure. Using label-free proteomic analysis, we found that TNFα-CKO altered the distribution of several muscle development-related proteins, such as Hira, Casz1, Casp7, Arhgap10, Gas1, Diaph1, Map3k20, Cfl2, and Igf2, in the nucleus and cytoplasm. Gene set enrichment analysis (GSEA) further revealed that TNFα deficiency resulted in positive enrichment in oxidative phosphorylation and MyoD targets and negative enrichment in JAK-STAT signaling. These findings suggest that TNFα-CKO positively regulates muscle growth and development, possibly via these newly identified targets and pathways.

Skeletal Muscle UCHL1 Negatively Regulates Muscle Development and Recovery after Muscle Injury.

Ubiquitin C-terminal hydrolase L1 (UCHL1) is a deubiquitinating enzyme originally found in the brain. Our previous work revealed that UCHL1 was also expressed in skeletal muscle and affected myoblast differentiation and metabolism. In this study, we further tested the role of UCHL1 in myogenesis and muscle regeneration following muscle ischemia-reperfusion (IR) injury. In the C2C12 myoblast, UCHL1 knockdown upregulated MyoD and myogenin and promoted myotube formation. The skeletal muscle-specific knockout (smKO) of UCHL1 increased muscle fiber sizes in young mice (1 to 2 months old) but not in adult mice (3 months old). In IR-injured hindlimb muscle, UCHL1 was upregulated. UCHL1 smKO ameliorated tissue damage and injury-induced inflammation. UCHL1 smKO also upregulated myogenic factors and promoted functional recovery in IR injury muscle. Moreover, UCHL1 smKO increased Akt and Pink1/Parkin activities. The overall results suggest that skeletal muscle UCHL1 is a negative factor in skeletal muscle development and recovery following IR injury and therefore is a potential therapeutic target to improve muscle regeneration and functional recovery following injuries.

Adenine base editing-mediated exon skipping restores dystrophin in humanized Duchenne mouse model.

Duchenne muscular dystrophy (DMD) affecting 1 in 3500-5000 live male newborns is the frequently fatal genetic disease resulted from various mutations in DMD gene encoding dystrophin protein. About 70% of DMD-causing mutations are exon deletion leading to frameshift of open reading frame and dystrophin deficiency. To facilitate translating human DMD-targeting CRISPR therapeutics into patients, we herein establish a genetically humanized mouse model of DMD by replacing exon 50 and 51 of mouse Dmd gene with human exon 50 sequence. This humanized mouse model recapitulats patient's DMD phenotypes of dystrophin deficiency and muscle dysfunction. Furthermore, we target splicing sites in human exon 50 with adenine base editor to induce exon skipping and robustly restored dystrophin expression in heart, tibialis anterior and diaphragm muscles. Importantly, systemic delivery of base editor via adeno-associated virus in the humanized male mouse model improves the muscle function of DMD mice to the similar level of wildtype ones, indicating the therapeutic efficacy of base editing strategy in treating most of DMD types with exon deletion or point mutations via exon-skipping induction.

Far-infrared therapy promotes exercise capacity and glucose metabolism in mice by modulating microbiota homeostasis and activating AMPK.

The benefits of physical exercise on human health make it desirable to identify new approaches that would mimic or potentiate the effects of exercise to treat metabolic diseases. However, whether far-infrared (FIR) hyperthermia therapy could be used as exercise mimetic to realize wide-ranging metabolic regulation, and its underling mechanisms remain unclear. Here, a specific far-infrared (FIR) rays generated from graphene-based hyperthermia devices might promote exercise capacity and metabolisms. The material characterization showed that the graphene synthesized by chemical vapour deposition (CVD) was different from carbon fiber, with single-layer structure and high electrothermal transform efficiency. The emission spectra generated by graphene-FIR device would maximize matching those adsorbed by tissues. Graphene-FIR enhanced both core and epidermal temperatures, leading to increased blood flow in the femoral muscle and the abdominal region. The combination of microbiomic and metabolomic analysis revealed that graphene-FIR modulates the metabolism of the gut-muscle axis. This modulation was characterized by an increased abundance of short-chain fatty acids (SCFA)-producing bacteria and AMP, while lactic acid levels decreased. Furthermore, the principal routes involved in glucose metabolism, such as glycolysis and gluconeogenesis, were found to be altered. Graphene-FIR managed to stimulate AMPK activity by activating GPR43, thus enhancing muscle glucose uptake. Furthermore, a microbiota disorder model also demonstrated that the graphene-FIR effectively restore the exercise endurance with enhanced p-AMPK and GLUT4. Our results provided convincing evidence that graphene-based FIR therapy promoted exercise capacity and glucose metabolism via AMPK in gut-muscle axis. These novel findings regarding the therapeutic effects of graphene-FIR suggested its potential utility as a mimetic agent in clinical management of metabolic disorders.

