Progressive Loss Of Muscle Mass Research Articles

Zingiber Officinale Roscoe Prevents Cellular Senescence of Myoblasts in Culture and Promotes Muscle Regeneration.

Background Ageing resulted in a progressive loss of muscle mass and strength. Increased oxidative stress in ageing affects the capacity of the myoblast to differentiate leading to impairment of muscle regeneration. Zingiber officinale Roscoe (ginger) has potential benefits in reversing muscle ageing due to its antioxidant property. This study aimed to determine the effect of ginger in the prevention of cellular senescence and promotion of muscle regeneration. Methods Myoblast cells were cultured into young and senescent state before treated with different concentrations of ginger standardised extracts containing different concentrations of 6-gingerol and 6-shogaol. Analysis on cellular morphology and myogenic purity was carried out besides determination of SA-β-galactosidase expression and cell cycle profile. Myoblast differentiation was quantitated by determining the fusion index, maturation index, and myotube size. Results Treatment with ginger extracts resulted in improvement of cellular morphology of senescent myoblasts which resembled the morphology of young myoblasts. Our results also showed that ginger treatment caused a significant reduction in SA-β-galactosidase expression on senescent myoblasts indicating prevention of cellular senescence, while cell cycle analysis showed a significant increase in the percentage of cells in the G0/G1 phase and reduction in the S-phase cells. Increased myoblast regenerative capacity was observed as shown by the increased number of nuclei per myotube, fusion index, and maturation index. Conclusions Ginger extracts exerted their potency in promoting muscle regeneration as indicated by prevention of cellular senescence and promotion of myoblast regenerative capacity.

Sarcopenia in patients with chronic obstructive pulmonary disease: A study of prevalence and associated factors in Western Greek population.

Background:Chronic obstructive pulmonary disease (COPD) is associated with a progressive loss of muscle mass and function and a systemic inflammatory process that can cause sarcopenia.Objective:The objective of this study is to estimate the prevalence rate of sarcopenia in COPD patients and to determine the factors associated with sarcopenic patients living in Western Greece.Methods:European Working Group on Sarcopenia in Older People criteria were applied to 69 outpatients with stable COPD. Body composition, exercise capacity, functional performance, physical activity, and health status were also assessed. COPD disease severity (COPD stage) was evaluated with the Global Initiative for chronic obstructive lung disease. The study protocol was approved by the Ethical Committee of the Technological Educational Institute of Western Greece.Results:The sample comprised 69 patients (59 women and 10 men), with a mean age of 71.33 ± 7.48 years. The prevalence of sarcopenia was 24.6% (n = 17). A high percentage (82.6%; n = 57) of the 69 Greek participants did not perform any regular exercise. The findings of this study demonstrated that sarcopenia was positively associated with COPD, age, body mass index, skeletal muscle mass, hand grip strength, and 4 m test.Conclusions:In conclusion, there is a 24.6% prevalence of sarcopenia in patients with COPD. Further research with larger samples would be indicated to clarify the precise association of specific characteristics of patients with sarcopenia and COPD.

Isolation, Culture, and Differentiation of Primary Myoblasts Derived from Muscle Satellite Cells

The skeletal muscle is key for body mobility and motor performance, but aging and diseases often lead to progressive loss of muscle mass due to wasting or degeneration of muscle cells. Muscle satellite cells (MuSCs) represent a population of tissue stem cells residing in the skeletal muscles and are responsible for homeostatic maintenance and regeneration of skeletal muscles. Growth, injury, and degenerative signals activate MuSCs, which then proliferate (proliferating MuSCs are called myoblasts), differentiate and fuse with existing multinuclear muscle cells (myofibers) to mediate muscle growth and repair. Here, we describe a protocol for isolating MuSCs from skeletal muscles of mice for in vitro analysis. In addition, we provide a detailed protocol on how to culture and differentiate primary myoblasts into myotubes and an immunofluorescent staining procedure to characterize the cells. These methods are essential for modeling regenerative myogenesis in vitro to understand the dynamics, function and molecular regulation of MuSCs.

Sarcopenia in COPD: a systematic review and meta-analysis.

