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Sarcopenia (muscle wasting) and cachexia share some pathophysiological aspects. Sarcopenia affects approximately 20 %, cachexia <10 % of ambulatory patients with heart failure (HF). Whilst sarcopenia means loss of skeletal muscle mass and strength that predominantly affects postural rather than non-postural muscles, cachexia means loss of muscle and fat tissue that leads to weight loss. The wasting continuum in HF implies that skeletal muscle is lost earlier than fat tissue and may lead from sarcopenia to cachexia. Both tissues require conservation, and therapies that stop the wasting process have tremendous therapeutic appeal. The present paper reviews the pathophysiology of muscle and fat wasting in HF and discusses potential treatments, including exercise training, appetite stimulants, essential amino acids, growth hormone, testosterone, electrical muscle stimulation, ghrelin and its analogues, ghrelin receptor agonists and myostatin antibodies.

\"Research shows that building muscle helps the body burn more calories 24/7 and that resistance training is the most effective way to torch body fat. Yet that message is still lost on many women who fear that weight lifting will make them bulky, turn their skin green, and give them Incredible Hulk muscles like their boyfriends'. Women have more options than step aerobics or running on a treadmill to shed pounds: They can weight-train in a very specific manner designed to make the most of a woman's unique physiology. Lift to Get Lean is the first beginner's guide to strength training from Women's Health that is written specifically for women by a woman. Holly Perkins is a certified strength and conditioning specialist (CSCS) who has been teaching the fat-burning secrets of weight training exclusively to women for more than 20 years. Perkins doesn't follow men's rules when it comes to building muscle. Her Lift to Get Lean delivers a three-step system: Technique, Movement Speed, and the Last 2 Reps Rule, which make all the difference in developing the kind of strong, lean, and sexy body women want. Perkins offers four different 90-day training programs that efficiently build functional strength along with leaner legs, stronger arms, and a sexier butt\"-- Provided by publisher.

Background Insulin resistance and muscle loss are interrelated processes linked to cardiovascular disease (CVD), but they are rarely assessed together. We investigated the association between a novel integrated biomarker—triglyceride–glucose muscle-loss index (TyG–MLI)—and incident CVD in a large prospective cohort. Methods A total of 277,418 UK Biobank participants free of CVD at baseline were included. TyG–MLI was calculated as ln[(triglycerides × fasting glucose)/2] × (cystatin C/creatinine). Incident CVD was identified through hospital admissions and death registries. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results Over a median follow-up of 15.1 years, 40,398 participants developed CVD. Crude CVD incidence increased steadily across TyG–MLI quartiles, and the cumulative incidence curves demonstrated clear separation on Kaplan–Meier analysis (log-rank p  < 0.001). Higher TyG–MLI was independently associated with greater CVD risk when modeled either continuously (per 1-SD: HR 1.17; 95% CI 1.16–1.18) or categorically (Q4 vs. Q1: HR 1.48; 95% CI 1.44–1.53). Restricted cubic spline analyses demonstrated a non-linear association across the TyG–MLI distribution. Sensitivity analyses yielded consistent results. In body mass index-stratified analyses, TyG–MLI showed stronger associations with CVD than TyG index, particularly among normal-weight and underweight individuals. Conclusions TyG–MLI, a composite marker reflecting insulin resistance and muscle loss, was independently associated with incident CVD in this large population-based cohort. These findings suggest that TyG–MLI captures cardiometabolic risk beyond traditional measures and may be particularly informative in individuals without obesity. Graphical abstract

