To investigate the relationship between respiratory sarcopenia with physical tests and a set of inflammatory biomarkers, seventy-one older women from the community with age 75 ± 7 years and BMI 26 ± 4 kg/m² were evaluated for appendicular lean mass using Dual X-ray Absorptiometry, respiratory muscle strength using an analog manuvacuometer, physical tests using handgrip strength, timed up and go and sit to stand in chair tests, and a panel of inflammatory biomarkers was measured, containing Adiponectin, BNDF, IFN, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, Leptin, Resistin, TNF and their soluble receptors sTNFr-1 and sTNFr-2. The analyzes suggest that older women with respiratory sarcopenia also had significantly low physical function and higher concentrations of sTNFr-2 (> 2241pg/ml), additionally respiratory muscle strength was inversely associated with sTNFr-2 concentrations (MIP: β = -0.48; R² = 0.24; p < 0.001; MEP: β = -0.35; R² = 0.12; p = 0.003). These results contribute to the discussion about the pathophysiology and to the strategies for diagnosing and monitoring respiratory sarcopenia in community-dwelling older women.

Age-related muscle function decline is a major impediment to healthy ageing. We aimed to investigate the association between a panel of Alzheimer's disease-related biomarkers and longitudinal trajectories of muscle strength, while exploring the influence of cognitive function.

In this cohort study, we gathered data from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K), an ongoing prospective study that includes adults aged 60 years and older, from central Stockholm, Sweden. We included data from baseline to the fourth follow-up (March 21, 2001, to Dec 31, 2016). Seven Alzheimer's disease-related blood biomarkers were measured in dementia-free, community dwelling participants: total tau, phosphorylated tau181 (p-tau181), phosphorylated tau217 (p-tau217), amyloid β 40 and 42, neurofilament light chain, and glial fibrillary acidic protein (GFAP). Muscle strength was measured through the handgrip strength and chair-stand tests. Linear mixed models were used to explore the association between baseline Alzheimer's disease-related biomarkers and muscle strength trajectories.

The baseline SNAC-K cohort included 3363 individuals, of whom 1953 participants were included in our analyses (mean age 70·2 [SD 9·1] years; 780 [39·9%] male and 1173 [60·1%] female participants). In adjusted models, higher concentrations of p-tau181 (β per year 0·93 [95% CI 0·71 to 1·16]; p<0·0001), p-tau217 (β per year 1·31 [1·03 to 1·58]; p<0·0001), neurofilament light chain (β per year 0·76 [0·56 to 0·96]; p<0·0001), and GFAP (β per year 0·37 [0·21 to 0·53]; p<0·0001) were associated with an accelerated decline of chair-stand performance over time. The adjustment for Mini-Mental State Examination (MMSE) score led to the attenuation of these associations. Higher concentrations of p-tau181 (β per year -0·12 [95% CI -0·17 to -0·07]; p<0·0001), p-tau217 (β per year -0·13 [-0·20 to -0·07]; p<0·0001), and neurofilament light chain (β per year -0·05 [-0·09 to -0·001]; p=0·047) were also associated with faster handgrip strength decline, with no attenuation after adjusting for MMSE score. Sex-specific differences were observed, with female participants showing a stronger association between biomarker concentrations and muscle strength decline than male participants, particularly in the chair-stand test.

Our findings suggest that blood Alzheimer's disease-related biomarkers might help estimate progressive muscle strength decline among older adults, elucidating the influence of brain pathology and cognitive ageing on this association. These Alzheimer's disease-related biomarkers could aid in identifying individuals for early intervention to prevent sarcopenia.

The Swedish Research Council, the Swedish Ministry of Health and Social Affairs, and the County Councils and Municipalities.

Sarcopenia is recognized as a complex and multifactorial disorder that includes nutritional deficiency, inactivity, proinflammatory status, hormonal changes, neurological degeneration, and metabolic disturbances. It's pathogenesis is not fully understood. Therefore, identifying specific biomarkers of sarcopenia will help us understand its pathophysiology. The most frequently reported blood-derived biomarkers of sarcopenia are growth factors, neuromuscular junctions, endocrine systems, mitochondrial dysfunction, inflammation-mediated and redox processes, muscle protein turnover, blood metabolomics, and behavior-mediated biomarkers. Here, we address the implications of sarcopenia biomarkers based on our research experience with Korean Frailty and Aging Cohort Study cohort data. It includes free testosterone, myostatin, fibroblast growth factor 21 (FGF-21), growth differentiation factor 15 (GDF-15), procollagen type III N-terminal peptide (P3NP), creatinine-based biomarkers, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), brain-derived neurotrophic factor (BDNF), metabolites (proline, alanine, tryptophan), and multi-biomarker risk score. We attempted to explain the paradoxical findings of myostatin and FGF-21 levels in relation to sarcopenia. GDF-15 levels were associated with sarcopenia prevalence but not its incidence. Plasma P3NP and BDNF levels may be biomarkers of muscle quality rather than quantity. Lower erythrocyte eicosapentaenoic acid (EPA) and docosahexaenoic acid levels were associated with slow gait speed, and erythrocyte EPA levels were associated with low handgrip strength. We developed a multi-biomarker risk score for sarcopenia and found that its accuracy in diagnosing sarcopenia was higher than that of any single biomarker.

Investigating relationships between nutritional and clinical biochemistry biomarkers and skeletal muscle mass, strength and function (sarcopenic indices) may 1) highlight micronutrients of interest for potential preventive or treatment strategies for sarcopenia, or 2) highlight biomarkers that may be useful for identifying individuals at risk of sarcopenia.

Investigate associations between nutritional biomarkers (vitamin D, vitamin B12, folate, magnesium, potassium, calcium, and iron), clinical biomarkers (hemoglobin, ferritin, albumin, creatinine, and hemoglobin A1c: HbA1c), and sarcopenic indices (appendicular lean mass: ALM); height-adjusted ALM: ALMht; fat-free mass as a percentage of total body weight; extended short physical performance battery score: extSPPB; height-adjusted hand grip strength: HGSht; height-adjusted knee extension concentric strength, and; height-adjusted knee extension isometric strength) in males and females.

Using multivariable linear regression analysis, we investigated cross-sectional associations between biomarkers and sarcopenic indices in data collected from 1761 participants (age 22-103 y) from the Baltimore Longitudinal Study of Aging.

Hemoglobin was positively associated with ALM (β = 0.20, P = 0.021), HGSht (β = 0.25, P = 0.001), and extSPPB (β = 0.13, P = 0.024) in males, and with extSPPB in females (β = 0.15, P = 0.019). In males, serum iron was positively associated with ALMht (β = 0.0021, P = 0.038) and extSPPB (β = 0.0043, P = 0.045). In females, ferritin was positively associated with knee-extension strength measurements. Serum creatinine was positively associated with lean mass measures in males and females and with muscle strength and function measures in males with normal renal function (estimated glomerular filtration rate ≥60 mL/min/1.73 m2). In males, high HbA1c was associated with lower ALMht (β = -0.21, P = 0.023), extSPPB (β = -0.40, P = 0.027), and HGSht (β = -0.56, P = 0.031). In males and females, magnesium was positively associated with extSPPB, and potassium was positively associated with measures of knee-extension strength.

The associations found between measures of iron status and creatinine and sarcopenic indices, in males in particular, indicate potential importance for muscle health. Future longitudinal and intervention studies are warranted to confirm these findings.

