Loss Of Muscle Function Research Articles

Associations of dietary oxidative balance score with sarcopenia in adults: an NHANES-based cross-sectional study

BackgroundSarcopenia, a prevalent muscle disorder in the older adults, is characterized by accelerated loss of muscle mass and function, contributing to increased risks of falls, functional decline, and mortality. The relationship between dietary oxidative balance score (DOBS) and sarcopenia, however, remains unclear.MethodsWe conducted a cross-sectional analysis of the National Health and Nutritional Examination Survey (NHANES) 2011–2018 cohort, which included 8,240 participants, aged 47.2 ± 17.6 years (48.6% male, 51.4% female). The participants were selected from geographic locations across all 50 states and the District of Columbia, using a stratified, multistage probability sampling design to collect health and nutritional data representative of the civilian, non-institutionalized U.S. population. We employed the generalized additive model to identify potential non-linear relationships and utilized the two-piecewise linear regression model to investigate the association between DOBS and sarcopenia in American adults.ResultsParticipants were categorized into quartiles based on their DOBS, and sarcopenia was diagnosed in 702 individuals (8.5%). In the unadjusted model, DOBS exhibited a significant negative correlation with sarcopenia (β = 0.97, 95% Confidence Interval (CI): 0.96 to 0.99, P < 0.001). This association remained consistent in the model with minimal adjustment for age and gender (β = 0.97, 95% CI: 0.96 to 0.98, P < 0.001) and in the fully adjusted model including additional covariates (β = 0.97, 95% CI: 0.96 to 0.99, P < 0.001). After adjusting for potential confounders, we identified a non-linear association DOBS and sarcopenia, with an inflection point at 23. The effect sizes and CIs to the left and right of the inflection point were 1.62 (95% CI: 1.09 to 2.41, P = 0.016) and 0.97 (95% CI: 0.95 to 0.98, P < 0.001), respectively. Subgroup analyses confirmed the stability of this relationship across various demographic and health-related variables.ConclusionsThis research provides new insights into the association between diet quality, as assessed by DOBS, and sarcopenia, reinforcing the critical role of a balanced, antioxidant-rich diet in adult muscle.

Oxygen transport across the lifespan of male Sprague Dawley rats.

Human populations are experiencing unprecedented growth and longevity with lingering knowledge gaps of the characteristics, mechanisms, and pathologies of senescence. Invasive measurements and long-term control conditions for longitudinal studies are infeasible, necessitating the need for surrogate animal models. Rats have short lifespans (2-3years) with translatable cardiovascular systems, and Sprague Dawley microcirculatory preparations are key to studying the oxygen transport mechanisms critical to the loss of skeletal muscle function in aging. Here we present baseline physiological data of 61 male, Sprague Dawley rats at 3, 6, 12, 18, and 24months of age. Anesthetized animals were surgically prepared for femoral arterial and venous cannulations, tracheal intubation, and exteriorization of the spinotrapezius muscle. Measurements included cardiovascular function, blood gases, and peripheral tissue interstitial oxygen tension (PISFO2) using phosphorescence quenching microscopy. Intrinsic heart rates decreased with age without significant changes to blood pressure. Arterial oxygen tension declined 17% by 18 and 24 Months (p < 0.05) while pACO2 and PISFO2 were unchanged. Lactate was elevated at 12 and 18 Months along with an alkaline shift in blood pH. Heart rate and decreased pAO2 decoupled from pACO2 are conserved phenomena in human aging. The continuity of resting PISFO2 despite an anaerobic shift in metabolism may be due to declining mitochondrial function and dysregulation of the vascular response to hypoxemia, which are also present in aged humans. These physiological and microcirculatory data offer a useful experimental model for investigating the detailed changes in oxygen supply and demand that affect senescing skeletal muscles in rats and humans.