Background Currently, the effect of skeletal muscle loss during neoadjuvant imatinib therapy on clinical outcomes in patients with locally advanced gastrointestinal stromal tumors (LA-GIST) remains unclear. This study aims to investigate the relationship between changes in skeletal muscle and postoperative complications, survival and tumor response in patients with LA-GIST during neoadjuvant therapy with imatinib. Methods We retrospectively analyzed pre- and post-treatment computed tomography images of 57 GIST patients who underwent radical surgery after neoadjuvant therapy with imatinib from January 2013 to March 2019. Skeletal muscle index (SMI) was measured at the L3 vertebral level in all patients. A cut-off value (SMI < 52.3 cm 2 /m 2 and < 38.6 cm 2 /m 2 for men and women, respectively) published in a previous study was used to define sarcopenia. Based on gender, we defined ΔSMI (%)/250 days above 9.69% for men and ΔSMI (%)/250 days above 7.63% for women as significant muscle loss (SML). Factors associated with postoperative complications and tumor response were analyzed using logistic regression, and predictors affecting patient prognosis were analyzed using Cox regression. Results Of the 57 patients, sarcopenia was present before and after neoadjuvant therapy in 20 (35.09%) and 28 (49.12%) patients, respectively. It was not associated with immediate or long-term clinical outcomes. However, patients with SML during neoadjuvant therapy had a higher incidence of postoperative complications (60.00% vs. 25.00%, p  = 0.008), worse pathological regression (44.00% vs. 75.00%, p  = 0.017) and worse 3-year survival (Male, 68.75% vs. 95.45%, p  = 0.027; Female, 66.67% vs. 100.00%, p  = 0.046) than patients without SML. Conclusion The development of SML during neoadjuvant therapy in LA-GIST patients, rather than pre- and post-treatment sarcopenia, is a major prognostic factor for the long-term prognosis and is also associated with recent postoperative complication rates and pathological regression.

Background/Objectives: Sarcopenia, defined as the progressive loss of muscle mass and function, is increasingly recognized in pediatric cancer patients as a significant clinical and prognostic factor. Sarcopenia in children arises from malignancy-related inflammation, malnutrition, and treatment toxicity, negatively affecting treatment response, recovery, and quality of life. Methods: We searched MEDLINE and Scopus for English-written articles published over the last five years using synonyms for the terms “sarcopenia” and “pediatric cancer”. Screening and data extraction were performed in a duplicate-blinded method. We qualitatively synthesized eligible articles. Results: Recent studies identify pre-treatment sarcopenia as a marker of poor prognosis, especially in hepatoblastoma and neuroblastoma. Total psoas muscle area (tax) and skeletal muscle index (SMI) are emerging diagnostic tools, though standardized methods remain lacking. Sarcopenia’s etiology is multifactorial, involving impaired mitochondrial metabolism, chemotherapy-induced appetite loss, and systemic inflammation. Sarcopenic obesity is common, particularly among leukemia survivors, often masked by normal BMI. Survivors also face reduced bone density, impaired immunity, and persistent muscle loss, linked to prior therapies such as radiotherapy and hematopoietic stem cell transplantation. Increase in muscle mass post-treatment correlates with better survival outcomes. Conclusions: Early detection of sarcopenia can support timely interventions such as nutritional support and physical activity. Yet, significant diagnostic heterogeneity across existing studies hampers definitive conclusions regarding its true prevalence and the optimal assessment method. Standardized diagnostic criteria are urgently needed to enable more reliable prevalence estimates and evidence-based clinical strategies.

There is currently a substantial volume of research underway to develop more effective approaches for the regeneration of functional muscle tissue as treatment for volumetric muscle loss (VML) injury, but few studies have evaluated the relationship between injury and the biomechanics required for normal function. To address this knowledge gap, the goal of this study was to develop a novel method to quantify the changes in gait of rats with tibialis anterior (TA) VML injuries. This method should be sensitive enough to identify biomechanical and kinematic changes in response to injury as well as during recovery. Control rats and rats with surgically-created VML injuries were affixed with motion capture markers on the bony landmarks of the back and hindlimb and were recorded walking on a treadmill both prior to and post-surgery. Data collected from the motion capture system was exported for analysis in OpenSim and Matlab. force testing indicated that the VML injury was associated with a significant deficit in force generation ability. Analysis of joint kinematics showed significant differences at all three post-surgical timepoints and gait cycle phase shifting, indicating augmented gait biomechanics in response to VML injury. In conclusion, this method identifies and quantifies key differences in the gait biomechanics and joint kinematics of rats with VML injuries and allows for analysis of the response to injury and recovery. The comprehensive nature of this method opens the door for future studies into dynamics and musculoskeletal control of injured gait that can inform the development of regenerative technologies focused on the functional metrics that are most relevant to recovery from VML injury.