COPD is associated with a progressive loss of muscle mass and function. However, there is an unmet need to define and standardise methods to estimate the prevalence of sarcopenia in COPD patients.We performed a systematic review and meta-analysis of the prevalence of this extrapulmonary manifestation in COPD patients. We searched Embase, Medline (Ovid), CINAHL (EBSCO), Web of Science, Scopus and Google Scholar for studies published up to January 17, 2019, assessing sarcopenia in COPD patients based on low muscle mass and decreased muscle function. Interventional studies, in vitro experiments, protocols or reviews and meta-analyses were excluded. We estimated heterogeneity (I2) and assessed significance (Q) using a Chi-squared test for estimates obtained from random-effects models.4465 articles were initially identified. After removing the duplicates and applying the selection criteria, we reviewed 62 full-text articles. Finally, 10 articles (n=2565 COPD patients) were included in this systematic review and meta-analyses. Overall, the prevalence of sarcopenia in patients with COPD was 21.6% (95% CI 14.6-30.9%, I2=94%), ranging from 8% in population-based to 21% in clinic-based studies, and 63% in COPD patients residing in nursing homes.Sarcopenia is frequently observed in COPD patients, with varying prevalence across population settings. Sarcopenia in COPD should be assessed using standardised tests and cut-off points from sarcopenia consensus criteria for clinical practice and international comparisons.

Progressive loss of muscle mass could be an adverse prognostic factor of 28-day mortality in septic shock patients

A decrease in skeletal muscle mass has been shown to increase hospital mortality. Nevertheless, little is known about the association between progressive muscle loss over time and clinical outcomes. We aimed to evaluate whether progressive loss of muscle mass in septic shock patients was associated with mortality. We reviewed prospectively enrolled registry of septic shock which had 817 consecutive patients. Of these, 175 patients who had computed tomography (CT) at a time of admission as well as 3–6 months prior to admission were included. Between these two CTs, the change in total abdominal muscle area index (TAMAI) was evaluated for progressive muscle loss. The change in TAMAI was higher in the non-survivors (−7.6 cm2/m2, 19.0% decrease) than the survivors (−4.0 cm2/m2, 10.5% decrease) with statistical significance (p = 0.002). Multiple logistic regression showed that the patients who had more than a 6.4 cm2/m2 (16.7%) reduction of TAMAI had a 4.42-fold higher risk for mortality at 28 days (OR, 4.42; 95% CI, 1.41–13.81, p = 0.011). Our study suggested that progressive loss of muscle mass might be a useful prognostic factor for septic shock patients. This implication will need to be further explored in future prospective studies.

Low Appendicular Lean Mass Index and Associations with Metabolic and Demographic Parameters in Wheelchair Athletes with Spinal Cord Injury.

People suffering from spinal cord injury (SCI) undergo metabolic and physical disturbances that target the skeletal muscle, causing a progressive loss of muscle mass. To estimate the appendicular lean mass index (ALMI) in athletes with traumatic (T-group) and non-traumatic (NT-group) SCI, and its association with metabolic and demographic parameters. Wheelchair athletes with SCI aged 18 to 52 years old were included (n = 62). From DEXA assessment, we estimated the ALM index (ALMI = appendicular lean mass/height2) and classified participants according to the degree of muscle loss (ALMI < 2 SD from the reference populations). Fasting blood was assayed for glycaemia, insulin, cortisol, and IGF-1 serum levels. Data were compared by T-test and Fisher's Exact Test; predictors of ALMI were investigated by linear regression models. The frequency of low ALMI was 63% in overall sample, 55% T-group and 71% NT-group. Low ALMI had no significant association with the origin of injury (X2 = 1.1, p = 0.29). Linear regression analyses showed significant association, in the whole sample, between ALMI and serum levels of IGF-1 (Beta = 0.69; p < 0.001), age (Beta=-5.8; p < 0.001), percentage fat mass (Beta=-0.26; p = 0.001), and energy intake (Beta = 0.32; p = 0.02). These significances were not maintained in the NT-group sub-analyses. Low ALMI was very frequent in our SCI participants, despite exercising and independently of the type of injury. Metabolic and demographic variables associated with low ALMI were different according to the origin of injury, which possibly relies on physiopathology particularities. More studies are necessary to clarify our findings.