Plumbagin alleviates muscle atrophy in female mice through inhibiting the DANCR/NF-κB axis

BackgroundMuscle atrophy is a condition of the skeletal muscular system closely related to inflammation and significantly affects a person's quality of life and physical activity. It is characterized primarily by the progressive loss of muscle mass, strength, and function. Plumbagin (PB), the main bioactive component of the traditional Chinese medicine Plumbago zeylanica L., has bFeen shown to treat various inflammatory diseases, such as osteoporosis, osteoarthritis, and sepsis. Furthermore, many biological processes, including inflammation, involve differentiation antagonistic nonprotein-coding RNA (DANCR). However, their role and clinical importance in myogenesis and amyotrophy are not well understood. PurposeThis study aimed to explore the role of DANCR and the inflammatory response in the anti-muscle atrophy effects of PB. MethodsThe expression of DANCR in muscle atrophic mice and during myogenic differentiation was examined using quantitative reverse transcription PCR (RT‒qPCR). The mechanism of DANCR in muscle atrophy was confirmed through gene knockdown, RNA sequencing (RNA-seq), RNA pull-down, RNA immunoprecipitation (RIP), immunofluorescence (IF), and luciferase reporter gene assays. Bioinformatics was utilized to investigate the mechanism by which PB treatment affects muscle atrophy. The relationship between PB and DANCR was verified by surface plasmon resonance (SPR) and RT‒qPCR. Additionally, the role of PB in muscle atrophy was explored through its control of DANCR-mediated regulation of the NF-κB pathway. Finally, the effect of PB on the myogenic differentiation of human skeletal muscle cells (HsKMCs) was investigated. ResultsDANCR expression was upregulated in the muscle tissues of mice with muscle atrophy and downregulated during myogenic differentiation. Knockout of DANCR promoted myogenic differentiation and significantly alleviated the loss of muscle mass, strength, and function in mice with muscle atrophy. The primary mechanism involved DANCR directly binding to the p65 protein to regulate NF-κB pathway activity. Experiments revealed that PB could target the degradation of DANCR, reduce the nuclear entry of p65, and inhibit the activation of the NF-κB pathway. Consequently, PB significantly inhibited myotube atrophy and the inflammatory response in HsKMCs and promoted their myogenic differentiation by regulating the NF-κB pathway. ConclusionsOur results suggest that PB regulates myogenesis and prevents amyotrophy by targeting the degradation of DANCR and inhibiting the activation of the NF-κB pathway. This study reveals the crucial role of DANCR in maintaining muscle physiology during muscle atrophy and identifies PB as an effective drug that can target DANCR degradation to alleviate muscle atrophy.

Novel functional electrical stimulation parameter optimization for neurorehabilitation using both conventional and AI techniques

Neurological conditions such as stroke or spinal cord trauma often attenuate or disrupt nerve connections, leading to loss of muscle function, sensation, or responsiveness. The application of physical and occupational therapy rehabilitation protocols can help regain some of the lost functions and significantly improve a patient’s quality of life. These protocols leverage the principle of neuroplasticity, an inherent property of the brain which allows the formation of new neural connections in response to external stimuli. Electrical Muscle Stimulation (EMS) has been proven to amplify the effects of rehabilitation as it adds new stimuli in the form of suitable electric pulse trains directly to the neuromuscular system. Certain rehabilitation protocols incorporate functional exercises which mimic natural movements, which can in turn benefit by the application of synchronized electric pulses. This process, known as Functional Electrical Stimulation (FES), has been demonstrated to be beneficial with respect to the nature and longevity of neuromuscular adaptations as well as brain reorganization. This paper considers techniques for the optimization of these parameters and presents preliminary in vivo experimental results demonstrating the proposed methodology.

Association Between Dynapenia/Sarcopenia, Extrapyramidal Symptoms, Negative Symptoms, Body Composition, and Nutritional Status in Patients with Chronic Schizophrenia.