Background: The assessment of appendicular skeletal muscle mass (ASM) is central to the diagnosis of sarcopenia (SA). We developed an anthropometric model for estimating ASM and tested its validity to identify SA and associated risk of disability (RSA) in older women. Methods: The equation was developed with 89 women (60-88 years, 72 ± 6 years), with a cross-validation sample of 12 women (60-84 years, 67 ± 5 years). Validity was determined through concordance between actual versus estimated ASMs, correlations between actual/estimated ASM versus peak torque (PT) and total work (TW) during isokinetic knee extension/flexion and handgrip strength, and agreement of patients classified with SA and RSA. Results: The predictive equation was ASM (kg) = 0.177 (body mass, kg)-0.075 (arm circumference, cm) + 0.020 (thigh circumference, cm) + 5.376 (R = 0.905; R 2 = 0.819; R 2ad = 0.809; F = 86.96; p < 0.0001; SEE = 1.35 kg). Agreement between actual and estimated ASMs was confirmed by validation (ICC = 0.81; p < 0.0001) and cross-validation samples (ICC = 0.72, p < 0.035). Regression characteristics in PRESS statistics (R 2 PRESS = 0.79; SEE-PRESS = 1.61) were compatible with the original model. Percent agreements for the classification of SA and RSA from indices calculated using actual/estimated ASM were 98% (gamma = 0.98, p = 0.015) and 68% (gamma = 0.89, p < 0.0001) in validation and 67% (gamma = 1.0, p = 0.032) and 70% (gamma = 0.84, p < 0.001) in cross-validation samples. Correlations between actual/estimated ASM versus PT (range 0.57-0.76, p < 0.05), TW (range 0.51-0.75, p < 0.05), and handgrip (range 0.67-0.74, p < 0.001) were theoretically consistent, being moderate and similar in both samples. Conclusion: This new anthropometric model has satisfactory prediction qualities and could be applied as a simple and practical method for estimating ASM in Brazilian older women.

Chemotherapy remains a central component of breast cancer treatment, significantly improving patient survival rates. However, its toxic side effects, along with cancer-related paraneoplastic syndromes, can lead to the loss of skeletal muscle mass and function, impairing physical abilities and increasing the risk of complications during treatment. Chemotherapeutic agents directly impact skeletal muscle cells by promoting protein degradation, inhibiting protein synthesis, and triggering systemic inflammation, all of which contribute to muscle atrophy. Additionally, these drugs can interfere with the proliferation and differentiation of stem cells, such as satellite cells, disrupting muscle regeneration and repair while inducing abnormal differentiation of intermuscular tissue, thereby worsening muscle wasting. These effects not only reduce the effectiveness of chemotherapy but also negatively affect patients' quality of life and disease prognosis. Recent studies have emphasized the role of exercise as an effective non-pharmacological strategy for preventing muscle loss and preserving muscle mass in cancer patients. This review examines the clinical manifestations of muscle dysfunction following breast cancer chemotherapy, the potential mechanisms underlying these changes, and the evidence supporting exercise as a therapeutic approach for improving muscle function.

The study aims to investigate the therapeutic effects of the aqueous extract of Atractylodes macrocephala Koidz. (AEA) on dexamethasone (Dex) -induced sarcopenia in mice and to explore its possible mechanisms of action.

This study utilized bioinformatics analysis to explore the primary pathogenic mechanisms of age-related sarcopenia and Dex-induced muscle atrophy. In animal experiments, a mouse model of muscle atrophy was established using Dex, and different doses of AEA were administered for treatment. The therapeutic effects of AEA were evaluated through tests of motor ability and histological analysis, and the molecular mechanisms predicted by bioinformatics were verified by measuring the expression levels of related genes.

Bioinformatics analysis suggests that there may be shared pathogenic mechanisms related to mitochondrial function and structure between age-related sarcopenia and Dex-induced muscle atrophy. Dex significantly reduced the mass, function, and cross-sectional area of muscle fibers in mice, and also induced changes in muscle fiber types. In contrast, AEA significantly ameliorated the aforementioned atrophic effects caused by Dex. The modulation of mitochondrial biogenesis and dynamics may be a crucial mechanism by which AEA exerts its anti-sarcopenia effects.

AEA can significantly alleviate the symptoms of Dex-induced skeletal muscle atrophy in mice by improving mitochondrial function, indicating its potential for clinical application in the prevention and treatment of age-related sarcopenia.

The Klotho gene is recognized for its anti-aging properties. Its downregulation leads to aging-like phenotypes, whereas overexpression can extend lifespan. Klotho protein exists in three forms: α-klotho, β-klotho and γ-klotho. The α-klotho has two isoforms: a membrane-bound form, primarily in the kidney and brain, and a secreted klotho protein present in blood, urine, and cerebrospinal fluid. Klotho functions as a co-receptor for fibroblast growth factor-23 (FGF23), regulating phosphate metabolism. The membrane-bound form controls various ion channels and receptors, while the secreted form regulates endocrine FGFs, including FGF19 and FGF21. The interaction between β-klotho and FGF21 in muscle is critical in the development of sarcopenic obesity. This systematic review, registered in PROSPERO and conducted following PRISMA guidelines, evaluates klotho levels in individuals with obesity or sarcopenic obesity. The study includes overweight, obese, and sarcopenic obese adults compared to those with a normal body mass index. After reviewing 713 articles, 20 studies were selected, including observational, cross-sectional, cohort studies, and clinical trials. Significant associations between klotho levels and obesity, metabolic syndrome (MS), and cardiovascular risk were observed. Exercise and dietary interventions positively influenced klotho levels, which were linked to improved muscle strength and slower decline. Klotho is a potential biomarker for obesity, MS, and sarcopenic obesity. Further research is needed to explore its mechanisms and therapeutic potential.

Sarcopenia is an age-related syndrome marked by a gradual decline in skeletal muscle mass and function. While various factors influencing sarcopenia have been studied, the link between daily sedentary time and sarcopenia remains underexplored.

This study analyzed the association between daily sitting time and sarcopenia using data from the National Health and Nutrition Examination Survey (NHANES 2011-2018). Daily sitting time was assessed through questionnaires, while sarcopenia was measured using body mass index (BMI) adjusted appendicular skeletal muscle mass (ASM). The relationship was analyzed using weighted logistic regression models and smoothing curves. Stratified analyses and interaction testing were employed to investigate population-specific characteristics of this association. Furthermore, chi-square test and grouped logistic regression were used to further analyze the impact of vigorous activity on the relationship between the two variables.

This study included 9998 participants with complete information. The fully adjusted model showed a significant positive correlation between daily sitting time and the prevalence of sarcopenia (OR = 1.07, 95% CI: 1.03-1.10, P = 0.0026). The group with daily sitting time ≥ 9 h had a 90% higher risk of sarcopenia compared to the < 4 h group (OR = 1.90, 95% CI: 1.22-2.84, P = 0.0040). Smooth curve fitting analysis showed a linear correlation between this relationship. Stratified analysis shows that non-Hispanic white men with a lower BMI (BMI < 25) have a higher risk of sarcopenia. Compared to those who actively participate in vigorous activities, individuals who lack recreational activities have a higher prevalence and risk of sarcopenia.

Our research has found that increased sedentary time significantly increases the risk of sarcopenia, especially among non-Hispanic white men with lower BMI. Additionally, individuals who lack vigorous physical activity also have a higher prevalence and risk of sarcopenia. Therefore, reducing sedentary behavior and increasing moderate exercise may be effective prevention strategies.

Body composition abnormalities are prognostic markers in several types of cancer, including colorectal cancer (CRC). Using our data distribution on body composition assessments and classifications could improve clinical evaluations and support population-specific opportune interventions. This study aimed to evaluate the distribution of body composition from computed tomography and assess the associations with overall survival among patients with CRC. In this multicenter cohort study, patients (N = 635) aged 18 years and older with CRC were observed for 12 to 36 months to assess outcomes. Skeletal muscle area (SM) and index (SMI), skeletal muscle radiodensity (SMD), intermuscular adipose tissue (IMAT), subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT) were evaluated, and classified based on tertile distributions. Low muscle mass (SMI) and poor muscle composition (SMD) were independent predictors of mortality regardless of follow-up period. This risk of mortality increased to more than 3-fold when combining both low SMI and low SMD (HRadjusted 3.1, 95% CI 1.8 to 5.4, respectively). Our study indicates that body composition characteristics may vary across countries, highlighting the need for developing sex- and population-specific cutoff values for computed tomography assessments in patients with different types of cancer.