246 A Clinical Audit of Detection and Management of Sarcopenia in Older Persons’ Specialist Rehabilitation Services in an Academic Teaching Hospital

Abstract Background Sarcopenia, characterised by progressive loss of muscle mass and strength, is associated with increased morbidity, mortality and poorer quality of life. International and European clinical practice guidelines on diagnosis and management of sarcopenia suggest the algorithm: Find Cases through screening, Assess Strength with validated outcome measures, Confirm Diagnosis with muscle quantity analysis and Determine Severity with validated physical performance measures (PPMs). Treatment recommendations include progressive resistance training (PRT) and a protein-rich diet. This audit aimed to investigate our specialist gerontological services’ adherence to these guidelines. Methods Using a custom-designed audit tool, patient medical records (PMRs) were reviewed in two inpatient rehabilitation wards and one Day Hospital (DH). Patients were included if under the care of a geriatrician and reviewed two or more times by a physiotherapist. Results Thirty PMRs were reviewed (18 DH, 12 inpatient). 0% of patients were screened for sarcopenia using a validated screening tool. 83.3% (n=15) of DH patients and 33.3% (n=4) of inpatients underwent a validated strength assessment. 0% of patients underwent muscle quantity analysis. 66.6% (n=12) of DH patients and 33.3% (n=4) of inpatients had validated PPMs performed. Probable sarcopenia was identified in 75% of DH and 100% of inpatients who had PPMs conducted. PRT was prescribed in 94% (n=17) and 50% (n=6) of DH patients and inpatients respectively. 16.6% (n=3) of DH patients and 75% (n=9) of inpatients were referred for nutritional assessment. 100% (n=9) of patients assessed by clinical nutrition were prescribed a high-protein/high-calorie diet. Conclusion This audit demonstrates limitations in identifying and managing sarcopenia as per the most recent international and European clinical practice guidelines. It is recognised that a multi-disciplinary approach is required to improve adherence to these guidelines. A multi-disciplinary sarcopenia management pathway is being implemented to facilitate this. Re-audit is planned to ensure the effectiveness of this pathway.

Efficacy of Nutritional Interventions as Stand-Alone or Synergistic Treatments with Exercise for the Management of Sarcopenia.

Sarcopenia is an age-related and accelerated process characterized by a progressive loss of muscle mass and strength/function. It is a multifactorial process associated with several adverse outcomes including falls, frailty, functional decline, hospitalization, and mortality. Hence, sarcopenia represents a major public health problem and has become the focus of intense research. Unfortunately, no pharmacological treatments are yet available to prevent or treat this age-related condition. At present, the only strategies for the management of sarcopenia are mainly based on nutritional and physical exercise interventions. The purpose of this review is, thus, to provide an overview on the role of proteins and other key nutrients, alone or in combination with physical exercise, on muscle parameters.

The Biological Foundations of Sarcopenia: Established and Promising Markers.

Sarcopenia, the progressive loss of muscle mass and strength, is one of the major health issues in older adults, given its high prevalence accompanied by huge clinical and socioeconomic implications. Age-related changes in skeletal muscle can be attributed to mechanisms both directly and indirectly related to muscle homeostasis. Indeed, a wide spectrum of age-related modifications in the organism was shown to play a key role in the pathogenesis of sarcopenia. Not surprisingly, sarcopenia has sometimes been indicated as a syndrome stemming from the aging process, and not as univocal standalone disease. Due to the multidimensionality of sarcopenia, a single biomarker approach is not enough to explain the biology of this condition. The aim of this review is to suggest innovative and promising sarcopenia markers investigating the link between skeletal muscle and brain. Indeed, as a neurological origin of sarcopenia has been hypothesized, a new perspective on sarcopenia biomarkers may focus on the dysfunction of the neuromuscular junctions (NMJs). The core SNARE synaptosomal-associated protein of 25 kDa (SNAP25) accumulates in the plasma membrane of nerve terminals at NMJs and regulates exocytosis at peripheral and central synapses. Interestingly, mice studies have shown that SNAP25 affects the neuromuscular function. SNARE complex and, in particular, SNAP25 may represent a promising pathway to explore the molecular and cellular mechanisms regulating muscular homeostasis and concur at profiling the sarcopenia biological background.