Background/Objectives: This study aimed to determine the association between chronic schizophrenia, extrapyramidal symptoms (EPSs), body composition, nutritional status, and dynapenia/sarcopenia. Methods: Data from 68 chronic patients with schizophrenia were analyzed using Spearman's rho correlation coefficients, Kruskal-Wallis test, Mann-Whitney U test, and Cramér's V statistics. Results: Among the participants, 32.4% had no loss of muscle mass or function, 39.7% had dynapenia, and 27.9% had sarcopenia. This study identified five key findings: (1) Bilateral grip strength, skeletal muscle index, and walking speed are interrelated, with higher negative symptom scores linked to slower movement and rigidity, particularly in the sarcopenia group, indicating that negative symptoms may contribute to muscle weakness and progression to sarcopenia. (2) Increasing age is associated with a decrease in chlorpromazine equivalent dose and an increase in the severity of EPSs. (3) Blood urea nitrogen (BUN)/creatinine ratio and all sarcopenia risk indicators were significantly negatively correlated. (4) Dynapenia and sarcopenia groups exhibited significant differences in muscle mass and nutritional status compared to the non-penia group, including reduced muscle mass, lower basal metabolic rate, and lower visceral fat levels. (5) There was an association between the Barthel Index (BI) score for activities of daily living (ADL) and dynapenia/sarcopenia. Particularly with regard to ADL, it seems necessary to pay attention to muscle weakness in partially independent patients who score 60 points or more. Conclusions: BUN/creatinine ratio, BI, EPSs, body mass index, grip strength, total protein, and albumin were useful indicators for detecting the risk of dynapenia/sarcopenia in routine psychiatric care.

Duchenne Muscular Dystrophy: An Overview of Diagnosis, Management, and Pharmacological Treatment

Background: Duchenne muscular dystrophy (DMD) is a severe inherited neuromuscular disorder, primarily affecting males, characterized by progressive muscle weakness due to mutations in the dystrophin gene. This gene encodes dystrophin, a protein crucial for maintaining muscle cell integrity. DMD leads to the progressive loss of muscle function, cardiac complications, and intellectual disability. The disease typically results in wheelchair dependence by the early teens and early mortality due to respiratory or cardiac complications in the twenties. Aim: This overview aims to examine the diagnosis, management strategies, and pharmacological treatments for Duchenne muscular dystrophy. Methods: The article reviews current literature on the genetic basis, epidemiology, pathophysiology, and clinical manifestations of DMD. It also explores diagnostic methods including serum biomarkers, genetic testing, and muscle biopsy, as well as treatment options, particularly glucocorticoid therapy, and ongoing pharmacological interventions. Results: Early detection of elevated serum creatine kinase (CK) levels, along with genetic testing, is key to confirming DMD. Current pharmacological treatments primarily focus on corticosteroids to slow muscle degeneration, and new investigational therapies are exploring gene editing and protein restoration. Additionally, cardiomyopathy, a major complication, requires regular monitoring and management. Conclusion: Duchenne muscular dystrophy remains a challenging condition with significant impact on patients and their families. Early diagnosis and intervention are essential for improving outcomes, while ongoing research offers hope for more effective therapies. Effective management includes a multidisciplinary approach focusing on pharmacological, physical, and cardiac care.

Exploring the association between pro-inflammatory mediators and sarcopenia in cancer patients through different diagnostic tools: a narrative review.

Sarcopenia, characterized by the progressive loss of skeletal muscle mass (MM) and muscle function, is a common and debilitating condition in cancer patients, significantly impacting their quality of life, treatment outcomes, and overall survival. The pathophysiology of sarcopenia is multifactorial, involving metabolic, hormonal, and inflammatory changes. Recent research highlights the role of chronic inflammation in the development and progression of sarcopenia, with pro-inflammatory cytokines being key mediators of muscle catabolism. The primary objective of this study was to assess the role of pro-inflammatory cytokines in identifying sarcopenia among cancer patients. As a secondary objective, we aim to investigate whether the methods used for assessing sarcopenia, both imaging and functional, align with established guidelines. A search of the Web of Science was conducted for English-language articles published since 2005, with the following terms: "Cancer" AND "Sarcopenia" AND "Pro-inflammatory cytokine*" OR "Interleukin*". Inclusion criteria included peer-reviewed controlled trials, observational studies, case reports, and case series. To avoid redundancy, articles with results which were included in systematic reviews, narrative reviews, or scoping reviews were excluded from this review. The analysis of 10 selected papers, including 1,138 cancer patients, revealed a lack of assessment of muscle strength (MS) and muscle functional performance in most of the studies on sarcopenia, contradicting the comprehensive nature of sarcopenia that includes MM, MS, and muscle functionality. There is no standardization of pro-inflammatory mediators for sarcopenia identification. Future research should focus on establishing cutoff points for inflammatory mediators and identifying which cytokines are linked to sarcopenia. Given the complexity of sarcopenia in different cancers, new projects should investigate whether cytokine expression depends on the tumor type. Moreover, considering that the majority of the study population comprised elderly individuals with primary sarcopenia, it is crucial to discern the extent to which the findings are influenced by age versus cancer-related factors.

