Stroke-associated sarcopenia is a serious post-stroke complication that can have a significant impact on patient’s functional recovery. However， currently available assessment tools for sarcopenia require specialized equipment and personnel， which are difficult to access in resource-limited settings. This article presents the role of biomarkers as an objective method in the pathogenesis， prevention， diagnosis， and prognostic assessment of stroke-associated sarcopenia， with the focus on neuromuscular， inflammatory， metabolic， and nutritional indicators.
Stroke ; Sarcopenia ; Biomarkers

Objective To investigate the incidence rate of sarcopenia and related risk factors in patients with stroke. Methods A retrospective analysis was performed for the patients with stroke who were admitted to the stroke center of a grade A tertiary hospital in Changchun， China， from March 2023 to June 2024. The method of bioelectrical impedance was used to perform body composition analysis for all patients on day（7.0±1.0）after admission， and the incidence rate of stroke-related sarcopenia was analyzed. A binary logistic regression analysis was used to investigate the risk factors for stroke-related sarcopenia. Results A total of 666 patients were included in the study， among whom 150（22.5%） developed sarcopenia （95%CI 0.193‒ 0.257）. Low body mass index， low phase angle， low triglyceride， advanced age， and low Barthel index were risk factors for the early onset of sarcopenia in patients with stroke. Conclusion There is a relatively high incidence rate of sarcopenia in stroke patients， with complex influencing factors. Medical staff should pay more attention to the elderly stroke patients， as well as those patients with emaciation， low phase angle， low triglyceride， and limited activities of daily living. Early nutritional supplementation and functional exercise can help to prevent the onset of stroke-related sarcopenia.
Stroke ; Sarcopenia

Aging is typically associated with decreased musculoskeletal function, leading to reduced mobility and increased frailty. As a hallmark of aging, cellular senescence plays a crucial role in various age-related musculoskeletal diseases, including osteoporosis, osteoarthritis, intervertebral disc degeneration, and sarcopenia. The detrimental effects of senescence are primarily due to impaired regenerative capacity of stem cells and the pro-inflammatory environment created by accumulated senescent cells. The secreted senescence-associated secretory phenotype (SASP) can induce senescence in neighboring cells, further amplifying senescent signals. Although the removal of senescent cells and the suppression of SASP factors have shown promise in alleviating disease progression and restoring musculoskeletal health in mouse models, clinical trials have yet to demonstrate significant efficacy. This review summarizes the mechanisms of cellular senescence in age-related musculoskeletal diseases and discusses potential therapeutic strategies targeting cellular senescence.
Humans ; Cellular Senescence/physiology* ; Musculoskeletal Diseases/pathology* ; Aging/pathology* ; Animals ; Senescence-Associated Secretory Phenotype/physiology* ; Sarcopenia ; Osteoporosis

BACKGROUND

Hand grip strength (HGS) is a tool to measure muscle strength, which is an important component in sarcopenia and frailty. Grip strength (GS) in midlife can predict physical disability in senior years and help evaluate a patient's overall health.

The general purpose of this study is to validate the HGS using an aneroid sphygmomanometer and Jamar dynamometer as a diagnostic tool for sarcpenia. The specific aims of this study are (a) to determine the concurrent criterion validity, (b) to determine the reliability, and (c) to measure the inter-rater agreement of the aneroid sphygmomanometer against the Jamar dynamometer in measuring HGS.

This prospective validation study measures HGS using an aneroid sphygmomanometer and Jamar dynamometer obtained from seventy participants 50 years old and above. Statistical methods used in data analysis include Spearman Rho, univariate linear regression analyses, intra-class correlation, inter-rater reliability, intra-rater reliability, Bland-Altman plots, and Lin’s concordance.

There was a significant correlation of HGS with the Jamar dynamometer and aneroid sphygmomanometer regardless of the rater [Spearman Rho (rs=0.762 to 0.778, p=0.001)]. Jamar GS is comparable to GS using a sphygmomanometer with the formula of [Jamar = 0.54 x sphygmomanometer (mmHg) - 45.12].

Aneroid sphygmomanometer can be used as an option to measure GS and has a valid value to predict the Jamar GS value. Hence, it can be an alternate tool for diagnosing sarcopenia.

