Skeletal Muscle Content Research Articles

Показники компонентного складу тіла кваліфікованих хокеїстів на траві у передзмагальному мезоциклі підготовчого періоду

Annotation. Topicality. Indicators of the component composition of the body are an integral part of the basic models of preparedness and competitive activity of athletes. Based on the values of body composition indicators of qualified field hockey players, training effects are corrected at different stages of the annual macrocycle. The purpose of the study is to determine the indicators of the component composition of the body of qualified field hockey players in the pre-competition mesocycle of the preparatory period of the macrocycle. Material and methods of the study. The study involved qualified field hockey players of the Vinnytsia Specialized Children's and Youth Field Hockey School (n= 20). Average age – 19.8±2.14 years. Sports qualification – 1st category, candidate for master of sports. Consent to participate in the study was obtained from the players in accordance with the Helsinki Declaration of Human Rights 2008. The study was conducted during the preparatory period of the 2nd cycle of player training in the 2024-2025 season. The following methods were used in the study: theoretical analysis of literary sources, morphofunctional methods, methods of mathematical statistics. Research results. The values of the body composition of qualified field hockey players in the pre-competition mesocycle of the preparatory period of the macrocycle were determined: age – 19.8±2.14 years; body length – 1.77±0.07 m; body weight – 75.9±10.8 kg; body mass index – 22.6±3.86 kg·m-2; percentage fat content – 18.8±4.77%; percentage skeletal muscle content – 39.0±3.97%; energy expenditure in a state of homeostasis – 1696.8±213.67 kcal; level of visceral fat – 4.9±1.87 standard units. It was found that a statistically significant difference in the values of body composition between skilled and highly skilled field hockey players is observed in terms of age (p <0.05), % fat (p <0.01), % skeletal muscle (p <0.01). Conclusions. Analysis of body composition indicators of qualified field hockey players allows for more targeted training effects on players, taking into account an individual approach.

Prognostic impact of body composition and immune-nutritional status in oligometastatic NSCLC patients receiving radiotherapy

BackgroundMetabolic and nutritional status are recognized as prognostic and predictive biomarkers in cancer treatment. However, there is limited research on oligometastatic non-small cell lung cancer (NSCLC) patients undergoing radiotherapy. We aimed to explore the independent and synergistic effects of body composition and immune-nutritional status on survival outcomes in these patients.MethodsPatients with oligometastatic NSCLC who underwent radiotherapy between 2017 and 2022 were retrospectively included. The evaluated outcomes were overall survival (OS) and progression-free survival (PFS). The skeletal muscle index (SMI), subcutaneous fat index (SFI), and pericardial fat index (PFI) were obtained using computed tomography (CT) and normalized by height squared. Laboratory biomarkers were utilized to assess immune-nutritional status. Univariate chi-square tests and multivariate logistic regression analyses were employed to determine correlations between hematological parameters and body composition. We conducted K-M analyses, along with univariate and multivariate Cox regression analyses to evaluate survival outcomes.Results102 patients [mean age 61.44 years, 51 males (50%)] were included. Compared to non-responders, responders exhibited a significantly lower prevalence of sarcopenia (44.93 vs. 55.07%, P = 0.007) and demonstrated relatively better immune-nutritional scores. Logistic regression analyses revealed that a low Prognostic Nutritional Index (PNI) was a risk factor for SMI, SFI, and PFI. Multivariate Cox analyses revealed that C reactive protein-to-albumin ratio (CAR) (HR = 0.26; 95% CI 0.11–0.61; P = 0.002) and PFI (HR = 2.73; 95% CI 1.06–7.01; P = 0.037) were predictive factors for OS. CAR (HR = 0.34, P = 0.001) and SFI (HR = 1.82, P = 0.049) were independent prognostic markers for PFS. K-M analyses indicated that the group with high PNI and high SFI exhibited markedly improved OS and PFS, as well as the one with high PNI and without sarcopenia (P < 0.001).ConclusionAmong oligometastatic NSCLC patients receiving radiotherapy, higher skeletal muscle and fat content, along with better immune-nutritional status, correlated with improved survival outcomes.