Care Pathway Heterogeneity in Amyotrophic Lateral Sclerosis: Effects of Gender, Age, and Onset

Background and Objectives: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron degeneration resulting in loss of muscle function. Care management is restricted to symptomatic and palliative strategies, while clinical manifestations are heterogeneous. However, assessing the timing and benefits of ALS major clinical interventions remains challenging, with varying and nonspecific time-to-events estimates reported in the literature. Consequently, we proposed a retrospective cohort study leveraging healthcare system data to investigate ALS patients care pathway stratified by gender, age class, and onset site to describe strategies diversity and temporality. Methods: We developed an algorithm to identify incident ALS patients in the French hospitalization registry and assessed its quality through comparison with literature. We described 7 states, encompassing patient status regarding clinical intervention history, considered 15 transitions, and stratified the analysis depending on 12 different patient profiles, defined according to gender, the presence of symptoms indicative of disease onset site, and age class, to model profile-specific care pathway trajectories. Alongside analysis of median time before transition, we compared acceleration factors resulting from accelerated failure time and time-inhomogeneous models. Results: We identified 21,153 incident patients with ALS between 2013 and 2022 with a mean age of 67.7±13.1 years at time of in-registry detection, male/female and spinal/bulbar ratios of 1.2 and 1.9, respectively. Noninvasive ventilation (NIV), gastrostomy, tracheostomy, or death at hospital were recorded for 55.24% of the study population. We identified significant variations in utilization based on gender, age class, and onset site. Notably, older age and bulbar onset site accelerated gastrostomy use and spinal onset site was associated with delayed NIV initiation while tracheostomy, mainly considered for younger patients (<64 years), is rarely indicated in ALS care management. Alongside investigation of time-to-event speed, we report extensively the patient profile-specific estimated median delay before clinical event start. Conclusion: Leveraging real-world data from hospital registries provides a large sample size to investigate low prevalence diseases. In conjunction with multistate models, such data enable a comprehensive analysis of care pathways, which revealed variations in ALS management strategies based on patient profiles. By identifying these disparities, our study contributes to enhancing the foreseeability of support strategies for ALS patients.

Periodic paralysis across the life course: age-related phenotype transition and sarcopenia overlap.

In Periodic Paralysis (PP), a rare inherited condition caused by mutation in skeletal muscle ion channels, the phenotype changes with age, transitioning from the episodic attacks of weakness that give the condition its name, to a more degenerative phenotype of permanent progressive weakness and myopathy. This leads to disability and reduced quality of life. Neither the cause of this phenotype transition, nor why it occurs around the age of 40 is known. However, 40 is also the age of onset of 'normal' age-related physiological decline when we consider (a) muscle mass and strength (b) physical function at the world class level and (c) age-related mitochondrial dysfunction. Elevated Na+, mitochondrial dysfunction and sarcoplasmic Ca2+ leak via the skeletal muscle ryanodine receptor (RyR1) have been implicated in both periodic paralysis myopathy and skeletal muscle ageing. We suggest this combination may trigger a negative spiral ultimately leading to progressive muscle failure. Understanding the interaction between ageing physiology and disease phenotype will provide a window into the healthy ageing process but also help understand how, and why PP phenotype changes with age. Understanding the mechanism underlying PP phenotype-transition and its link with ageing physiology, not only has the potential to identify the first disease modifying therapies for PP, but also to identify novel and potentially tractable mechanisms that contribute to sarcopenia, the pathological loss of muscle mass and function with age.

Weight loss in patients on osimertinib for metastatic EGFR-mutant non-small cell lung cancer.