BACKGROUND

Curcumin has been investigated as a potential natural solution to prevent or even treat skeletal muscle decline. There are a number of externally sourced finished products (ie, those imported from other countries) containing curcumin, but high cost limits their usage. The emerging research and development of locally sourced curcumin is an opportunity to produce high-quality oral supplements comparable to existing imported products.

The primary purpose of this study is to determine the effects of oral administration of a local curcumin formulation on skeletal muscle using an animal model that similarly demonstrated the course of human sarcopenia.

Purpose-bred 11- to 12-week-old female Sprague Dawley (SD) rats will be used in this study. SD rats are extensively used in animal models of human diseases and conditions such as diabetes, obesity and sarcopenia. Female rats have been selected because they do not demonstrate more temperature or activity variance and have more stable behavior compared to males. To simulate sarcopenia in this animal model, the tail suspension (TS) method was utilized. The TS method involves decreased hind limb function by suspending the animal’s tail for the duration of treatment. The laboratory animals will be randomized to receive any of the four treatments: (1) low-dose curcumin + vehicle; (2) high-dose curcumin + vehicle; (3) vehicle only; and (4) control (distilled water). The interventions will be subdivided into two: 2-week treatment and 4-week treatment. The gastrocnemius muscles on both sides will be excised and weighed, and the muscle tissues subjected to rapid freezing in acetone-dry ice and sliced into 10 μm-thick sections for staining. Examination of muscle architecture and computation of atrophy factors will be performed. The presence of connective tissue, fat tissue and number of atrophic muscle cells will be determined. Accurate quantitative detection of the rat total AMP (adenosine monophosphate)-Activated Protein Kinase will be performed in the gastrocnemius muscle tissue utilizing the enzyme-linked immunosorbent assay kit.

OBJECTIVE: To assess the impacts of electroacupuncture (EA) on the gait, oxidative stress, inflammatory reaction, and protein degradation in the rats of denervated skeletal muscle atrophy, and explore the potential mechanism of EA for alleviating denervated skeletal muscle atrophy. METHODS: Forty male SD rats, 8 weeks old, were randomly assigned to a sham-surgery group, a model group, an EA group, and a p38 MAPK inhibitor group, with 10 rats in each group. The right sciatic nerve was transected to establish a rat model of denervated skeletal muscle atrophy in the model group, the EA group and the p38 MAPK inhibitor group. In the sham-surgery group, the nerve was exposed without transection. One day after successful modeling, the rats in the EA group received EA at "Huantiao" (GB30) and "Zusanli" (ST36) on the right side, using a continuous wave with a frequency of 2 Hz and current intensity of 1 mA, for 15 min in each session, EA was delivered once a day, 6 times a week. In the p38 MAPK inhibitor group, the rats received the intraperitoneal injection with SB203580 (5 mg/kg), once a day, 6 times a week. The intervention was composed of 3 weeks in each group. After the intervention completion, the CatWalk XT 10.6 animal gait analysis system was used to record the gait parameters of rats. The wet weight ratio of the gastrocnemius muscle was calculated after the sample collected. Using HE staining, the fiber morphology and cross-sectional area of the gastrocnemius muscle were observed; ELISA was employed to measure the content of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α in the gastrocnemius muscle; the biochemical hydroxyamine method was adopted to detect the content of superoxide dismutase (SOD) and malondialdehyde (MDA) in the gastrocnemius muscle; with immunohistochemistry and Western blot used, the expression of p38 mitogen-activated protein kinase (p38 MAPK), phosphorylated (p)-p38 MAPK, muscle atrophy F-box gene (Atrogin-1), muscle RING finger 1 (Murf-1), nuclear factor E2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) was detected in the gastrocnemius muscle. RESULTS: Compared to the sham-surgery group, in the model group, the standing duration, the swing time and the step cycle were increased (P<0.001), the footprint area of the maximum contact time, the print area, the average intensity of the maximum contact time, the average intensity, the swing speed, and the step length were decreased (P<0.001); the wet weight ratio of gastrocnemius muscle and fiber cross-sectional area were reduced (P<0.001); the content of IL-6, IL-1β, TNF-α and MDA in gastrocnemius muscle elevated (P<0.001), and that of SOD reduced (P<0.001); the positive and protein expression of p-p38 MAPK, Atrogin-1 and Murf-1 elevated (P<0.001) and that of Nrf2 and HO-1 dropped (P<0.001). When compared with the model group, in the EA group and the p38 MAPK inhibitor group, the standing duration, the swing time and the step cycle decreased (P<0.01), the footprint area of the maximum contact time, the print area, the average intensity of the maximum contact time, the average intensity, the swing speed, and the step length increased (P<0.01); the wet weight ratio of gastrocnemius muscle and fiber cross-sectional area were improved (P<0.01, P<0.05); the content of IL-6, IL-1β, TNF-α and MDA in gastrocnemius muscle dropped (P<0.05, P<0.01), and that of SOD elevated (P<0.01, P<0.05); the positive and protein expression of p-p38 MAPK, Atrogin-1 and Murf-1 dropped (P<0.01, P<0.05) and that of Nrf2 and HO-1 increased (P<0.01, P<0.05). CONCLUSION Electroacupuncture may alleviate skeletal muscle atrophy in denervated skeletal muscle atrophy rats by mediating the p38 MAPK activity, thereby suppressing oxidative stress, inflammatory reaction, and protein degradation.
Animals ; Electroacupuncture ; Male ; Rats ; p38 Mitogen-Activated Protein Kinases/genetics* ; Rats, Sprague-Dawley ; Muscular Atrophy/metabolism* ; Muscle, Skeletal/metabolism* ; Humans ; Signal Transduction ; Superoxide Dismutase/genetics* ; Tumor Necrosis Factor-alpha/genetics* ; Oxidative Stress ; MAP Kinase Signaling System ; Acupuncture Points