One of the most pressing challenges facing society today is the rising prevalence of physical and cognitive frailty. This geriatric condition makes older adults more vulnerable to disability, illness, and a heightened risk of mortality. In this scenario, Parkinson's disease (PD) and geriatric frailty, which share several common characteristics, are becoming increasingly prevalent worldwide, underscoring the urgent need for innovative strategies. Nutraceuticals are naturally occurring bioactive compounds contained in foods, offering health benefits over and above essential nutrition. By examining the literature from the past decade, this review highlights how nutraceuticals can act as complementary therapies, addressing key processes, such as oxidative stress, inflammation, and neuroprotection. Notably, the antioxidant action of nutraceuticals appears particularly beneficial in regard to PD and geriatric frailty. For instance, antioxidant-rich nutraceuticals may mitigate the oxidative damage linked to levodopa therapy in PD, potentially reducing the side effects and enhancing treatment sustainability. Similarly, the antioxidant effects of nutraceuticals may amplify the benefits of physical activity, enhancing muscle function, cognitive health, and resilience, thereby reducing the risk of frailty. This review proposes a holistic approach integrating nutraceuticals with exercise, pharmacotherapy, and lifestyle adjustments. It promises to transform the management of ARD, prolong life, and improve the quality of life and well-being of older people.

As a common clinical manifestation, muscle weakness is prevalent in people with mobility disorders. Further studies of muscle weakness have found that patients with muscle weakness present with persistent muscle inflammation, loss of muscle fibers, fat infiltration, and interstitial fibrosis. Therefore, we propose the concept of muscle microenvironment homeostasis, which explains the abnormal pathological changes in muscles through the imbalance of muscle microenvironment homeostasis. And we identified an interstitial progenitor cell FAP during the transition from normal muscle microenvironment homeostasis to muscle microenvironment imbalance caused by muscle damage diseases. As a kind of pluripotent stem cell, FAPs do not participate in myogenic differentiation, but can differentiate into fibroblasts, adipocytes, osteoblasts, and chondrocytes. As a kind of mesenchymal progenitor cell, it is involved in the generation of extracellular matrix, regulate muscle regeneration, and maintain neuromuscular junction. However, the muscle microenvironment is disrupted by the causative factors, and the abnormal activities of FAPs eventually contribute to the complex pathological changes in muscles. Targeting the mechanisms of these muscle pathological changes, we have identified appropriate signaling targets for FAPs to improve and even treat muscle damage diseases. In this review, we propose the construction of muscle microenvironmental homeostasis and find the key cells that cause pathological changes in muscle after homeostasis is broken. By studying the mechanism of abnormal differentiation and apoptosis of FAPs, we found a strategy to inhibit the abnormal pathological changes in muscle damage diseases and improve muscle regeneration.

The objective of the present randomized trial was to verify the effect of twelve weeks of strength training with self-selected and imposed loads on muscle function, functionality, muscle quality, and perceptual and affective responses in elderly men and women. Twenty-four volunteers were divided into two groups of 12 individuals each: self-selected group (SS) (8 women, 4 men; mean age=66.92±6.18 years) and imposed group (IMP) (8 women, 4 men; mean age=65.33±2.42 years). The strength exercise program lasted 12 weeks (3 d/w). All exercises were performed on machines. The SS group was instructed to select a weight that would allow them to complete three sets of 10 repetitions, while the IMP group had the load imposed by the researchers following the exercise prescription model recommended by American College of Sports Medicine (ACSM). Rated perceived exertion (RPE) and affective responses were recorded at the end of each session. Muscle function, functionality, and muscle quality were assessed before and after the intervention. Both groups demonstrated similar improvements in strength and functional capacity. Furthermore, the SS group reported lower RPE and higher affective responses compared to the IMP group at 8-12 weeks. In summary, the findings from this study highlighted the effectiveness of both IMP and SS intensity resistance training programs in enhancing muscle strength and functional capacity among older adults.

Sarcopenia is a loss of muscle strength, muscle mass, and function that can increase a patient's risk of injury, illness, and can even severely impair quality of life and increase a patient's risk of death. A growing body of research suggests that sarcopenia and urinary tract disorders are closely related. In this review, we aimed to emphasize the definition of skeletal sarcopenia, summarize the methods used to diagnose skeletal sarcopenia, discuss the advances in the study of sarcopenia in benign diseases of the urinary system, discuss the advances in the study of sarcopenia in malignant diseases of the urinary system. Sarcopenia and urologic diseases interact with each other; urologic diseases cause sarcopenia, and sarcopenia aggravates the condition of the original disease, thus falling into a vicious circle. This review provides a comprehensive understanding of sarcopenia in urologic diseases, which is very important for the management and prognosis of urologic diseases.

There is an emerging and urgent need to identify biomarkers of sarcopenia. A novel sarcopenia index (SI), based on serum creatinine and cystatin C, has emerged as a potential biomarker for use. The SI can predict clinical outcomes and discriminate between the presence of sarcopenia in a range of chronic and acute conditions. However, the SI has not yet been tested in a large real-world general population dataset. This study aimed to investigate the accuracy of the SI in the identification of sarcopenia in a large prospective general population cohort.

Data were taken from UK Biobank, a large prospective epidemiological study in the United Kingdom (UK). Serum creatinine and cystatin C values were used to calculate the SI [creatinine (mg/dl)/cystatin C (mg/dl) × 100]. Probable sarcopenia was defined by maximum handgrip strength (HGS). Muscle mass was assessed using bioelectrical impedance analysis. Low muscle mass was defined as an appendicular lean mass (ALM) index below prespecified thresholds. Confirmed sarcopenia was defined as both low HGS and low muscle mass. Pearson correlation coefficients and logistic regression were used to explore the association between various sarcopenia traits (probable sarcopenia, low ALM index, and confirmed sarcopenia) and the SI. The diagnostic value of the SI was investigated using the area under the receiver operating characteristic curve (area under the curve, AUC).

458,702 participants were included in the analysis (46.4% males, mean age, males: 68.7 (±8.2) years; females: 68.2 (±8.0) years)). Probable sarcopenia was observed in 4.5% of males and 6.1% of females; low ALM index in 2.8% of males and 0.7% of females; confirmed sarcopenia in 0.3% of males and 0.1% of females. SI was significantly lower in individuals with confirmed sarcopenia (males: 86.3 ± 16.6 vs. 99.5 ± 15.3, p < .01; females: 73.6 ± 13.7 vs. 84.6 ± 14.0, p < .01). For every 1-unit increase in the SI, the odds of confirmed sarcopenia were reduced by 5% in males (odds ratio (OR): 0.95, p < 0.001) and 7% in females (OR: 0.923, p < 0.001). The AUC showed acceptable discriminative ability of confirmed sarcopenia (males: AUC = 0.731; females: AUC = 0.711).

Using a large real-world dataset of almost half a million people, our study indicated the SI has acceptable diagnostic accuracy when identifying those with sarcopenia and may be a useful biomarker to aid the stratification of those at risk and in need of intervention.

The emergency department is treating a growing number of older patients with frailty, which has been linked to poorer outcomes. Urgency is generally emphasized in the emergency department based on indicators such as triage scores and early warning scores for decision-making. However, this approach may not be sufficient for frail older people. The Frailty Index-laboratory (FI-lab) has been used as a simple assessment tool for frailty, but it may also reflect disease severity and predict adverse outcomes in the emergency care setting. Therefore, we aimed to evaluate the association between FI-lab in the emergency room and adverse outcomes during hospitalization through comparison with assessments using triage and early warning scores.

This was a retrospective cohort study conducted in a tertiary hospital. The study included patients aged 65 years or older who were admitted to the general internal medicine ward after being initially evaluated in the emergency department. FI-lab was calculated using 24 laboratory parameters from blood tests. The National Early Warning Score (NEWS), the Japan Triage and Acuity Scale (JTAS), and the modified JTAS were also used as prognostic indicators, and their association with adverse outcomes was compared with that of FI-lab.