Enhancing circulatory myokines and extracellular vesicle uptake with targeted exercise in patients with prostate cancer (the MYEX trial): a single-group crossover study.

INTRODUCTION: Physical activity is associated with improved disease progression and cancer-specific survival in patients with prostate cancer (PCa). However, the mechanisms underlying these associations remain unclear, while the relative impact of exercise modes is unknown. This study aims to examine the differential impact of exercise mode on tumour-suppressive skeletal muscle-associated systemic molecules as well as their delivery mechanism. This study will compare the effects of the two main exercise modes, aerobic and resistance, on (1) circulatory myokine levels, (2) skeletal muscle-induced extracellular vesicle abundance and cargo contents, and (3) uptake of extracellular vesicles (EVs) in PCa cells in patients with localised or advanced PCa. METHODS: A single-group cross-over design will be used for patients at opposite ends of the disease spectrum. A total of 32 patients (localised PCa, n = 16; metastatic castrate-resistant PCa, n = 16) will be recruited while capitalising on two ongoing studies. Ethics amendment has been approved for two ongoing trials to share data, implement the acute exercise sessions, and collect additional blood samples from patients. The patients will undertake two exercise sessions (aerobic only and resistance only) in random order one week apart. Blood will be collected before, after, and 30 min post-exercise. Circulating/EV-contained myokine levels (irisin, IL-6, IL-15, FGF-21, and SPARC) and plasma skeletal muscle-induced EVs will be measured using ELISA and flow cytometry. PCa cell line growth with or without collected plasma will be examined using PCa cell lines (LNCaP, DU-145, and PC-3), while evaluating cellular uptake of EVs. Ethics amendments have been approved for two capitalising studies to share data, implement acute exercise sessions and collect additional samples from the patients. DISCUSSION: If findings show a differential impact of exercise mode on the establishment of an anti-cancer systemic environment, this will provide fundamental knowledge for developing targeted exercise prescriptions for patients with PCa across different disease stages. Findings will be reported in peer-reviewed publications and scientific conferences, in addition to working with national support groups to translate findings for the broader community. TRIAL REGISTRATION: The registration for the two capitalising studies are NCT02730338 and ACTRN12618000225213.

NeuroMotion: Open-source platform with neuromechanical and deep network modules to generate surface EMG signals during voluntary movement.

Neuromechanical studies investigate how the nervous system interacts with the musculoskeletal (MSK) system to generate volitional movements. Such studies have been supported by simulation models that provide insights into variables that cannot be measured experimentally and allow a large number of conditions to be tested before the experimental analysis. However, current simulation models of electromyography (EMG), a core physiological signal in neuromechanical analyses, remain either limited in accuracy and conditions or are computationally heavy to apply. Here, we provide a computational platform to enable future work to overcome these limitations by presenting NeuroMotion, an open-source simulator that can modularly test a variety of approaches to the full-spectrum synthesis of EMG signals during voluntary movements. We demonstrate NeuroMotion using three sample modules. The first module is an upper-limb MSK model with OpenSim API to estimate the muscle fibre lengths and muscle activations during movements. The second module is BioMime, a deep neural network-based EMG generator that receives nonstationary physiological parameter inputs, like the afore-estimated muscle fibre lengths, and efficiently outputs motor unit action potentials (MUAPs). The third module is a motor unit pool model that transforms the muscle activations into discharge timings of motor units. The discharge timings are convolved with the output of BioMime to simulate EMG signals during the movement. We first show how MUAP waveforms change during different levels of physiological parameter variations and different movements. We then show that the synthetic EMG signals during two-degree-of-freedom hand and wrist movements can be used to augment experimental data for regressing joint angles. Ridge regressors trained on the synthetic dataset were directly used to predict joint angles from experimental data. In this way, NeuroMotion was able to generate full-spectrum EMG for the first use-case of human forearm electrophysiology during voluntary hand, wrist, and forearm movements. All intermediate variables are available, which allows the user to study cause-effect relationships in the complex neuromechanical system, fast iterate algorithms before collecting experimental data, and validate algorithms that estimate non-measurable parameters in experiments. We expect this modular platform will enable validation of generative EMG models, complement experimental approaches and empower neuromechanical research.