Cachexia is characterized by weight loss and decline in muscle mass and function and is a poor prognostic factor among patients with cancer. Patients with metastatic EGFR-mutant non-small cell lung cancer (NSCLC) derive remarkable survival benefits with osimertinib, a third-generation EGFR tyrosine kinase inhibitor. It is not known whether patients treated with osimertinib experience any weight loss or whether weight loss impacts patient outcomes. Therefore, we sought to describe the frequency and consequences of weight loss in this patient population. We conducted a single-center retrospective pilot study of 56 patients treated with first-line osimertinib for metastatic EGFR-mutant NSCLC. We defined on-treatment weight loss as a loss of ≥5% body weight at 6 or 12 months of treatment. We described the characteristics of patients with and without on-treatment weight loss and differences in progression-free survival (PFS), time on treatment with osimertinib, and overall survival (OS). Forty-six percent (n = 26) of patients met the criteria for on-treatment weight loss. There were no significant differences in patient or disease characteristics between patients with and without weight loss. Compared to patients without weight loss, patients with weight loss had similar PFS and time on treatment with osimertinib. Yet, patients with weight loss had significantly worse overall survival (HR 4.91, 95% CI, 1.56-15.5, P = .007). Weight loss was observed in nearly half of patients with metastatic EGFR-mutant NSCLC treated with osimertinib, and patients with weight loss had significantly worse overall survival.

Effect of Preoperative Body Composition on Postoperative Anastomotic Leakage in Oncological Ivor Lewis Esophagectomy—A Retrospective Cohort Study

Background: Surgery for esophageal cancer has an associated high rate of postoperative complications such as anastomotic leakage (AL) and fistulas. Pre-operative sarcopenia as a loss of skeletal muscle mass and function is identified as a potential prognostic factor in determining the outcomes of oncological surgical resections for esophageal cancers. In this study, we evaluated the impact of body composition on postoperative complications in esophageal cancer surgery. Methods: In this cohort study, we analyzed patients’ body composition at the level of the third lumbar vertebra on CT scans before Ivor Lewis resections for esophageal cancers between January 2015 and December 2022. Patients with a skeletal muscle index (SMI) ≤ 38.5 cm2/m2 in women and ≤52.4 cm2/m2 in men were classified as sarcopenic. Postoperative complications were categorized following the Dindo–Clavien classification and included AL, postoperative pneumonia, length of hospital stay, and failure-to-rescue which were compared between the sarcopenic and non-sarcopenic patients. Results: From a group of 111 patients with Ivor Lewis esophagectomy, 70 patients (63.1%) were classified as sarcopenic based on the SMI and the previously published gender-specific cut-off values. AL occurred at 12.6% (5.6% in adenocarcinoma). Within the whole cohort, patients with AL had a significantly low SMI of 43.487 ± 8.088 vs. 48.668 ± 7.514; p = 0.012. Additionally, the SMI showed a negative correlation to the length of postoperative hospital stay (r = −0.204; p = 0.032; N = 111). The failure-to-rescue rate was higher in the group of sarcopenic patients (12.8% vs. 8%). Conclusions: Our data showed a correlation between SMI and AL. This effect could not be seen in gender-specific SMI. This study showed a lower failure-to-rescue rate in non-sarcopenic patients after Ivor Lewis esophagectomy. These findings underscore the crucial role of determining the preoperative nutritional and body composition status as measured by the preoperative CT scans.

Accelerated Sarcopenia Phenotype in the DJ-1/Park7-Knockout Zebrafish.

Age-dependent loss of muscle mass and function is associated with oxidative stress. DJ-1/Park7 acts as an antioxidant through multiple signalling pathways. DJ-1-knockout zebrafish show a decline in swimming performance and loss of weight gain between 6 and 9 months of age. Here, we address the degree to which this is associated with muscle degeneration and identify molecular changes preceding dysregulation of muscle performance. Loss of DJ-1 reduced the skeletal muscle fibre cross-section area. The highly mitochondrial-dependent red slow muscle was more affected than the white muscle, and degeneration of sub-sarcolemma red muscle mitochondria was observed. Using TandemMassTag-based quantitative proteomics, we identified a total of 3721 proteins in the multiplex sample of 4 and 12-month-old muscles. A total of 68 proteins, mainly associated with inflammation and mitochondrial function, were dysregulated in the young DJ-1-null adults, with Annexin A3, Sphingomyelin phosphodiesterase acid-like 3B, Complement C3a, and 2,4-dienoyl CoA reductase 1 being the most affected. The loss of DJ-1 also accelerated molecular features associated with sarcopenia, such as a decrease in the NAD+/NADH ratio and a reduction in Prostaglandin reductase 2 and Cytosolic glycerol-3-phosphate dehydrogenase levels. In view of the experimental power of zebrafish, the DJ-1-null zebrafish makes a valuable model for understanding the connection between oxidative stress and age-dependent muscle loss and function.