In total, 872 patients (mean age, 80.9 years; male, 52.6 %) were analyzed. Patients who died during hospitalization had a higher FI-lab than those who survived. In multiple regression analysis, FI-lab, NEWS, and the modified JTAS were significantly associated with in-hospital death and prolonged length of hospital stay. In contrast, none of these indices were associated with in-hospital falls. The FI-lab was independently associated with the likelihood of discharge to home.

FI-lab evaluated in the emergency department reflected the severity of illness in acutely hospitalized older adults, similarly to NEWS and JTAS, and was a useful indicator for predicting adverse outcomes. These results may indicate the value of FI-lab for older adults in the acute care setting.

The progressive aging of the population has led to a rise in geriatric pathologies, with sarcopenia, characterized by muscle mass and function loss, becoming a crucial prognostic indicator. This study investigates sarcopenia in elderly hospitalized patients with advanced chronic liver disease (cirrhotic) and non-liver disease patients, comparing their prevalence and exploring correlations with anthropometric and biochemical factors. The cohort of 115 patients, including 50 cirrhotic and 65 non-cirrhotic individuals, exhibited significant comorbidities and a mean age of 78.4 years. Cirrhotic patients presented distinct laboratory parameters indicating liver damage. Applying European Working Group on Sarcopenia in Older People criteria, probable sarcopenia prevalence was similar in cirrhotic (62%) and non-cirrhotic (63%) patients. Stratifying probable sarcopenia into confirmed sarcopenia and dynapenia revealed no significant differences between populations. Correlation analyses demonstrated positive associations between Appendicular Skeletal Muscle Mass (ASM) and anthropometric parameters, malnutrition risk, and grip strength. In cirrhotic patients, muscle mass inversely correlated with liver damage. Odds ratio analysis highlighted the Mini Nutritional Assesment's (MNA) significant predictive capability for sarcopenia. ROC curve analysis affirmed MNA and biochemical markers' combined use, such as transferrin, albumin, total cholesterol, lymphocyte count and C-reactive protein as a strong predictor. Despite limitations, such as a small sample size, this study underscores the significance of thorough sarcopenia screening in elderly hospitalized patients, especially those with cirrhosis. Indeed, individuals with end-stage liver disease are particularly susceptible to sarcopenia. A more personalized approach utilizing tools like MNA and biochemical markers could prove beneficial. Further research is warranted to validate these findings and inform clinical interventions.

Recent studies have indicated that comorbidities such as sarcopenia and anemia can influence the prognosis of patients with colorectal cancer (CRC). However, the synergistic effects of sarcopenia and anemia on the survival of CRC patients are not yet comprehensively understood. This study aimed to investigate the relationship between anemia and sarcopenia and their synergistic effect on survival in patients with CRC.

A total of 1629 patients who underwent colorectal surgery were retrospectively reviewed. Patients were categorized into four hemoglobin-sarcopenia combined classifications (HS grade) according to their hemoglobin and skeletal muscle index (SMI) levels: hemoglobin low/SMI low (HS1), hemoglobin low/SMI high (HS2), hemoglobin high/SMI low (HS3), and hemoglobin high/SMI high (HS4). Association with overall survival (OS) was analyzed using both univariable and multivariable analyses.

In total, 1024 patients with stage I-III CRC were analyzed. Patient allocation according to HS grade was 124 (12.1%) in HS1, 298 (29.1%) in HS2, 135 (13.2%) in HS3, and 467 (45.6%) in HS4. The Kaplan-Meier curves of OS showed statistically significant differences according to anemia and sarcopenia status as well as to HS grade (all P < 0.001). Univariable analysis of factors associated with OS revealed statistical significance in absence of anemia (hazard ratio [HR] 0.550, 95% confidence interval [CI] 0.400-0.756, P < 0.001], absence of sarcopenia (HR 0.560, P < 0.001), and HS grade (HS2, HR 0.515, P = 0.002; HS3, HR 0.468, P = 0.006; HS4, HR 0.325, P < 0.001). Multivariable analysis showed that compared to the HS1 group, the HS2 and HS4 groups showed significantly better OS (HS2, HR 0.527, 95% CI 0.340-0.817, P = 0.004; HS4, HR 0.574, 95% CI 0.361-0.912, P = 0.018).

Sarcopenia, characterized by a low SMI and the presence of anemia before surgery, was associated with reduced OS among patients with non-metastatic CRC.

Plasma C-terminal agrin-fragment-22 (CAF22), a breakdown product of neuromuscular junction, is a potential biomarker of muscle loss. However, its levels from adolescence to octogenarians are unknown.

We evaluated young (18-34 years, n = 203), middle-aged (35-59 years, n = 163), and old men (60-87 years, n = 143) for CAF22, handgrip strength (HGS), appendicular skeletal-mass index (ASMI), and gait speed.

We found an age-associated increase in CAF22 from young (100.9 ± 29 pmol) to middle-aged (128.3 ± 38.7 pmol) and older men (171.5 ± 35.5 pmol) (all p<0.05). This was accompanied by a gradual reduction in HGS (37.7 ± 6.1 kg, 30.2 ± 5.2 kg, and 26.6 ± 4.7 kg, for young, middle-aged, and old men, respectively), ASMI (8.02 ± 1.02 kg/m2, 7.65 ± 0.92 kg/m2, 6.87 ± 0.93 kg/m2, for young, middle-aged, and old men, respectively), and gait speed (1.29 ± 0.24 m/s, 1.05 ± 0.16 m/s, and 0.81 ± 0.13 m/s, for young, middle-aged, and old men, respectively). After adjustment for age, we found negative regressions of CAF22 with HGS (- 0.0574, p < 0.001) and gait speed (- 0.0162, p < 0.001) in the cumulative cohort. The receiver operating characteristics analysis revealed significant efficacy of plasma CAF22 in diagnosing muscle weakness (HGS < 27 kg) (middle-aged men; AUC = 0.731, 95% CI = 0.629-0.831, p < 0.001, Older men; AUC = 0.816, 95% CI = 0.761-0.833, p < 0.001), and low gait speed (0.8 m/s) (middle-aged men; AUC = 0.737, 95% CI = 0.602-0.871, p < 0.001, older men; AUC = 0.829, 95% CI = 0.772-0.886, p < 0.001), and a modest efficacy in diagnosing sarcopenia (middle-aged men; AUC = 0.701, 95% CI = 0.536-0.865, p = 0.032, older men; AUC = 0.822, 95% CI = 0.759-0.884, p < 0.001) in middle-aged and older men.

Altogether, CAF22 increases with advancing age and may be a reliable marker of muscle weakness and low gait speed.

The present retrospective study reviewed the association among sarcopenia, myosteatosis, and overall survival (OS) in patients with postoperative colorectal cancer (CRC) with regard to age.

A retrospective study was conducted with a five-year follow-up.

Data from all patients with CRC, who underwent surgery between February 2005 and April 2014, were reviewed.

Data from 1053 patients (622 male [59.1%], 431 female [40.9%]; mean [± SD] age, 62.8 ± 11.8 years) were analyzed.

Patients were divided into three groups according to age: ≤50, 51-74, and ≥75 years. Data, including perioperative parameters, and the presence of sarcopenia and myosteatosis according to skeletal muscle index (SMI) and skeletal muscle radiodensity (SMD), respectively, were collected. Sarcopenia was evaluated using CT by calculating the SMI at the L3 level by dividing the area of the skeletal muscle by height squared (cm2/m2). SMD was also calculated using CT at the L3 level, but by evaluating fat attenuation according to Hounsfield units (HU).

Patient allocation according to age group was as follows: ≤50 years, n = 147 (14.0%); 51-74 years, n = 742 (70.5%); and ≥75 years, n = 164 (15.5%). The presence of sarcopenia and myosteatosis were statistically significant with increasing age (P = 0.004 and P < 0.001, respectively). The 51-74 years age group exhibited a significant association in OS for myosteatosis (P < 0.001) while the ≥75 years group was significantly associated with sarcopenia (P = 0.04) with regard to OS. Multivariable analysis also revealed a statistically significant association between myosteatosis in the 51-74 years age group (P = 0.033) and sarcopenia in the ≥75 years age group (P = 0.005) even when adjusted for recurrence status.