Background Decreased size and mass of paraspinal muscles are associated with lower vertebral bone mineral density, more postoperative complications, increased mortality, and spinal sagittal imbalance. However, it is difficult to determine muscle loss in older adults with overweight and obesity. This study aimed to investigate the effects of body mass index (BMI) and central obesity on paraspinal muscle aging and to determine cutoff values for low paraspinal muscle mass/quality in Chinese community populations. Methods In this nationwide cross-sectional study, abdominal CT scans and basic information were collected and analyzed from 4,305 community-dwelling adults from twelve representative cities in China between 2013 and 2017. Psoas and posterior paraspinal muscle index (PMI and PSMI) and density (PMD and PSMD) at the L3 level were measured using OsiriX software. Correlation analysis, multiple linear regression, and one-way ANOVA were performed for statistical analysis. Commonly used cutoff value calculations were applied to define low muscle index and density (Mean–2SD, 5th percentile in young people, and 20th percentile in older people) in the general population and individuals with different BMIs. Results Correlation analysis showed that the paraspinal muscle index and density were primarily correlated with sex, BMI, and age. Multiple linear regression analysis indicated that the paraspinal muscle index (PSMI and PMI) was primarily influenced by sex (β=–0.391 and − 0.599, p  < 0.001) and BMI (β = 0.442 and 0.371, p  < 0.001), followed by age and waist circumference. In contrast, muscle density (PSMD and PMD) was mainly associated with sex (β=–0.405 and − 0.317, p  < 0.001) and age (β=–0.409 and − 0.429, p  < 0.001), with a slight influence from WC and BMI. Considering the significant effect of BMI on muscle mass, we calculated BMI-stratified cutoffs for PSMI (as 12.3/10.6, 15.0/11.7, and 15.2/11.9 cm 2 /m 2 in normal, overweight, and obese men/women using M-2SD), PMI (as 3.8/2.9, 5.0/3.4, and 4.9/3.9 cm 2 /m 2 in normal, overweight and obese men/women using M-2SD), and unstratified cutoffs for PSMD (as 36.3 and 31.1 HU in men and women) and PMD (as 40.1 and 36.9 HU in men and women). Conclusions This study found that sex and BMI were key determinants of paraspinal muscle mass, with BMI influencing paraspinal muscle number more than age. In contrast, muscle density was primarily influenced by sex and age. This study provided BMI-stratified and non-stratified cutoff values for low paraspinal muscle index and density, which aided in the identification of spinal sarcopenia in individuals with different BMIs.

Age-related skeletal muscle loss, sarcopenia, cachexia and wider malnutrition (under nutrition) are complex in aetiology with interaction of clinical, social and economic factors. Weight loss and loss of skeletal muscle mass in older people are associated with increased morbidity and mortality with implications for increasing health and social care costs. There is insufficient evidence to identify the ideal treatment options. However, preventing weight loss and loss of skeletal muscle in older age will be keys to reducing morbidity and mortality. This will require all those coming into contact with older people to identify and address weight loss early, including through diet, improving physical activity and increasing social interaction. Public health messages on diet should, in the main, continue to focus on older people achieving current UK dietary recommendations for their age as visually depicted in the eatwell plate together with associated messages regarding dietary supplements where appropriate.

Background Surgery-related loss of muscle quantity negatively affects postoperative outcomes. However, changes of muscle quality have not been fully investigated. A perioperative intervention targeting identified risk factors could improve postoperative outcome. This study investigated risk factors for surgery-related loss of muscle quantity and quality and outcomes after liver resection for colorectal liver metastasis (CRLM). Methods Data of patients diagnosed with CRLM who underwent liver resection between 2006 and 2016 were analysed. Muscle quantity (psoas muscle index [PMI]), and muscle quality, (average muscle radiation attenuation [AMA] of the psoas), were measured using computed tomography. Changes in PMI and AMA of psoas after surgery were assessed. Results A total of 128 patients were analysed; 67 (52%) had surgery-related loss of muscle quantity and 83 (65%) muscle quality loss. Chronic obstructive pulmonary disease (COPD) ( P  = 0.045) and diabetes ( P  = 0.003) were risk factors for surgery-related loss of muscle quantity. A higher age ( P  = 0.002), open resection ( P  = 0.003) and longer operation time ( P  = 0.033) were associated with muscle quality loss. Overall survival was lower in patients with both muscle quantity and quality loss compared to other categories ( P  = 0.049). The rate of postoperative complications was significantly higher in the group with surgery-related loss of muscle quality. Conclusions Risk factors for surgery-related muscle loss were identified. Overall survival was lowest in patients with both muscle quantity and quality loss. Complication rate was higher in patients with surgery-related loss of muscle quality.