Ounce Equivalent Protein Ingestion Does Not Result in Equivalent Responses of Protein Kinetics (OR27-05-19)

ObjectivesThe progressive loss of muscle mass, or sarcopenia, is inherent to aging and related to functionality and independence. It is well established that the loss of muscle mass can be mitigated with adequate dietary protein intake. To help the consumers meet protein requirements utilizing a variety of protein food sources, the Dietary Guidelines for Americans (DGAs) published an “ounce equivalents” recommendation for protein food sources. However, the actual equivalency of these varied protein food groups has not been established. We examined the responses of protein kinetics in response to consumption of ounce equivalents of ground beef, sirloin, eggs, pork loin, kidney beans, peanut butter, tofu, and mixed nuts in young subjects. MethodsSubjects adhered to 3 days of activity and dietary control, and were then studied using an 8.5 h metabolic study which included a 4.5 h basal overnight-fasted period followed by a 4 h post-meal period. All groups were balanced by sex (4 males/4 females). ResultsConsumption of animal-based protein food sources resulted in higher whole body net balance than the plant-based protein food sources (P < 0.05). Consumption of beef sirloin, eggs, and pork loin induced a higher whole-body anabolic response than ground beef and the plant- based proteins. Consumption of tofu (soy-protein) induced a higher whole-body anabolic response than the other plant proteins (P < 0.05). The improvement in whole-body net balance with animal-based protein sources and tofu was due to a significant increase in protein synthesis (P < 0.05) as well as a significant suppression of protein breakdown in most protein sources (P < 0.05). Whole-body net balance was related to higher plasma EAA concentrations with animal-based protein sources and tofu realizing greater peripheral concentrations (P < 0.05). ConclusionsThe results of this study indicate that the “ounce equivalents” as expressed in the DGAs do not produce equivalent anabolic responses, nor are they equivalent in terms of the amount of protein provided, or the caloric cost of protein consumption. The magnitude of anabolic response appears to be largely determined by the amount of essential amino acids per gram of protein food source. Funding SourcesThe Beef Checkoff, National Pork Board, and Egg Nutrition Center.

Accelerated sarcopenia and outcomes in older adults with cancer: The Health ABC Study.

11526 Background: Progressive loss of muscle mass and strength (sarcopenia) is a well-known phenomenon of aging; however, little is known about the contribution of a cancer diagnosis to sarcopenia and its subsequent impact on disability. Using a prospective cohort of older adults from pre- to post-cancer diagnosis and a similarly-followed non-cancer cohort, we examined the trajectory of sarcopenia measures and their association with overall survival (OS) and major disability among those with cancer. Methods: The Health, Aging, and Body Composition (Health ABC) Study is a prospective longitudinal study where 3,075 community-dwelling older adults (70-79y) underwent 6 annual assessments of body composition and were followed for development of sentinel events (cancer, disability, death). Appendicular lean mass (ALM [kg]) was a sum of DXA-based lean tissue of all extremities. Hand grip strength (HGS [kg]) was averaged from 2 trials per hand. Gait speed (GS) was evaluated over a 20m course. We used linear mixed effect models to compare the change in ALM, HGS, and GS between individuals who subsequently developed cancer and those who did not, adjusting for age, race, gender, enrollment site. Among patients with cancer, we used multivariable cox regression for time from cancer diagnosis to mortality and major disability (cane/walker, inability to walk 0.25 mile/climb 10 steps, assistance with activities of daily living) treating sarcopenia measures as time-varying covariates. Results: Mean age at enrollment was 75y; 52% female; 42% black; 515 new cancers (prostate: 23%, colorectal: 15%, lung: 13%, breast: 11%). Compared with non-cancer controls, we found significantly steeper declines in HGS ( p= 0.03) and GS ( p&lt; 0.001), and a trend in ALM ( p= 0.07) prior to cancer diagnosis; and a significantly steeper decline in ALM ( p&lt; 0.001), but no difference in HGS ( p= 0.6) or GS ( p= 0.4) after cancer diagnosis. Slow GS was associated with a 44% increase in mortality ( p= 0.02) and a 70% increase in disability ( p= 0.02), but not ALM or HGS. Conclusions: Accelerated loss in sarcopenia measures both prior to and after a cancer diagnosis, and association with disability and mortality in older adults with cancer, present opportunities for targeted interventions.