INTRODUCTION: The diagnosis of sarcopenia relies on key indicators such as handgrip strength, walking speed and muscle mass. Developing a composite index that integrates these measures could enhance clinical evaluation in older adults. This study aimed to standardise and combine these metrics to establish a z score for the sarcopenia composite index (ZoSCI) tailored for the ageing population. Additionally, we explore the risk factors associated with ZoSCI to provide insights into early prevention and intervention strategies. METHOD: This retrospective study analysed data between January 2017 and December 2021 from an elderly health programme in Taiwan, applying the Asian Working Group for Sarcopenia criteria to assess sarcopenia. ZoSCI was developed by standardising handgrip strength, walking speed and muscle mass into z scores and integrating them into a composite index. Receiver operating characteristic (ROC) curve analysis was used to determine optimal cut-off values, and multiple regression analysis identified factors influencing ZoSCI. RESULTS: Among the 5047 participants, the prevalence of sarcopenia was 3.7%, lower than the reported global prevalence of 3.9-15.4%. ROC curve analysis established optimal cut-off points for distinguishing sarcopenia in ZoSCI: -1.85 (sensitivity 0.91, specificity 0.88) for males and -1.97 (sensitivity 0.93, specificity 0.88) for females. Factors associated with lower ZoSCI included advanced age, lower education levels, reduced exercise frequency, lower body mass index and creatinine levels. CONCLUSION This study introduces ZoSCI, a new compo-site quantitative indicator for identifying sarcopenia in older adults. The findings highlight specific risk factors that can inform early intervention. Future studies should validate ZoSCI globally, with international collaborations to ensure broader applicability.
Humans ; Sarcopenia/physiopathology* ; Male ; Aged ; Female ; Retrospective Studies ; Hand Strength ; Taiwan/epidemiology* ; ROC Curve ; Aged, 80 and over ; Risk Factors ; Walking Speed ; Geriatric Assessment/methods* ; Prevalence ; Muscle, Skeletal ; Middle Aged