Impact of Ghrelin‐Depleting Gastrectomy on Long‐Term Endocrine and Metabolic Health With a Focus on Skeletal Muscle and Bone Mineral Content

ABSTRACTBackgroundAdvances in diagnostic and surgical techniques have improved survival rates for gastric cancer patients. However, gastrectomy involving ghrelin‐secreting regions of the upper gastric greater curvature can lead to long‐term endocrine and metabolic disturbances, including reductions in serum ghrelin and insulin‐like growth factor‐1 (IGF‐1), potentially contributing to skeletal muscle and bone mineral loss.MethodsThis prospective observational study included 35 gastric cancer patients who underwent gastrectomy between 2016 and 2018, with follow‐up for 3–5 years. Patients were categorized into ghrelin‐depleted (total or proximal gastrectomy) and ghrelin‐preserved (distal gastrectomy) groups. Serum desacyl‐ghrelin, IGF‐1, and insulin‐like growth factor‐binding protein‐3 (IGFBP‐3) levels were measured, and skeletal muscle mass and bone mineral content were assessed.ResultsThe ghrelin‐depleted group exhibited significantly lower serum desacyl‐ghrelin (56.9 ± 27.9 vs. 111.2 ± 54.8 fmol/mL, p = 0.0006), skeletal muscle mass (87.7% ± 2.1% vs. 95.1% ± 2.4%, p = 0.0229), and bone mineral content (90.9% ± 13.0% vs. 99.5% ± 6.3%, p = 0.0249). Additionally, IGF‐1 levels showed a significant positive correlation with skeletal muscle mass (r = 0.53, p = 0.020). While the correlation between IGF‐1 and bone mineral content did not reach statistical significance, a positive trend was observed (r = 0.44, p = 0.062).ConclusionGastrectomy involving resection of ghrelin‐rich regions leads to long‐term reductions in serum desacyl‐ghrelin levels, adversely affecting skeletal muscle mass and bone mineral content. These findings highlight the importance of considering the endocrine consequences when selecting surgical procedures.

Association between skeletal muscle mass to visceral fat area ratio and insulin resistance in type 2 diabetes.

To investigate the correlation between skeletal muscle mass to visceral fat area ratio (SVR), neutrophil/lymphocyte ratio (NLR) and insulin resistance (IR) in patients with type 2 diabetes mellitus (T2DM). 246 T2DM patients who attended the outpatient clinics and wards of the Department of Endocrinology of the Seventh People's Hospital affiliated to Shanghai University of Traditional Chinese Medicine from June 2022 to March 2023 were selected as study subjects. General information of the study subjects was collected, body measurements were determined: height, weight, waist circumference, hip circumference, body mass index and waist-hip ratio (WHR) were calculated; biochemical indices were determined: NLR, fasting glucose (FPG), fasting insulin (FINS), and the homeostatic modeling was evaluated. Homeostatic Model Assessment of Insulin Resistance(HOMA-IR), and calculation of insulin sensitivity index (ISI). Skeletal muscle content (ASM), body fat mass(BMI), visceral fat area(VFA), and basal metabolism were determined by multifrequency bio resistive resistance method, and SVR were calculated. 82 cases in each group (50 males and 32 females) were divided into 3 groups according to the SVR level in three equal parts. Differences between groups were analyzed by one-way ANOVA. The correlation between NLR and SVR, HOMA-IR, ISI was analyzed using Pearson/Spearman correlation. Multiple linear regression analysis was used to analyze the relationship between SVR and IR. Compared with the Q3 group, NLR, FINS, HOMA-IR were elevated in the Q1 and Q2 groups (P < 0.005), and ISI and SVR were decreased (P < 0.005). Correlation analysis showed that NLR was negatively correlated with SVR, and ISI (P < 0.005) and positively correlated with HOMA-IR (P < 0.005). Multiple linear regression analysis showed that SVR and HOMA-IR were independently correlated (F = 25.584,P < 0.001); and SVR and HOMA-IR were independently correlated (F = 46.105,P < 0.001). SVR is correlated with IR in T2DM patients, suggesting that SVR has some clinical value for early warning of IR in T2DM.