Different age groups exhibited significantly variable skeletal muscle indices. Although an abundance of irrefutable results demonstrated a correlation between CT-defined sarcopenia, myosteatosis, and clinical prognosis, data regarding age-dependent correlations are scarce. Results of this study demonstrated that sarcopenia and myosteatosis did not influence the prognosis of young patients with postoperative CRC (≤50 years of age), inferring the existence of significantly different skeletal muscle-related parameters according to age. Patients over 75 years of age showed significant association with sarcopenia while those in the 51-74 age group displayed significant link to myosteatosis. Clinicians should consider the impact of sarcopenia and myosteatosis on patient prognosis and should also be aware that the effect may differ according to patient age.

Given the high incidence of sarcopenia among Asians, it is imperative to identify appropriate intervention methods. The International Clinical Practice Guidelines for Sarcopenia, developed by the International Conference on Sarcopenia and Frailty Research (ICFSR) task force, recommends resistance training (RT) as a primary treatment for managing sarcopenia. Inflammatory biomarkers serve as indicators of sarcopenia. However, there is currently insufficient conclusive evidence regarding the effectiveness of RT in modulating inflammatory biomarker levels among Asian participants with sarcopenia.

Four databases were utilized for this study until October 9, 2023. This study focused on randomized controlled trials (RCTs) that examined the effects of RT on interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), and interleukin-10 (IL-10) about sarcopenia. This study has been registered in the PROSPERO database (CRD42024501855).

The meta-analysis included six studies from Asians involving 278 participants. The results showed a significant decrease in RT for IL-6 (weighted mean difference (WMD) = -0.73, 95% confidence interval (CI) = -1.02 to -0.44; n=5). However, no significant differences were found for TNF-α (WMD = -1.00, 95% CI = -2.47 to 0.46; n=5), CRP (WMD = -0.45, 95% CI = -1.14 to 0.23; n=3), and IL-10 (WMD = 0.13, 95% CI = -3.99 to 4.25; n=2). Subgroup analysis revealed that factors including gender selection, intervention methods, frequency, period, and duration could have a particular effect on the part of inflammatory biomarkers.

RT has been shown to reduce part of the level of inflammatory markers, specifically IL-6, in Asian sarcopenia participants. However, other inflammatory factors, such as TNF-α, CRP, and IL-10, did not show significant changes. Further research should confirm the impact of RT on these indicators and explore the potential effects of various factors on different inflammatory markers, such as diet, body composition, and medications.

https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=501855, identifier CRD42024501855.

The serum creatinine/cystatin C ratio (CCR) and the sarcopenia index (SI) are novel indicators for sarcopenia, but their accuracy may depend on various confounders. To assess CCR and SI diagnostic accuracy, we studied the clinical and biophysical parameters associated with sarcopenia or sarcopenic obesity. A total of 79 elderly patients (65-99 yrs, 33 females) underwent clinical, anthropometric, body composition, geriatric performance, and blood chemistry evaluation. The CCR and SI accuracy were assessed to identify sarcopenia. Sarcopenia was confirmed in 40.5%, and sarcopenic obesity in 8.9% of the subjects. Sarcopenic patients showed an increased Charlson comorbidity index, cardiovascular disease (CVD) rates and frailty, and decreased physical performance than non-sarcopenic subjects. Patients with sarcopenic obesity had increased body fat and inflammatory markers compared to obese subjects without sarcopenia. Sarcopenia was associated with a decreased CCR and SI. However, when the logistic regression models were adjusted for possible confounders (i.e., age, gender, Charlson comorbidity index, presence of CVD, and frailty score), a significant OR was confirmed for the CCR (OR 0.021, 95% CI 0.00055-0.83) but not for the SI. The AUC for the CCR for sarcopenia discrimination was 0.72. A higher performance was observed in patients without chronic kidney diseases (CKD, AUC 0.83). CCR, more than the SI, is a useful, non-invasive, and cost-effective tool to predict sarcopenia, irrespective of the potential confounders, particularly in subjects without CKD.

Cardiovascular disease (CVD) is closely associated with sarcopenia. We aimed to examine the relationship between Life's Essential 8 (LE8) and the incidence of sarcopenia among adults in the United States. In this study, a cross-sectional analysis was conducted using data from the National Health and Nutrition Examination Survey from 2013 to 2018 and included 5999 adult participants. LE8 score was categorized into low (< 49), moderate (49-79), and high CVH (≥ 79) groups and consisted of health behavior score and health factor score based on American Heart Association definitions. Sarcopenia was defined according to The Foundation for the National Institutes of Health Sarcopenia Project. Multivariate logistic regressions, restricted cubic spline regressions, and subgroup analyses were used to assess the association between LE8 and sarcopenia. LE8 and its subscales score were negatively associated with the incidence of sarcopenia in US adults.

Complex inflammatory crosstalk between muscular and adipose organs during ageing is controlled by adipokines and myokines. The Adiponectin/Leptin ratio (A/L ratio) has proven to be a promising biomarker for identifying insulin sensitivity, cardiovascular risk and adipose tissue inflammation. Although the A/L ratio has been related to inflammatory conditions, its ability to associate with or indicate the behavior of other inflammatory mediators remains unknown. The present study aimed to verify the association between the A/L ratio and a panel of inflammatory biomarkers in community-dwelling older women. The plasmatic concentrations of adiponectin, leptin, resistin, brain-derived neurotrophic factor (BDNF), interferon-gamma (IFN-γ), interleukins 2, 4, 5, 6, 8 and 10, tumour necrosis factor (TNF) and its soluble receptors (sTNF-r) 1 and 2 were evaluated in 71 community-dwelling older women with 75 (±7) years. The A/L ratio was negative and inverse correlated with BNDF (r = -0.29; p = 0.01), IL-8 (r = -0.37; p = 0.001) and sTNFr- 1 (r = -0.98; p < 0.001) levels. A strong and inverse association, with proportional effect, between A/L ratio and sTNFr-1 concentrations was found (Adjusted R2 = 0.22; β = -0.48; p > 0.001). It suggests that the presence of sTNFr-1 causes an inflammatory effect that affect cross-talk between muscle and adipose tissue, contributing to pro-inflammatory imbalance, which may have molecular and functional consequences. In addition, we provide insights into diagnostic biomarkers for inflammation, especially related to muscle wasting and intrinsic capacity in older people.

Progressive loss of peripheral muscle strength is highly pronounced in patients receiving maintenance hemodialysis (MHD), of which the pathological mechanism tends to be multifactorial. Plasma nickel was reportedly correlated with muscular strength in non-dialysis patients. However, scarce is known regarding the association between blood nickel level and handgrip strength among the patients undergoing MHD.

This cross-sectional study included patients undergoing MHD at our center in October 2021. Blood samples were collected before the hemodialysis sessions. Nickel level was measured using inductively coupled plasma mass spectrometry. Eligible patients were stratified into three groups by the blood nickel level: tertile 1 (≥ 5.2 ug/L); tertile 2 (< 5.2 ug/L and ≥ 4.5 ug/L); and tertile 3 (< 4.5 ug/L). Handgrip strength measurement was used to evaluate the muscle status. Spearman's analyses and multivariable linear regression analyses were performed to study the relationship between blood nickel level and handgrip strength.

A total of 236 patients were enrolled, with an average age of 55.51 ± 14.27 years and a median dialysis vintage of 83 (IQR: 48-125) months. Patients in group with a higher blood nickel level (tertile 1) tended to be female, had longer dialysis vintage and higher Kt/V, but lower BMI, serum creatinine, hemoglobin, and handgrip strength level (all p < 0.05). After adjustment for confounding factors in multivariable models, for every 1ug/L increase in nickel level, the patient's handgrip strength decreases by 2.81 kg (β: - 2.810, 95% confidence interval: - 5.036 to - 0.584, p = 0.014). Restricted cubic spline confirmed the relationship was nearly linear.