This study aims to explore the role and mechanism of CXC chemokine receptor 3 (CXCR3) in cisplatin-induced skeletal muscle atrophy. Wild-type mice were divided into two groups: cisplatin group and control group (treated by normal saline). The results showed that, compared to the control group, the expression levels of CXCR3 mRNA and protein were significantly up-regulated in the skeletal muscle of the cisplatin group, suggesting that CXCR3 may play an important role in the model of cisplatin-induced skeletal muscle atrophy. To further investigate its role and potential mechanisms, CXCR3 knockout mice and wild-type mice were treated with cisplatin to induce skeletal muscle atrophy. The results revealed that CXCR3 knockout not only failed to alleviate cisplatin-induced skeletal muscle atrophy, but also further reduced body weight, skeletal muscle mass, and muscle fiber cross-sectional area. Further analysis showed that, in the cisplatin-induced muscle atrophy model, CXCR3 knockout significantly up-regulated the expression levels of E3 ubiquitin ligases in skeletal muscle and down-regulated the expression levels of myogenic regulatory factors. To explore the molecular mechanism by which CXCR3 gene deletion exacerbated cisplatin-induced skeletal muscle atrophy, transcriptomic sequencing was performed on the atrophied skeletal muscles of wild-type and CXCR3 knockout mice. The results showed that, compared to wild-type mice, 14 genes were significantly up-regulated and 12 genes were significantly down-regulated in the skeletal muscle of CXCR3 knockout mice. Gene set enrichment analysis (GSEA) revealed a significant enrichment of genes related to fatty acid β-oxidation. Quantitative real-time PCR validation results were consistent with the transcriptomic sequencing results. These findings suggest that CXCR3 may counteract cisplatin-induced skeletal muscle atrophy by up-regulating E3 ubiquitin ligases, down-regulating myogenic regulatory factors, and enhancing the recruitment of fatty acid β-oxidation-related genes.
Animals ; Cisplatin/adverse effects* ; Muscular Atrophy/physiopathology* ; Mice ; Receptors, CXCR3/metabolism* ; Ubiquitin-Protein Ligases/metabolism* ; Mice, Knockout ; Oxidation-Reduction ; Fatty Acids/metabolism* ; Muscle, Skeletal/metabolism* ; Mice, Inbred C57BL ; Male

The increasing prevalence of aging has led to a rising incidence of comorbidity of sarcopenia and obesity, posing significant burdens on socioeconomic and public health. Current research has systematically explored the pathogenesis of each condition; however, the mechanisms underlying their comorbidity remain unclear. This study reviews the current literature on sarcopenia and obesity in the aging population, focusing on their shared biological mechanisms, which include loss of autophagy, abnormal macrophage function, mitochondrial dysfunction, and reduced sex hormone secretion. It also identifies metabolic mechanisms such as insulin resistance, vitamin D metabolism abnormalities, dysregulation of iron metabolism, decreased levels of nicotinamide adenine dinucleotide, and gut microbiota imbalances. Additionally, this study also explores the important role of genetic factors, such as alleles and microRNAs, in the co-occurrence of sarcopenia and obesity. A better understanding of these mechanisms is vital for developing clinical interventions and preventive strategies.
Humans ; Sarcopenia/physiopathology* ; Obesity/physiopathology* ; Aging/physiology* ; Autophagy/physiology* ; Insulin Resistance ; Comorbidity ; Vitamin D/metabolism* ; Gonadal Steroid Hormones/metabolism* ; Gastrointestinal Microbiome ; Mitochondria ; MicroRNAs

Skeletal muscle atrophy is characterized by a reduction in both the size and quantity of skeletal muscle fibers, resulting in impaired muscle strength and function. It mainly includes disuse muscle atrophy, aging muscle atrophy, denervated muscle atrophy and muscle atrophy caused by disease etc. As a cost-effective way, exercise has been widely used in the prevention and treatment of skeletal muscle atrophy, but its mechanism for improving skeletal muscle atrophy remains unclear. Recent studies have indicated that insulin-like growth factor 1 (IGF-1) plays an important role in improving muscle atrophy through exercise, in addition to promoting the survival of neurons, lowering blood sugar, and anti-inflammation. This article reviews recent findings on the mechanisms by which IGF-1 mediates exercise-induced improvement in skeletal muscle atrophy, providing a theoretical basis for the prevention and treatment of this disease.
Insulin-Like Growth Factor I/physiology* ; Muscular Atrophy/therapy* ; Humans ; Exercise/physiology* ; Muscle, Skeletal ; Animals ; Insulin-Like Peptides