Histological, immunohistochemical assessment and DNA fingerprint species identification of some meat products in Egypt

A total of sixty commercial beef products, represented by minced meat, sausage, kofta, and burger, with fifteen samples per product, were collected randomly from different markets in Assiut city, Egypt. Samples were examined histologically, immunohistochemically and molecularly to investigate tissue composition and species substitution. Polymerase Chain Reaction (PCR) was applied to confirm the beef origin of different marketed beef products and determine if there are any adulteration and/or contamination with rodents and canine species. The histological investigation finds significant differences in skeletal muscle content, with the highest proportion in minced meat, whereas the lowest detected in kofta. Several animal tissues were detected, including adipose tissue, collagen, cartilage, and bone, where kofta showed the highest levels. We also detected plant tissues, predominantly found in burger samples. Expression Bcl2 indicated the maximum intensity in sausage, while burger showed the lowest expression. PCR results revealed that 89.13% were pure beef products, 10.87% were with rat meat contamination, and 100% of examined samples were negative for canine species. These results highlight the efficacy of histology, Bcl2 immunohistochemistry and PCR in assessing meat quality and distinguishing adulteration.

Research progress on resistance exercise therapy for improving cognitive function in patients with AD and muscle atrophy.

Alzheimer's disease (AD) significantly reduces the quality of life of patients and exacerbates the burden on their families and society. Resistance exercise significantly enhances the overall cognitive function of the elderly and patients with AD while positively improving memory, executive function, and muscle strength, reducing fall risks, and alleviating psychological symptoms. As AD is a neurodegenerative disorder, some nerve factors are readily activated and released during exercise. Therefore, several prior studies have concentrated on exploring the molecular mechanisms of resistance exercise and their impact on brain function and neural plasticity. Recent investigations have identified an intrinsic relationship between individuals with AD and the pathological mechanisms of skeletal muscle atrophy, establishing a correlation between patients with AD cognitive level and skeletal muscle content. Resistance exercise primarily targets the skeletal muscle, which improves cognitive impairment in patients with AD by reducing vascular and neuroinflammatory factors and further enhances cognitive function in patients with AD by restoring the structural function of skeletal muscle. Furthermore, the effects of resistance training vary among distinct subgroups of cognitive impairment. Individuals exhibiting lower cognitive function demonstrate more pronounced adaptive responses in physical performance over time. Consequently, further investigation is warranted to determine whether tailored guidelines-such as variations in the frequency and duration of resistance exercise-should be established for patients with varying levels of dementia, in order to optimize the benefits for those experiencing cognitive impairment. This study aimed to review the relationship between AD and skeletal muscle atrophy, the impact of skeletal muscle atrophy on AD cognition, the mechanism by which resistance exercise improves cognition through skeletal muscle improvement, and the optimal resistance exercise mode to elucidate the additional advantages of resistance exercise in treating cognitive function in patients with AD and skeletal muscle atrophy.

Skeletal muscle effects of antisense oligonucleotides targeting glycogen synthase 1 in a mouse model of Pompe disease.