Fatty infiltration in the musculoskeletal system: pathological mechanisms and clinical implications.

Fatty infiltration denotes the anomalous accrual of adipocytes in non-adipose tissue, thereby generating toxic substances with the capacity to impede the ordinary physiological functions of various organs. With aging, the musculoskeletal system undergoes pronounced degenerative alterations, prompting heightened scrutiny regarding the contributory role of fatty infiltration in its pathophysiology. Several studies have demonstrated that fatty infiltration affects the normal metabolism of the musculoskeletal system, leading to substantial tissue damage. Nevertheless, a definitive and universally accepted generalization concerning the comprehensive effects of fatty infiltration on the musculoskeletal system remains elusive. As a result, this review summarizes the characteristics of different types of adipose tissue, the pathological mechanisms associated with fatty infiltration in bone, muscle, and the entirety of the musculoskeletal system, examines relevant clinical diseases, and explores potential therapeutic modalities. This review is intended to give researchers a better understanding of fatty infiltration and to contribute new ideas to the prevention and treatment of clinical musculoskeletal diseases.

Inhibition of skeletal muscle differentiation by calciprotein particles in human primary myoblasts.

Sarcopenia is a common complication of chronic kidney disease (CKD) and has a detrimental effect on prognosis. Previous studies have explored the role of secondary calciprotein particles (CPP2) in determining the progression of complications and poor outcomes in patients with CKD. However, no study has demonstrated that CPP2 impairs skeletal myogenesis. Our study revealed that CPP2 exposure inhibits skeletal myogenesis by suppressing myotube formation and expression of skeletal muscle-specific myosin heavy chain and actin in human primary myoblasts. Moreover, CPP2 exposure altered the expression patterns of lineage-determinative transcription factors responsible for regulating myotube differentiation marker genes. This study first demonstrated that CPP2 interferes with myoblast differentiation and myotube formation in vitro.

Early Predictors of Recovery From Nonoperatively Treated Achilles Tendon Rupture: 1 Year Follow-Up Study.

PURPOSE: To investigate early structural and mechanical predictors of plantarflexor muscle strength and the magnitude of Achilles tendon (AT) nonuniform displacement at 6 and 12 months after AT rupture. METHODS: Thirty-five participants (28 males and 7 females; mean ± SD age 41.7 ± 11.1 years) were assessed for isometric plantarflexion maximal voluntary contraction (MVC) and AT nonuniformity at 6 and 12 months after rupture. Structural and mechanical AT and plantarflexor muscle properties were measured at 2 months. Limb asymmetry index (LSI) was calculated for all variables. Multiple linear regression was used with the 6 and 12 month MVC LSI and 12 month AT nonuniformity LSI as dependent variables and AT and plantarflexor muscle properties at 2 months as independent variables. The level of pre- and post-injury sports participation was inquired using Tegner score at 2 and 12 months (scale 0-10, 10 = best possible score). Subjective perception of recovery was assessed with Achilles tendon total rupture score (ATRS) at 12 months (scale 0-100, 100=best possible score). RESULTS: Achilles tendon resting angle (ATRA) symmetry at 2 months predicted MVC symmetry at 6 and 12 months after rupture (ß = 2.530, 95% CI 1.041-4.018, adjusted R2 = 0.416, p = 0.002; ß = 1.659, 95% CI 0.330-2.988, adjusted R2 = 0.418, p = 0.016, respectively). At 12 months, participants had recovered their pre-injury level of sports participation (Tegner 6 ± 2 points). The median (IQR) ATRS score was 92 (7) points at 12 months. CONCLUSION: Greater asymmetry of ATRA in the early recovery phase may be a predictor of plantarflexor muscle strength deficits up to 1 year after rupture. TRIAL REGISTRATION: This research is a part of "nonoperative treatment of Achilles tendon rupture in Central Finland: a prospective cohort study" that has been registered in ClinicalTrials.gov (NCT03704532).