Our study highlighted that blood nickel level was related to handgrip strength in patients undergoing MHD. Prospective studies with larger sample sizes are still needed to confirm the result.

Untargeted metabolomics can be used to expand our understanding of the pathogenesis of sarcopenia. However, the metabolic signatures of sarcopenia patients have not been thoroughly investigated. Herein, we explored metabolites associated with sarcopenia by untargeted gas chromatography (GC)/liquid chromatography (LC)-mass spectrometry (MS) and identified possible diagnostic markers.

Forty-eight elderly subjects with sarcopenia were age and sex matched with 48 elderly subjects without sarcopenia. We first used untargeted GC/LC-MS to analyze the plasma of these participants and then combined it with a large number of multivariate statistical analyses to analyze the data. Finally, based on a multidimensional analysis of the metabolites, the most critical metabolites were considered to be biomarkers of sarcopenia.

According to variable importance in the project (VIP > 1) and the p-value of t-test (p < 0.05), a total of 55 metabolites by GC-MS and 85 metabolites by LC-MS were identified between sarcopenia subjects and normal controls, and these were mostly lipids and lipid-like molecules. Among the top 20 metabolites, seven phosphatidylcholines, seven lysophosphatidylcholines (LysoPCs), phosphatidylinositol, sphingomyelin, palmitamide, L-2-amino-3-oxobutanoic acid, and palmitic acid were downregulated in the sarcopenia group; only ethylamine was upregulated. Among that, three metabolites of LysoPC(17:0), L-2-amino-3-oxobutanoic acid, and palmitic acid showed very good prediction capacity with AUCs of 0.887 (95% CI = 0.817-0.957), 0.836 (95% CI = 0.751-0.921), and 0.805 (95% CI = 0.717-0.893), respectively.

These findings show that metabonomic analysis has great potential to be applied to sarcopenia. The identified metabolites could be potential biomarkers and could be used to study sarcopenia pathomechanisms.

Background: Physical weakness and cardiovascular risk increase significantly with age, but the underlying biological mechanisms remain largely unknown. This study aims to reveal the causal effect of circulating metabolites on frailty, sarcopenia and vascular aging related traits and diseases through a two-sample Mendelian Randomization (MR) analysis. Methods: Exposures were 486 metabolites analyzed in a genome-wide association study (GWAS), while outcomes included frailty, sarcopenia, arterial stiffness, atherosclerosis, peripheral vascular disease (PAD) and aortic aneurysm. Primary causal estimates were calculated using the inverse-variance weighted (IVW) method. Methods including MR Egger, weighted median, Q-test, and leave-one-out analysis were used for the sensitive analysis. Results: A total of 125 suggestive causative associations between metabolites and outcomes were identified. Seven strong causal links were ultimately identified between six metabolites (kynurenine, pentadecanoate (15:0), 1-arachidonoylglycerophosphocholine, androsterone sulfate, glycine and mannose) and three diseases (sarcopenia, PAD and atherosclerosis). Besides, metabolic pathway analysis identified 13 significant metabolic pathways in 6 age-related diseases. Furthermore, the metabolite-gene interaction networks were constructed. Conclusion: Our research suggested new evidence of the relationship between identified metabolites and 6 age-related diseases, which may hold promise as valuable biomarkers.

Skeletal muscle plays a critical role throughout the aging process. People living with sarcopenia, a progressive and generalized loss of skeletal muscle mass and function, often experience diminished quality of life, which can be attributed to a long period of decline and disability. Therefore, it is important to identify modifiable factors that preserve skeletal muscle and promote successful aging (SA). In this review, SA was defined as (1) low cardiometabolic risk, (2) preservation of physical function, and (3) positive state of wellbeing, with nutrition as an integral component. Several studies identify nutrition, specifically high-quality protein (eg, containing all essential amino acids), and long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), as positive regulators of SA. Recently, an additive anabolic effect of protein and n-3 PUFAs has been identified in skeletal muscle of older adults. Evidence further suggests that the additive effect of protein and n-3 PUFAs may project beyond skeletal muscle anabolism and promote SA. The key mechanism(s) behind the enhanced effects of intake of protein and n-3 PUFAs needs to be defined. The first objective of this review is to evaluate skeletal muscle as a driver of cardiometabolic health, physical function, and wellbeing to promote SA. The second objective is to examine observational and interventional evidence of protein and n-3 PUFAs on skeletal muscle to promote SA. The final objective is to propose mechanisms by which combined optimal intake of high-quality protein and n-3 PUFAs likely play a key role in SA. Current evidence suggests that increased intake of protein above the Recommended Dietary Allowance and n-3 PUFAs above the Dietary Guidelines for Americans recommendations for late middle-aged and older adults is required to maintain skeletal muscle mass and to promote SA, potentially through the mechanistical target of rapamycin complex 1 (mTORC1).

Sarcopenia is characterized by skeletal muscle quantitative and qualitative alterations. A marker of collagen turnover, procollagen type III N-terminal peptide (P3NP), seems to be related to those conditions. This study aims to assess the predictive role of P3NP in muscle density and physical performance changes. In the InCHIANTI study, a representative sample from the registry lists of two towns in Tuscany, Italy, was recruited. Baseline data was collected in 1998, and follow-up visits were conducted every 3 years. Out of the 1453 participants enrolled at baseline, this study includes 1052 participants. According to P3NP median levels, population was clustered in two groups; 544 (51.7%) of the 1052 subjects included were classified in the low median levels (LM-P3NP); at the baseline, they were younger, had higher muscle density, and performed better at the Short Physical Performance Battery (SPPB), compared to the high-median group (HM-P3NP).LM-P3NP cases showed a lower risk to develop liver chronic diseases, CHF, myocardial infarction, and osteoarthritis. HM-P3NP levels were associated with a longitudinal reduction of muscle density, and this effect was potentiated by the interaction between P3NP and leptin. Moreover, variation in physical performance was inversely associated with high level of P3NP, and directly associated with high fat mass, and with the interaction between P3NP and muscle density. Our data indicate that P3NP is associated with the aging process, affecting body composition, physical performance, and clinical manifestations of chronic degenerative age-related diseases.

This study aimed to examine the effects of 12 weeks of resistance training (RT) and vitamin D (VitD) supplementation on muscle strength and C-terminal agrin fragment (CAF) and Neurotrophin-3 (NT-3) concentrations as potential biomarkers in postmenopausal women.

This was a randomized double-blind placebo-controlled study. Forty-four healthy postmenopausal women (55.84 ± 4.70 years and 29.61 ± 4.26 kg/m2) were randomly assigned into four groups: (1) Resistance training + placebo (RT + PLA), (2) Vitamin D supplementation (VitD), (3) Resistance training + vitamin D (RT + VitD), and (4) Placebo (PLA). VitD was supplemented as an oral capsule containing 50000 IU of cholecalciferol every two weeks. RT involved leg press, chest press, leg extension, leg curl, and shoulder press exercises, performed with 3-4 sets at 70-85 % of 1RM, three times a week.

Circulating levels of CAF and NT-3 did not significantly change following the intervention period in the study groups (p > 0.05). There were significant increases in upper and lower body muscle strength and power for RT + VitD and RT + PLA ( < 0.05), but not for VitD or PLA (p > 0.05). The muscle function gains for RT + VitD and RT + PLA were higher than those for VitD and PLA but did not differ between them.

12-week of RT interventions resulted in significant increases in muscle strength and power in postmenopausal women. However, VitD supplementation did not result in any additional benefits. The positive changes in muscle function promoted by RT do not seem to be associated with changes in the neuromuscular joint via the CAF or NT-3 as potential biomarkers.