Effects of Alnus japonica Hot Water Extract and Oregonin on Muscle Loss and Muscle Atrophy in C2C12 Murine Skeletal Muscle Cells.

Background/Objectives: Sarcopenia is characterized by the loss of muscle mass and function, increases in mortality rate, and risk of comorbidities in the elderly. This study evaluated the effects of Alnus japonica hot water extract (AJHW) and its active compound, oregonin, on muscle atrophy and apoptosis in vitro. Methods: AJHW underwent phytochemical analysis. C2C12 cells were subjected to H2O2 and dexamethasone to induce oxidative stress and muscle loss, after which AJHW and oregonin were administered to assess their impacts on cell viability, apoptosis, muscle protein synthesis stimulation, and muscle protein degradation inhibition. Cell viability was assessed via an MTT assay, and apoptosis was analyzed by measuring Bcl-2, Bax, cleaved caspase-3, and cleaved PARP through Western blotting. Western blotting and RT-PCR were utilized to analyze MyoD, Myogenin, Atrogin-1, and MuRF1 protein and gene expression in a muscle atrophy model, as well as the Akt/mTOR and FoxO3α pathways. Results: AJHW was confirmed to contain oregonin, an active compound. AJHW and oregonin significantly increased cell viability and reduced apoptosis by upregulating Bcl-2 and downregulating Bax, cleaved caspase-3, and cleaved PARP. They significantly enhanced muscle protein synthesis through the upregulation of MyoD and Myogenin, while diminishing muscle degradation by downregulating Atrogin-1 and MuRF1. The activation of the Akt/mTOR pathway and inhibition of the FoxO3α pathway were also observed. Conclusions: AJHW and oregonin effectively prevented muscle cell apoptosis, promoted muscle protein synthesis, and inhibited muscle protein degradation in vitro. These results suggest that AJHW and oregonin could serve as therapeutic agents to prevent and treat sarcopenia.

Circulating small extracellular vesicles as blood-based biomarkers of muscle health in aging nonhuman primates.

Age-associated loss of muscle mass and function and subsequent mobility decline define poor health outcomes, reduced quality of life, and mortality risk. The rate and extent of aging-related muscle loss varies across older adults. It is challenging to understand the molecular pathogenesis of mobility decline, as anthropometric and imaging techniques, primarily used in muscle function assessment, do not offer much molecular information. Small extracellular vesicles (sEV) are lipid membrane-bound, nano-sized (≤ 200nm) vesicles which carry a wide array of biomolecules as their cargo. sEV contain cell/tissue-specific signatures on their surface and can be isolated from biofluids. These properties pose sEV as a minimally invasive means to monitor the functional and biological health of difficult-to-access tissues, establishing them as a promising liquid biopsy tool. Here, we first isolated skeletal muscle-derived sEV (sEVSKM) from the serum of vervet monkeys (16 to < 25years old) using alpha sarcoglycan (SGCA) as a muscle-specific sEV surface marker. sEVSKM were extensively characterized for size, concentration, purity, and specificity. Further, sEVSKM isolated from young (11-15years) and old (25-29years) monkeys' serum were characterized for oxidized proteins by mass spectrometry and miRNAs by small-RNAseq. Notably, the analysis of oxidized proteins indicated perturbation of metabolic pathways, actin cytoskeleton, muscle cytoskeleton regulation, and HIF-1 signaling in older monkeys. Furthermore, small-RNAseq analysis identified differential expression of several miRNAs regulating metabolic pathways, inflammation, and stress signaling. Altogether, these results suggest that it is feasible to isolate sEVSKM and use them to identify molecular biomarkers that reflect the physiological state of muscle tissue.