Pompe disease (PD) is a progressive myopathy caused by the aberrant accumulation of glycogen in skeletal and cardiac muscle resulting from the deficiency of the enzyme acid alpha-glucosidase (GAA). Administration of recombinant human GAA as enzyme replacement therapy (ERT) works well in alleviating the cardiac manifestations of PD but loses sustained benefit in ameliorating the skeletal muscle pathology. The limited efficacy of ERT in skeletal muscle is partially attributable to its inability to curb the accumulation of new glycogen produced by the muscle enzyme glycogen synthase 1 (GYS1). Substrate reduction therapies aimed at knocking down GYS1 expression represent a promising avenue to improve Pompe myopathy. However, finding specific inhibitors for GYS1 is challenging given the presence of the highly homologous GYS2 in the liver. Antisense oligonucleotides (ASOs) are chemically modified oligomers that hybridise to their complementary target RNA to induce their degradation with exquisite specificity. In the present study, we show that ASO-mediated Gys1 knockdown in the Gaa-/- mouse model of PD led to a robust reduction in glycogen accumulation in skeletal muscle. In addition, combining Gys1 ASO with ERT slightly further reduced glycogen content in muscle, eliminated autophagic buildup and lysosomal dysfunction, and improved motor function in Gaa-/- mice. Our results provide a strong foundation for validation of the use of Gys1 ASO, alone or in combination with ERT, as a therapy for PD. We propose that early administration of Gys1 ASO in combination with ERT may be the key to preventative treatment options in PD. KEY POINTS: Antisense oligonucleotide (ASO) treatment in a mouse model of Pompe disease achieves robust knockdown of glycogen synthase (GYS1). ASO treatment reduces glycogen content in skeletal muscle. Combination of ASO and enzyme replacement therapy (ERT) further improves motor performance compared to ASO alone in a mouse model of Pompe disease.

Seasonal Changes in Fatty Acid Content in Skeletal Muscle of the Long-Tailed Ground Squirrel Urocitellus undulatus

Seasonal Changes in Fatty Acid Content in Skeletal Muscle of the Long-Tailed Ground Squirrel Urocitellus undulatus

Chronic alcohol-related myopathy: a closer look at the role of lipids.

Chronic alcohol-related myopathy (CAM), characterized by muscle atrophy and weakness, arises from prolonged excessive ethanol (EtOH) intake. The precise mechanisms by which EtOH induces skeletal muscle atrophy are not fully understood. This article posits that the pathophysiology of CAM may be significantly influenced by how EtOH modifies lipid profiles and alters lipid composition and content in skeletal muscle. We review existing literature on lipid alterations in CAM-afflicted individuals and analogous animal models, discuss EtOH's direct and indirect effects on skeletal muscle lipids, and present specific instances where lipids contribute to muscle atrophy. This article advocates for a novel viewpoint, suggesting that lipid dysregulation may be the principal factor in EtOH-induced muscle wasting, offering a different angle to approach CAM research and treatment strategies.

Endurance exercise attenuates Gαq-RNAi induced hereditary obesity and skeletal muscle dysfunction via improving skeletal muscle Srl/MRCC-I pathway in Drosophila

G protein alpha q subunit (Gαq) can binds to the G protein-coupled receptor (GPCR) for signaling and is closely related to lipid metabolism. Endurance exercise is an effective means of combating acquired obesity and its complications, but the mechanisms by which endurance exercise modulates hereditary obesity and its complications are unknown. In this study, we achieved knockdown of Gαq in drosophila adipose tissue and skeletal muscle by constructing the Gαq-UAS-RNAi/Ppl-Gal4 and Gαq-UAS-RNAi/Mef2-GAl4 systems. Drosophila were subjected a three-week endurance exercise intervention, and changes in relevant indicators were detected and observed by RT-PCR, ELISA, oil red staining, immunofluorescence staining, and transmission electron microscopy. The results showed that knockdown of Gαq in both adipose tissue and skeletal muscle induced a significant increase in triglycerides accompanied by a decrease in rapid climbing ability, a decrease in Superoxide Dismutase (SOD) activity level, and a decrease in Mitochondrial respiratory chain complexI (MRCC I) content in Drosophila whole body and skeletal muscle, and down-regulated the expression of the G protein alpha q subunit (Gαq), the skeletal muscle myosin heavy chain expression gene (Mhc), mitochondrial biogenesis gene Spargal(the PGC-1alpha homologue in Drosophila). Endurance exercise significantly improved the triglyceride levels in the whole body and skeletal muscle of drosophila with Gαq knockdown in adipose tissue and skeletal muscle, as well as their ability to climb, increased SOD activity level and MRCCI content level, and up-regulated the expression of Gαq, Mhc, and Spargal(Srl). Thus, the present findings suggest that genetic defects in the Gαq gene in adipose and skeletal muscle tissues induce hereditary obesity and skeletal muscle dysfunction, and that endurance exercise attenuates this hereditary obesity and concomitant skeletal muscle dysfunction in drosophila by improving skeletal muscle fiber contractile proteins, mitochondrial function and function, and antioxidant capacity via mediating the Gαq/Mhc, Gαq/Srl/MRCC-I, and Gαq/SOD pathways.