Sarcopenia is a skeletal muscle disorder characterized by progressive and generalized decline in muscle mass and function. Although it is mostly known as an age-related disorder, it can also occur secondary to systemic diseases such as malignancy or organ failure. It has demonstrated a significant relationship with adverse outcomes, e.g., falls, disabilities, and even mortality. Several breakthroughs have been made to find a pharmaceutical therapy for sarcopenia over the years, and some have come up with promising findings. Yet still no drug has been approved for its treatment. The key factor that makes finding an effective pharmacotherapy so challenging is the general paradigm of standalone/single diseases, traditionally adopted in medicine. Today, it is well known that sarcopenia is a complex disorder caused by multiple factors, e.g., imbalance in protein turnover, satellite cell and mitochondrial dysfunction, hormonal changes, low-grade inflammation, senescence, anorexia of aging, and behavioral factors such as low physical activity. Therefore, pharmaceuticals, either alone or combined, that exhibit multiple actions on these factors simultaneously will likely be the drug of choice to manage sarcopenia. Among various drug options explored throughout the years, testosterone still has the most cumulated evidence regarding its effects on muscle health and its safety. A mas receptor agonist, BIO101, stands out as a recent promising pharmaceutical. In addition to the conventional strategies (i.e., nutritional support and physical exercise), therapeutics with multiple targets of action or combination of multiple therapeutics with different targets/modes of action appear to promise greater benefit for the prevention and treatment of sarcopenia.

Sarcopenia, a geriatric syndrome characterized by progressive skeletal muscle mass and function decline, poses a significant health risk among the elderly, contributing to frailty, falls, hospitalization, loss of independence and mortality. The prevalence of sarcopenia varies significantly based on various factors, such as living status, demographics, measurement techniques and diagnostic criteria. Although the overall prevalence is reported at 10% in individuals aged 60 and above, disparities exist across settings, with higher rates in nursing homes and hospitals. Additionally, the differences in prevalence between Asian and non-Asian countries highlight the impact of cultural and ethnic factors, and variations in diagnostic criteria, cut-off values and assessment methods contribute to the observed heterogeneity in reported rates. This review outlines diverse diagnostic criteria and several measurement techniques supporting decision making in clinical practice. Moreover, it facilitates the selection of appropriate tools to assess sarcopenia, emphasizing its multifactorial nature. Various scientific groups, including the European Working Group of Sarcopenia in Older People (EWGSOP), the International Working Group on Sarcopenia (IWGS), the Asian Working Group on Sarcopenia (AWGS), the American Foundation for the National Institutes of Health (FNIH) and the Sarcopenia Definition and Outcomes Consortium (SDOC), have published consensus papers outlining diverse definitions of sarcopenia. The choice of diagnostic criteria should be aligned with the specific objectives of the study or clinical practice, considering the characteristics of the study population and available resources.

Sarcopenia, a complex and debilitating condition characterized by progressive deterioration of skeletal muscle, is the primary cause of age-associated disability and significantly impacts healthspan in elderly patients. Despite its prevalence among the aging population, the underlying molecular mechanisms are still under investigation. The NLRP3 inflammasome is crucial in the innate immune response and has a significant impact on diseases related to inflammation and aging. Here, we investigated the expression of the NLRP3 inflammasome pathway and pro-inflammatory cytokines in skeletal muscle and peripheral blood of dependent and independent patients who underwent hip surgery. Patients were categorized into independent and dependent individuals based on their Barthel Index. The expression of NLRP3 inflammasome components was significantly upregulated in sarcopenic muscle from dependent patients, accompanied by higher levels of Caspase-1, IL-1β and IL-6. Among older dependent individuals with sarcopenia, there was a significant increase in the MYH3/MYH2 ratio, indicating a transcriptional shift in expression from mature to developmental myosin isoforms. Creatine kinase levels and senescence markers were also higher in dependent patients, altogether resembling dystrophic diseases and indicating muscle degeneration. In summary, we present evidence for the involvement of the NLRP3/ASC/NEK7/Caspase-1 inflammasome pathway with activation of pro-inflammatory SASP in the outcome of sarcopenia in the elderly.

Biomarkers are emerging as a potential tool for screening or diagnosing sarcopenia. We aimed to summarize the current evidence on the diagnostic test accuracy of biomarkers for sarcopenia. We comprehensively searched Ovid MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials up to January 2023 and only included diagnostic test accuracy studies. We identified 32 studies with 23,840 participants (women, 58.26%) that assessed a total of 30 biomarkers. The serum creatinine to cystatin C ratio (Cr/CysC) demonstrated a pooled sensitivity ranging from 51% (95% confidence interval [CI] 44-59%) to 86% (95% CI 70-95%) and a pooled specificity ranged from 55% (95% CI 38-70%) to 76% (95% CI 63-86%) for diagnosing sarcopenia defined by five different diagnostic criteria (11 studies, 7240 participants). The aspartate aminotransferase to alanine aminotransferase ratio demonstrated a pooled sensitivity of 62% (95% CI 56-67%) and a pooled specificity of 66% (95% CI 60-72%) (3 studies, 11,146 participants). The other 28 blood biomarkers exhibited low-to-moderate diagnostic accuracy for sarcopenia regardless of the reference standards. In conclusion, none of these biomarkers are optimal for screening or diagnosing sarcopenia. Well-designed studies are needed to explore and validate novel biomarkers for sarcopenia.

It is required to consider multiple biomarkers simultaneously to predict sarcopenia and to understand its complex pathological mechanisms. This study aimed to develop multiple biomarker panels for predicting sarcopenia in older adults and to further examine its association with the incidence of sarcopenia.

A total of 1,021 older adults were selected from the Korean Frailty and Aging Cohort Study. Sarcopenia was defined by the Asian Working Group for Sarcopenia 2019 criteria. Among the 14 biomarker candidates at baseline, eight biomarkers that could optimally detect individuals with sarcopenia were selected to develop a multi-biomarker risk score (range from 0 to 10). The utility of developed multi-biomarker risk score in discriminating sarcopenia was investigated using receiver operating characteristic (ROC) analysis.

The multi-biomarker risk score had an area under the ROC curve (AUC) of 0.71 with an optimal cut-off of 1.76 score, which was significantly higher than all single biomarkers with AUC of <0.7 (all, p<0.01). During the two-year follow-up, the incidence of sarcopenia was 11.1%. Continuous multi-biomarker risk score was positively associated with incidence of sarcopenia after adjusting confounders (odds ratio [OR]=1.63; 95% confidence interval [CI]=1.23-2.17). Participants with a high risk score had higher odds of sarcopenia than those with a low risk score (OR=1.82; 95% CI=1.04-3.19).

Multi-biomarker risk score, which was a combination of eight biomarkers with different pathophysiologies, better discriminated the presence of sarcopenia than a single biomarker, and it could further predict the incidence of sarcopenia over two years in older adults.

Sarcopenia involves in the loss of muscle mass associated with aging, which is the major cause of progressive muscle weakness and deterioration in older adults. Muscle atrophy is a direct presentation of sarcopenia, and it greatly contributes to the decline in quality of life among older adults. Neuromuscular junction (NMJ) stability is the key link to maintain muscle function. Besides, the degenerative change of NMJ promotes the process of muscle atrophy in the elderly. Based on previous transcriptome sequencing and bioinformatics analyses of aged muscle, this study used the 18-month-old aged mouse model and the 6-month-old young mouse model to deliberate the role and underlying mechanisms of Cullin-3 (Cul3) in age-related muscle atrophy. The results of reverse transcriptase polymerase chain reaction (RT-PCR) and immunoblotting analysis showed that the expression of CUL3 increased in aged muscle tissue, while the expression level of postsynaptic membrane nicotinic acetylcholine receptors (nAChRs) decreased significantly, which manfested a negative correlation. Meanwhile, immunofluorescence demonstrated that Cul3 was highly expressed in senile muscle NMJ. The results of ubiquitin indicated that the ubiquitin level of aged muscle nAChRs was evidently increased. Co-immunoprecipitation furtherly verified the correlation between Cul3 and nAChRs. Taken together, Cul3 may mediate the ubiquitination degradation of nAChRs protein at the NMJ site in aged mice, leading to NMJ degeneration and accelerated atrophy of fast-twitch muscle fibers in aged muscle. As a prominent element to maintain the stability of NMJ, Cul3 is supposed to be one of candidate intervention targets in sarcopenia.