Automated Assessment of Sarcopenia with Hounsfield Unit Average Calculation in Computed Tomography Scans Using Deep Learning Techniques

Abstract Introduction Skeletal muscle is increasingly plastic with an ability to gain or lose tissue. Depletion of muscle mass and quality occurs due to various factors such as aging, disease, and disuse. Sarcopenia can be loosely defined as a significant loss of muscle mass and function. Sarcopenia is now recognized as an independent risk factor for various patient-related negative outcomes after various surgeries. Various computed tomography (CT) based imaging indices for assessment of sarcopenia exist in practice. The psoas muscle Hounsfield unit average calculation (HUAC) has been proven to be an effective one as it is independent of patient anthropometric data, and it can be calculated in the images provided. Aim The aim of this study is to develop automated tools for estimation of the HUAC using deep learning algorithms. Materials and Methods A total of 41 abdominal CTs were used. Ground truth was established and validated by two radiologists with more than 5 and 10 years of experience each. Models were trained to identify the psoas muscle among the slices and calculate the HUAC. Results At inference, an average intersection over union (IoU) value of 90% was obtained between the deep learning model outputs and the original annotated test images for the CT slices. The Dice coefficient was 0.90 between the ground truth labels and the output from the model. Conclusion We have demonstrated the accuracy of our deep learning–based algorithm for quantifying the psoas muscle HUAC, which is a marker for sarcopenia. There is a potential for a fully automated measure to calculate the HUAC for any patient undergoing CT scan.

Skeletal Muscle Stem Cells and the Microenvironment Regulation in Sarcopenia:A Review.

Sarcopenia is an age-related degenerative skeletal muscle disorder characterized by the loss of skeletal muscle mass and function during aging.Sarcopenia can impair the elderly's ability to perform daily activities and is associated with high risks of falls,fractures,and hospitalization.It seriously affects the quality of life of the elderly and becomes one of the major health problems in the aging society.Skeletal muscle stem cells,also known as muscle satellite cells,play a key role in supporting muscle regeneration and homeostasis maintenance.Studies have suggested that muscle satellite cell functions are tightly regulated by microenvironment signals in the skeletal muscle.Of note,skeletal muscle fibers,serving as an immediate niche of muscle satellite cells,regulate their activation,proliferation,and self-renewal.This article reviews the research progress in the regulatory roles of skeletal muscle stem cells and their microenvironment in sarcopenia during aging,providing theoretical support for potential treatment of sarcopenia via modifying skeletal muscle microenvironment and regulating muscle satellite cell functions.

Reactive oxygen species in skeletal muscle injury, fatigue, regeneration and ageing: In memory of John Faulkner

One of the most critical factors impacting healthspan in the elderly is the loss of muscle mass and function, clinically referred to as sarcopenia. Muscle atrophy and weakness lead to loss of mobility, increased risk of injury, metabolic changes and loss of independence. Thus, defining the underlying mechanisms of sarcopenia is imperative to enable the development of effective interventions to preserve muscle function and quality in the elderly and improve healthspan. Over the past few decades, understanding the roles of mitochondrial dysfunction and oxidative stress has been a major focus of studies seeking to reveal critical molecular pathways impacted during aging. In this review, we will highlight how oxidative stress might contribute to sarcopenia by discussing the impact of oxidative stress on the loss of innervation and alteration in the neuromuscular junction (NMJ), on muscle mitochondrial function and atrophy pathways, and finally on muscle contractile function.

Sarcopenia's Role in Neoadjuvant Chemotherapy Outcomes for Locally Advanced Breast Cancer: A Retrospective Analysis.