Nutritional intervention to enhance recovery after arthroscopic knee surgery in adults: a randomized controlled pilot trial

BackgroundEssential amino acid (EAA) and omega-3 fatty acid ingestion independently attenuate leg skeletal muscle disuse atrophy in uninjured persons. However, no data exist regarding the effectiveness of combined EAA and omega-3 fatty acid ingestion to mitigate skeletal muscle disuse atrophy in response to anterior cruciate ligament reconstruction (ACLR) surgery. This pilot trial will explore the feasibility of recruitment and retention of ACLR outpatients from a single center across 18 months to consume either a combination of omega-3 fatty acids and EAAs, or a placebo control, for 4 weeks before and 2 weeks after surgery.MethodsThirty adult (≥ 18 years old) ACLR outpatients will be recruited for this single center, double-blind, two-arm randomized controlled feasibility pilot trial. Participants will consume either 5 g⋅day−1 of omega-3 fatty acids (fish oil) and 40 g⋅day−1 of EAAs or 5 g⋅day−1 of a control fatty acid mixture (safflower oil) and 40 g⋅day−1 of non-essential amino acids (NEAAs). Fatty acid supplements will be consumed 4 weeks before and for 2 weeks after ACLR surgery, whereas the EAAs and NEAAs will be consumed 1 week before and for 2 weeks after ACLR surgery. The primary outcomes are feasibility of recruitment and retention, with the goal to recruit 30 outpatients across 18 months and retain 22 participants upon completion of the study protocol following 12 weeks of data collection. These results will be reported using descriptive statistics, along with reasons and timepoints for study dropout. Secondary exploratory outcomes will be reported using inferential statistics for purposes of hypothesis generation and elucidation of mechanistic targets for future work; no inferences to clinical efficacy will be made. These outcomes include integrated rates of skeletal muscle protein synthesis, skeletal muscle protein content and expression of translation factors, skeletal muscle and erythrocyte phospholipid composition, and measures of skeletal muscle mass, strength, and power.ImpactThis work will set the foundation for a future randomized controlled trial powered to detect an effect of EAA + omega-3 fatty acid intake on skeletal muscle size or function in response to ACLR surgery.Trial registrationClinicalTrials.gov, NCT06233825. Registered 31 January 2024. https://clinicaltrials.gov/study/NCT06233825?term=NCT06233825&rank=1

Water deprivation induces a systemic procatabolic state that differentially affects oxidative and glycolytic skeletal muscles in male mice.

Dehydration, characterized by the loss of total body water and/or electrolytes due to diseases or inadequate fluid intake, is prevalent globally but often underestimated. Its contribution to long-term chronic diseases and sarcopenia is recognized, yet the mechanisms involved in systemic and muscle protein metabolism during dehydration remain unclear. This study investigated metabolic adaptations in a 36-h water deprivation (WD) model of mice. Male C57BL/6 mice underwent 36-h WD or pair-feeding at rest, with assessments of motor skills along with biochemical and metabolic parameters. Dehydration was confirmed by hypernatremia, body mass loss, hyporexia, and increased activity of vasopressinergic and oxytocinergic neurons compared with controls. These results were associated with liver mass loss, decreased glycemia, and increased cholesterolemia. In addition, increased V̇o2 and a decreased respiratory exchange ratio indicated reduced carbohydrate consumption and potentially increased protein use during dehydration. Thus, skeletal muscle protein metabolism was evaluated due to its high protein content. In the oxidative muscles of the WD group, total and proteasomal proteolysis increased, which was associated with decreased Akt-mediated intracellular signaling. Interestingly, there was an increase in fiber cross-sectional area, likely due to higher muscle water content caused by increased intracellular osmolality induced by protein catabolism products. Conversely, no changes were observed in protein turnover or water content in glycolytic muscles. These findings suggest that short-term WD imposes a procatabolic state, depleting protein content in skeletal muscle. However, skeletal muscle may respond differently to dehydration based on its phenotype and might adapt for a limited time.NEW & NOTEWORTHY This study investigated the effects of WD on mouse homeostasis, focusing on energy substrates and skeletal muscle protein metabolism. Our findings revealed a shift toward reduced dependence on carbohydrate degradation and increased reliance on lipid oxidation, or even protein oxidation, as energy sources, since we observed increased proteolysis in one muscle phenotype. Despite body mass loss, soleus and EDL muscle masses were differently affected. These results indicate the procatabolic potential of short-term WD in mice.