KL-Biome (Postbiotic Formulation of Lactiplantibacillus plantarum KM2) Improves Dexamethasone-Induced Muscle Atrophy in Mice.

Sarcopenia refers to an age-related decrease in muscle mass and strength. The gut-muscle axis has been proposed as a promising target to alleviate muscle atrophy. The effect of KL-Biome-a postbiotic preparation comprising heat-killed Lactiplantibacillus plantarum KM-2, its metabolites, and an excipient (soybean powder)-on muscle atrophy was evaluated using dexamethasone (DEX)-induced atrophic C2C12 myoblasts and C57BL/6J mice. KL-Biome significantly downregulated the expression of genes (Atrogin-1 and MuRF1) associated with skeletal muscle degradation but increased the anabolic phosphorylation of FoxO3a, Akt, and mTOR in C2C12 cells. Oral administration of KL-Biome (900 mg/kg) for 8 weeks significantly improved muscle mass, muscle function, and serum lactate dehydrogenase levels in DEX-treated mice. KL-Biome administration increased gut microbiome diversity and reversed DEX-mediated gut microbiota alterations. Furthermore, it significantly increased the relative abundances of the genera Subdologranulum, Alistipes, and Faecalibacterium prausnitzii, which are substantially involved in short-chain fatty acid production. These findings suggest that KL-Biome exerts beneficial effects on muscle atrophy by regulating gut microbiota.

Gender Differences in Core Muscle Morphology of Elite Alpine Skiers: Insights from Ultrasonography.

This study investigates gender differences in core muscle morphology among elite alpine skiers using ultrasonography, highlighting significant disparities that could influence training and injury prevention strategies. METHODS: A cross-sectional design was employed, examining ultrasound imaging (USI) in 22 elite skiers (11 male, 11 female) to assess the thickness of the external oblique (EO), internal oblique (IO), transversus abdominis (TrAb), and rectus abdominis (RA) muscles. RESULTS: Significant differences were noted, with male skiers displaying greater muscle thickness, particularly in the right IO and RA and left IO, EO, TrAb, and RA. CONCLUSIONS: These findings suggest that male and female skiers may require different training approaches to optimize performance and reduce injury risks. This research contributes to a deeper understanding of the physical demands on elite skiers and underscores the need for gender-specific training regimens to enhance athletic outcomes and prevent injuries.

Using Resistance-Band Tests to Evaluate Trunk Muscle Strength in Chronic Low Back Pain: A Test-Retest Reliability Study.

Exercise is a front-line intervention to increase functional capacity and reduce pain and disability in people with low strength levels or disorders. However, there is a lack of validated field-based tests to check the initial status and, more importantly, to control the process and make tailored adjustments in load, intensity, and recovery. We aimed to determine the test-retest reliability of a submaximal, resistance-band test to evaluate the strength of the trunk stability muscles using a portable force sensor in middle-aged adults (48 ± 13 years) with medically diagnosed chronic low back pain and healthy peers (n = 35). Participants completed two submaximal progressive tests of two resistance-band exercises (unilateral row and Pallof press), consisting of 5 s maintained contraction, progressively increasing the load. The test stopped when deviation from the initial position by compensation movements occurred. Trunk muscle strength (CORE muscles) was monitored in real time using a portable force sensor (strain gauge). Results revealed that both tests were highly reliable (intra-class correlation [ICC] > 0.901) and presented low errors and coefficients of variation (CV) in both groups. In particular, people with low back pain had errors of 14-19 N (CV = 9-12%) in the unilateral row test and 13-19 N (CV = 8-12%) in the Pallof press. No discomfort or pain was reported during or after the tests. These two easy-to-use and technology-based tests result in a reliable and objective screening tool to evaluate the strength and trunk stability in middle-aged adults with chronic low back pain, considering an error of measurement < 20 N. This contribution may have an impact on improving the individualization and control of rehabilitation or physical training in people with lumbar injuries or disorders.