BACKGROUND Sarcopenia, characterized by loss of skeletal muscle mass and function, is linked to poor outcomes in cancer patients. In breast cancer, sarcopenia has been associated with reduced treatment tolerance and survival. However, its impact on patients with locally advanced breast cancer receiving neoadjuvant chemotherapy is understudied. This study aimed to assess sarcopenia's impact on outcomes in 226 women with advanced breast cancer, pre- and post-chemotherapy. MATERIAL AND METHODS This retrospective cohort study included 226 patients with stage II-III breast cancer who received neoadjuvant chemotherapy (NAC) between 2015 and 2021. Sarcopenia was assessed using psoas muscle area (PMA) from pre- and post-NAC computed tomography scans, with a 25th percentile cut-off (415.4 mm²). Pathological response was evaluated using the Miller-Payne grading system, and survival outcomes were analyzed using Kaplan-Meier curves. Statistical significance was set at P<0.05. RESULTS The mean PMA decreased significantly after NAC (502.8 mm2 to 454.3 mm², P<0.001). Pre-NAC, sarcopenia was present in 24.8% of patients. This increased to 40.7% after NAC. Sarcopenia was more prevalent in obese patients (P<0.001), but no significant association was found between sarcopenia and pathological complete response (pCR) or survival outcomes. Although pre- and post-NAC sarcopenia did not affect recurrence or mortality, non-sarcopenic patients were more likely to achieve pCR (P=0.012). Hematologic toxicity was higher in sarcopenic patients with comorbidities (P<0.05). CONCLUSIONS Sarcopenia significantly increases after NAC but does not independently impact pathological response, recurrence, or survival in locally advanced breast cancer. Obesity and comorbid conditions are key factors influencing sarcopenia, highlighting the need for comprehensive management to mitigate treatment-related sarcopenia.

Prevalence of sarcopenia after bariatric surgery: a systematic review and meta-analysis

Introduction: Bariatric surgery, after failed weight loss and comorbidity resolution, can lead to postoperative sarcopenia, characterized by the gradual loss of muscle mass and strength, impacting functionality and quality of life. Objective: This systematic review aims to determine the prevalence of sarcopenia after bariatric surgery. Methods: The protocol was registered on PROSPERO CRD42023447294). Comprehensive searches of electronic databases and journal references, without language restrictions, were conducted. Sarcopenia was defined as a progressive disorder involving muscle mass and function loss. The primary outcome was sarcopenia prevalence after bariatric surgery. Meta-analysis was realized using R software (version 4.1.0). Results: Among 1,445 reviewed studies from databases like MEDLINE, Embase, Web of Science, BVS, LILACS, and BDENF, eight met the criteria. The global sarcopenia prevalence was 32%, with an average age of 42 ± 10 years. It was higherin Roux-en-Y gastric bypass (RYGB) patients (59%). DXA was the primary data collection method (45%). After bariatric surgery, sarcopenia prevalence was 55% after more than a year, 3% within a year, and 24% at one year. Conclusion: The high sarcopenia prevalence highlights the need for healthcare professionals to enhance screening, intervention, and follow-up for this condition. Additional studies are needed to understand associated factors and develop interventions to prevent sarcopenia in this population.

Protective effects of elastic band training-detraining on Fall risk, power, body composition, and cognition in older adults with mild cognitive impairment: A 40-week trial

BackgroundPhysical inactivity exacerbates muscle function and mass loss, increasing the risk of falls in older adults. Regular exercise can prevent muscle loss, cognitive decline, and comorbidities, potentially reducing fall risk. Given the multifactorial nature of fall risk, a comprehensive assessment is required. ObjectiveTo investigate the effects of a 40-week intervention, including a long-term exercise program (16-weeks), detraining (8-weeks), and retraining (16-weeks), on fall risk and cognitive status in older adults with mild cognitive impairment. MethodsParticipants (≥70 years old) were divided into two groups: Elastic Band Resistance Training (EBRT, n = 22) and a control group with no treatment (n = 20). Cognitive profile, body composition, muscle power, and multifactorial fall risk assessments (Timed Up-and-Go Test (TUG), Falls Efficacy Scale (FES), Fall Risk Assessment Tool (FRAT), and sensorimotor platform) were evaluated at four time points. ResultsSignificant correlations between muscle power, fat-free mass, and cognitive status with fall risk assessments were observed at baseline. Both phases of the exercise intervention improved muscle power, body composition, cognitive profile, and fall risk status. The EBRT group showed significant improvements in muscle power (p ≤ 0.01), fall risk (FRAT, p ≤ 0.01), FES (p ≤ 0.05), sensorimotor performance (p ≤ 0.001), TUG (p ≤ 0.001), and cognitive status (MoCA, p ≤ 0.05). Protective effects persisted during the detraining phase. ConclusionThis study highlights significant improvements in fall risk assessment induced by EBRT, demonstrating its protective effects. The findings suggest that EBRT can enhance aspects related to fall risk, offering promising avenues for improving independence and quality of life in older adults prone to falls.