Normobaric hypoxia accelerates high-intensity intermittent training-induced mitochondrial biogenesis (PGC-1α)- and dynamics (OPA1)-related protein expressions in rat gastrocnemius muscle.

High-intensity intermittent training (HIIT) in a normobaric hypoxic environment enhances exercise capacity, possibly by increasing the mitochondrial content in skeletal muscle; however, the molecular mechanisms underlying these adaptations are not well understood. Therefore, we investigated whether HIIT under normobaric hypoxia can enhance the expression of proteins involved in mitochondrial biogenesis and dynamics in rat gastrocnemius muscle. Five-week-old male Wistar rats (n = 24) were randomly assigned to the following four groups: (1) sedentary under normoxia (20.9% O2) (NS), (2) training under normoxia (NT), (3) sedentary under normobaric hypoxia (14.5% O2) (HS), and (4) training under normobaric hypoxia (HT). The training groups in both conditions were engaged in HIIT on a treadmill five to six days per week for nine weeks. From the fourth week of the training period, the group assigned to hypoxic conditions was exposed to normobaric hypoxia. Forty-eight hours after completing the final training session, gastrocnemius muscles were surgically removed, and mitochondrial enzyme activity and mitochondrial biogenesis and dynamics regulatory protein levels were determined. Citrate synthase (CS) activity and mitochondrial oxygen phosphorylation (OXPHOS) subunits in the gastrocnemius muscle in the HT significantly exceeded those in the other three groups. Moreover, the levels of a master regulator of mitochondrial biogenesis, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), and a mitochondrial fusion-related protein, optic atrophy 1 (OPA1), were significantly increased by HIIT under normobaric hypoxia. Our data indicates that HIIT and normobaric hypoxia increase the expression of mitochondrial biogenesis- and dynamics-related proteins in skeletal muscles.

Functional Role of Extracellular Vesicles in Skeletal Muscle Physiology and Sarcopenia: The Importance of Physical Exercise and Nutrition.

Extracellular vesicles (EVs) play a key role in intercellular communication by transferring miRNAs and other macromolecules between cells. Understanding how diet and exercise modulate the release and content of skeletal muscle (SM)-derived EVs could lead to novel therapeutic strategies to prevent age-related muscle decline and other chronic diseases, such as sarcopenia. This review aims to provide an overview of the role of EVs in muscle function and to explore how nutritional and physical interventions can optimise their release and function. A literature review of studies examining the impact of exercise and nutritional interventions on MS-derived EVs was conducted. Major scientific databases, including PubMed, Scopus and Web of Science, were searched using keywords such as 'extracellular vesicles', 'muscle', 'exercise', 'nutrition' and 'sarcopenia'. The selected studies included randomised controlled trials (RCTs), clinical trials and cohort studies. Data from these studies were synthesised to identify key findings related to the release of EVs, their composition and their potential role as therapeutic targets. Dietary patterns, specific foods and supplements were found to significantly modulate EV release and composition, affecting muscle health and metabolism. Exercise-induced changes in EV content were observed after both acute and chronic interventions, with a marked impact on miRNAs and proteins related to muscle growth and inflammation. Nutritional interventions, such as the Mediterranean diet and omega-3 fatty acids, have also shown the ability to alter EV profiles, suggesting their potential to improve cardiovascular health and reduce inflammation. EVs are emerging as critical mediators of the beneficial effects of diet and exercise on muscle health. Both exercise and nutritional interventions can modulate the release and content of MS-derived EVs, offering promising avenues for the development of novel therapeutic strategies targeting sarcopenia and other muscle diseases. Future research should focus on large-scale RCT studies with standardised methodologies to better understand the role of EVs as biomarkers and therapeutic targets.