Skeletal muscle gauge (SMG) was recently introduced as an imaging indicator of sarcopenia. Computed tomography is essential for measuring SMG; thus, the use of SMG is limited to patients who undergo computed tomography. We aimed to develop a machine learning algorithm using clinical and inflammatory markers to predict SMG in patients with colorectal cancer.

The least absolute shrinkage and selection operator regression model was applied for variable selection and predictive signature building in the training set. The predictive accuracy of the least absolute shrinkage and selection operator model, defined as linear predictor (LP)-SMG, was compared using the area under the receiver operating characteristic curve and decision curve analysis in the test set.

A total of 1094 patients with colorectal cancer were enrolled and randomly categorized into training (n = 656) and test (n = 438) sets. Low SMG was identified in 142 (21.6%) and 90 (20.5%) patients in the training and test sets, respectively. According to multivariable analysis of the test sets, LP-SMG was identified as an independent predictor of low SMG (odds ratio = 1329.431; 95% CI, 271.684-7667.996; P < .001). Its predictive performance was similar in the training and test sets (area under the receiver operating characteristic curve = 0.846 versus 0.869; P = .427). In the test set, LP-SMG had better outcomes in predicting SMG than single clinical variables, such as sex, height, weight, and hemoglobin.

LP-SMG had superior performance than single variables in predicting low SMG. This machine learning model can be used as a screening tool to detect sarcopenic status without using computed tomography during the treatment period.

As clinical tests, such as gait speed, require nervous system integrity to be performed properly, sarcopenia shares features with neurological diseases. Neurofilament light chains (NF-L) are now used as a blood-biomarker of neuronal damage, and its expression might be altered in sarcopenia. We aimed to assess NF-L concentrations in a large cohort of older individuals screened for sarcopenia.

The SarcoPhAge cohort is a Belgian cohort of 534 community-dwelling older adults with an ongoing 10-year follow-up. Sarcopenia diagnosis was established at inclusion according to the European Working Group on Sarcopenia in Older People 2 (EWGSOP2) criteria. Muscle strength was evaluated with a hydraulic hand dynamometer, appendicular lean mass by Dual-Energy X-ray Absorptiometry (DXA) and physical performance by the Short Physical Performance Battery (SPPB). NF-L was measured on all available sera collected at the time of inclusion (n = 409) using SiMoA technology (Quanterix°).

In the multivariate model, NF-L was associated with performance tests such as gait speed (p < 0.0001) and SPPB scores (p = 0.0004). An association was also observed with muscle strength (p = 0.0123) and lean mass (p = 0.0279). In the logistic regression model, NF-L was an independent predictor of severe sarcopenia (p = 0.0338; OR = 20.0; 95% CI 1.39-287.7) with satisfactory diagnostic accuracy (AUC: 0.828) and subjects with an SPPB score ≤ 8 had higher odds of having increased NF-L (p < 0.0001; OR = 23.9; 95% CI 5.5-104).

These data highlight the potential for using NF-L to investigate the pathophysiology of sarcopenia severity and the neurological features associated with performance tests. However, these results need to be confirmed with other cohorts in different settings.

C-terminal agrin fragment (CAF) is a biomarker for neuromuscular junction degradation. This study aimed to investigate whether 110-kDa CAF (CAF110) was associated with the presence and incidence of low muscle mass and strength.

This cross-sectional retrospective cohort study comprised women aged ≥65 years. We measured muscle mass using a dual-energy X-ray absorptiometry scanner, hand-grip strength, and blood sampling between 2011 and 2012. A follow-up study with the same measurements was conducted between 2015 and 2017. Low muscle mass and strength were defined as an appendicular skeletal muscle mass index <5.4 kg/m2 and hand-grip strength <18 kg, respectively. The CAF110 level was measured using enzyme-linked immunosorbent assay kits.

In total, 515 women (74.3 ± 6.3 years) were included in this cross-sectional analysis. Of these, 101 (19.6%) and 128 (24.9%) women presented with low muscle mass and strength, respectively. For low muscle mass, the odds ratios (ORs) of the middle and highest CAF110 tertile groups, compared with the lowest group, were 1.93 (95% confidence interval: 1.09-3.43; P = 0.024) and 2.15 (1.22-3.80; P = 0.008), respectively. After adjusting for age, the ORs remained significant: 1.98 (1.11-3.52; P = 0.020) and 2.27 (1.28-4.03; P = 0.005), respectively. Low muscle strength ORs of all the CAF110 tertile groups were not significant. In the longitudinal analysis, 292 and 289 women were assessed for incidents of low muscle mass and strength, respectively. Of those, 34 (11.6%) and 20 (6.9%) women exhibited low muscle mass and strength, respectively. For incident low muscle mass, the crude OR of the CAF110 ≥ the median value group was marginally higher than that of the CAF110 < median value group (median [interquartile range]: 1.98 [0.94-4.17] (P = 0.072). After adjusting for age and baseline muscle mass, the OR was 2.22 [0.97-5.06] (P = 0.058). All low muscle strength ORs of the median categories of CAF110 were not significant.

CAF110 was not associated with low muscle strength. However, CAF110 may be a potential marker for the incidence of low muscle mass.

Sarcopenia and anemia are common diseases in the elderly and are caused by various factors. In this study, the association between sarcopenia and anemia in an elderly Korean population was examined. The Korea Centers for Disease Control and Prevention's cross-sectional, nationally representative Korea National Health and Nutrition Examination Survey (KNHANES, 2008-2011) served as the source of the data for this study. Of the 2769 participants (1167 men and 1602 women) included in this study, a significant association was found between sarcopenia and anemia in the elderly in Korea. In Model 1, unadjusted for covariates, the prevalence of sarcopenia in all participants was 1.805 (95% CI 1.364-2.388) and 2.746 (95% CI 1.740-4.334) in men, and 1.494 (95% CI 1.045-2.138) in women. In Model 4, adjusted for all covariates, the prevalence of sarcopenia in all participants was 1.455 (95% CI 1.064-1.989) and 2.649 (95% CI 1.475-4.755) in men, but it was insignificant in women. While prior studies failed to consider variables such as exercise status and nutritional intake, this research incorporated these factors as covariates. Despite this comprehensive approach, this study still revealed an independent association between sarcopenia and anemia. Moreover, a significant association was uncovered among elderly men, with no corresponding association identified among women.

Sarcopenia is highly prevalent in heart failure (HF) patients, and the involvement of biomarkers in its pathophysiology is suggested, but little has been studied concerning HF sarcopenic patients.

To evaluate the association between inflammatory and humoral markers with sarcopenia, as well as the impact of sarcopenia on quality of life and functional capacity in older HF patients.

In this cross-sectional study, 90 outpatient HF patients, aged ≥ 60 years, were evaluated for sarcopenia (EWGSOP2 diagnostic criteria), inflammation (high-sensitive C-reactive protein [hs-CRP], Interleukin-6 [IL-6], tumor necrosis factor alpha [TNF-α]) and humoral markers (total testosterone and insulin-like growth factor-1 [IGF-1]), physical activity (International Physical Activity Questionnaire), quality of life (Minnesota Living with Heart Failure Questionnaire), and functional capacity (6-minute walk test). The adopted level of significance was p<0.05.

Patients had a mean age of 69.4 ± 7.2 years, 67.8% were male, with left ventricular ejection fraction (LVEF) of 35.9 ± 11.9% and 22 (24.4%) were sarcopenic. Age (73.1 ± 8.1 and 68.3 ± 6.5 years; p= 0.006), body mass index (BMI) (23.1 ± 2.8 and 28.2 ± 4.2 kg/m2; p <0.001), and LVEF (29.9 ± 8.8 and 37.9 ± 12.1%; p= 0.005) were different between groups with and without sarcopenia, respectively. After adjusting for age, ethnicity, BMI, LVEF, and the use of angiotensin converting enzyme inhibitors/angiotensin receptor blockers, sarcopenia was associated with higher serum levels of IL-6 and worse functional capacity.

In HF patients, sarcopenia was associated with IL-6 levels and functional capacity.