Study on changes in serum irisin level in free-flap transplantation and the correlation of serum irisin level with flap blood flow

Study on changes in serum irisin level in free-flap transplantation and the correlation of serum irisin level with flap blood flow

Association of Questionnaire-Based Physical Activity Analysis and Body Composition Dynamics in Type 2 Diabetes: A Cross-Sectional Study.

Physical activity (PA) exerts an important influence on glycemic control in type 2 diabetes (T2D) patients. Alterations in body composition in patients with T2D may be involved in the overall pathophysiologic process, but PAs and alterations in body composition have been poorly studied. A total of 615 patients with T2D were selected by convenient sampling. The patients were investigated with the International Physical Activity Questionnaire (IPAQ-S). Moreover, biochemical indices were collected, and the progression of the body composition of the subjects was determined via dual-energy X-ray absorptiometry (DXA). The variables included lumbar bone mineral density (LSBMD), femoral neck bone mineral density (FNBMD), hip bone mineral density (HBMD), whole-body bone mineral density (TBMD), limb skeletal muscle mass index (ASMI), whole-body fat percentage (B-FAT) and trunk fat percentage (T-FAT). Moreover, the levels of physical activity (high level of physical activity [H-PA], medium level of physical activity [M-PA] and low level of physical activity [L-PA]) were divided into three groups to analyze the changes in patient body composition with changes in physical activity level. One-way analysis of variance showed that β-CTX, TP1NP, HbA1c, B-FAT and T-FAT increased significantly (p<0.05), while 25(OH)D, LSBMD, FNBMD, HBMD, TBMD and ASMI decreased significantly (p<0.001) with the decrease of physical activity. However, there was no significant difference in serum lipids between lnHOMA-ir and lnHOMA-β (p>0.05). Multiple linear regression model was established to gradually adjust for clinical confounding factors. It was found that physical activity level was independently positively correlated with LSBMD, FNBMD, HBMD, TBMD, and ASMI, and was independently negatively correlated with B-FAT and T-FAT in patients with type 2 diabetes. A lack of physical activity is an independent risk factor for decreased bone mineral density, decreased skeletal muscle content and increased fat content in patients with T2D.

IGF2 promotes the differentiation of chicken embryonic myoblast by regulating mitochondrial remodeling.

Skeletal muscle is crucial for animal movement and posture maintenance, and it serves as a significant source of meat in the livestock and poultry industry. The number of muscle fibers differentiated from myoblast in the embryonic stage is one of the factors determining the content of skeletal muscle. Insulin-like growth factor 2 (IGF2), a well-known growth-promoting hormone, is crucial for embryonic and skeletal muscle growth and development. However, the specific molecular mechanism underlying its impact on chicken embryonic myoblast differentiation remains unclear. To elucidate the molecular mechanism by which IGF2 regulates chicken myoblast differentiation, we manipulated IGF2 expression in chicken embryonic myoblast. The results demonstrated that IGF2 was upregulated during chicken skeletal muscle development and myoblast differentiation. On the one hand, we found that IGF2 promotes mitochondrial biogenesis through the PGC1/NRF1/TFAM pathway, thereby enhancing mitochondrial membrane potential, oxidative phosphorylation, and ATP synthesis during myoblast differentiation. This process is mediated by the PI3K/AKT pathway. On the other hand, IGF2 regulates BNIP3-mediated mitophagy, clearing dysfunctional mitochondria. Collectively, our findings confirmed that IGF2 cooperatively regulates mitochondrial biogenesis and mitophagy to remodel the mitochondrial network and enhance mitochondrial function, ultimately promoting myoblast differentiation.

Feasibility of calculating rocuronium dosage by skeletal muscle weight in patients with obesity.

This study aimed to investigate the dose-response relationship of rocuronium administered based on skeletal muscle weight and to assess the feasibility of calculating rocuronium dosage by skeletal muscle weight in short surgeries for patients with obesity. This single-center, randomized controlled clinical trial included 71 patients with obesity aged 28-70 years, with body fat percentages (PBF) >20% in men and > 28% in women, ASA status I-III, scheduled for tracheoscopy. Patients were randomly allocated into two groups: skeletal muscle group (SM group) received rocuronium based on the skeletal muscle content (1.0 mg/kg, n = 31), and the conventional administration group (conventional group) received rocuronium based on total body weight (0.45 mg/kg, n = 30). General anesthesia was administered using the same protocol. Parameters recorded included patients' general condition, muscle relaxant usage, onset time of muscle relaxants, non-response time, clinical effect time, 75% recovery time, and recovery index. Additionally, occurrences of body movement, choking, and incomplete muscle relaxation during surgery were recorded. Compared to the conventional group, the SM group required significantly less rocuronium dosage, resulting in significantly lower non-response time, clinical effect time, 75% recovery time, and recovery index (p < 0.05), and the onset time is slightly longer. Neither group experienced body movement, choking, or incomplete muscle relaxation (p > 0.05). Utilizing skeletal muscle weight to calculate rocuronium dosage in short surgeries for patients with obesity can reduce dosage, shorten recovery time, and prevent residual muscle relaxation while achieving satisfactory muscle relaxation to meet surgical requirements.

A non-antibiotic erythromycin derivative improves muscle endurance by regulating endogenous anti-fatigue protein orosomucoid in mice.

At present, there are no official approved drugs for improving muscle endurance. Our previous research found acute phase protein orosomucoid (ORM) is an endogenous anti-fatigue protein, and macrolides antibiotics erythromycin can elevate ORM level to increase muscle bioenergetics and endurance parameters. Here, we further designed, synthesized and screened a new erythromycin derivative named HMS-01, which lost its antibacterial activity in vitro and in vivo. Data showed that HMS-01 could time- and dose-dependently prolong mice forced-swimming time and running time, and improve fatigue index in isolated soleus muscle. Moreover, HMS-01 treatment could increase the glycogen content, mitochondria number and function in liver and skeletal muscle, as well as ORM level in these tissues and sera. In Orm-deficient mice, the anti-fatigue and glycogen-elevation activity of HMS-01 disappeared. Therefore, HMS-01 might act as a promising small molecule drug targeting ORM to enhance muscle endurance.

AMPK and glucose deprivation exert an isoform-specific effect on the expression of Na+,K+-ATPase subunits in cultured myotubes

In skeletal muscle, Na+,K+-ATPase (NKA), a heterodimeric (α/β) P-type ATPase, has an essential role in maintenance of Na+ and K+ homeostasis, excitability, and contractility. AMP-activated protein kinase (AMPK), an energy sensor, increases the membrane abundance and activity of NKA in L6 myotubes, but its potential role in regulation of NKA content in skeletal muscle, which determines maximum capacity for Na+ and K+ transport, has not been clearly delineated. We examined whether energy stress and/or AMPK affect expression of NKA subunits in rat L6 and primary human myotubes. Energy stress, induced by glucose deprivation, increased protein content of NKAα1 and NKAα2 in L6 myotubes, while decreasing the content of NKAα1 in human myotubes. Pharmacological AMPK activators (AICAR, A-769662, and diflunisal) modulated expression of NKA subunits, but their effects only partially mimicked those that occurred in response to glucose deprivation, indicating that AMPK does not mediate all effects of energy stress on NKA expression. Gene silencing of AMPKα1/α2 increased protein levels of NKAα1 in L6 myotubes and NKAα1 mRNA levels in human myotubes, while decreasing NKAα2 protein levels in L6 myotubes. Collectively, our results suggest a role for energy stress and AMPK in modulation of NKA expression in skeletal muscle. However, their modulatory effects were not conserved between L6 myotubes and primary human myotubes, which suggests that coupling between energy stress, AMPK, and regulation of NKA expression in vitro depends on skeletal muscle cell model.