Tetra-linoleoyl cardiolipin depletion plays a major role in the pathogenesis of sarcopenia

Sarcopenia, the progressive loss of muscle mass, strength, and physical performance that occurs during aging, is highly prevalent among the elderly. Sarcopenia increases the risk of falls, disability, and death. The biological basis for sarcopenia is not well understood. There are no specific preventive or therapeutic strategies for sarcopenia except exercise. The elucidation of biological pathways and identification of therapeutic targets for treating or preventing sarcopenia remain a high priority in aging research. Mitochondria play a critical role in skeletal muscle by providing energy in the form of ATP, regulation of signaling, calcium homeostasis, autophagy, and other functions. Cardiolipin, a unique dimeric phospholipid specific to mitochondria and an essential component of mitochondrial membranes, is involved in mitochondrial protein transport, maintaining structural organization of mitochondrial membranes, cellular signaling, regulating enzymes involved in β-oxidation of fatty acids, and facilitating normal electron transport chain (ETC) function and generation of ATP. The fatty acid species composition of cardiolipin is critical to mitochondrial bioenergetics, as cardiolipin affects membrane biophysical properties, binds and stabilizes ETC protein complexes, and shapes the curvature of the mitochondrial cristae. Tetra-linoleoyl cardiolipin (18:2)4 comprises ∼80% of cardiolipin in mitochondria in normal human skeletal and cardiac muscle and is optimal for effective ETC function and ATP generation. Aging is associated with a decrease in cardiolipin content, decrease in tetra-linoleoyl cardiolipin (18:2)4 and replacement of linoleic acid (18:2) with other fatty acids in cardiolipin composition, decline of ETC function, and increased generation of reactive oxygen species in muscle. Together, these findings from the literature prompt the hypothesis that depletion of the cardiolipin (18:2)4 species may be at the root of mitochondrial dysfunction with aging, in turn leading to sarcopenia. Corroboration of the tetra-linoleoyl cardiolipin depletion hypothesis suggests new leads for the prevention and treatment of sarcopenia by enhancing the biosynthesis, accretion, and integrity of tetra-linoleoyl cardiolipin.

Economic Impact of Hospitalizations in US Adults with Sarcopenia

BackgroundSarcopenia is characterized by progressive loss of muscle mass with corresponding decline in strength and/or physical function. The economic burden of sarcopenia-associated disability is considerable in the US.ObjectiveTo estimate the cost of hospitalizations in US adults with sarcopenia categorized by age, sex, and race/ethnicity.Design, setting and participantsA retrospective, prevalence based, economic burden study, consisting of 4011 adults aged ≥40 years with and without sarcopenia.MethodsData on prevalence of low lean mass, functional limitations, and hospitalizations were obtained from the National Health and Nutrition Examination Survey (1999–2004); cost of hospitalizations was obtained from the Healthcare Cost and Utilization Project — National Inpatient Sample (2014), and population estimates were obtained from the US Census (2014). Probability and cost of hospitalizations were estimated by multiple logistic regression and negative binomial regression models, respectively.ResultsThe total estimated cost of hospitalizations in individuals with sarcopenia was USD $40.4 billion with an average per person cost of USD $260. Within this category, average per person cost was highest for Hispanic women (USD $548) and lowest for Non-Hispanic Black women (USD $25); average per person cost was higher for older adults (≥65 years) (USD $375) than younger adults (40–64 years) (USD $204) with sarcopenia. The total cost of hospitalizations in individuals with sarcopenia (≥65 years) was USD $19.12 billion. Individuals with sarcopenia had greater odds of hospitalization (OR, 1.95; p<.001) compared to those without and had an annual marginal increase in cost of USD $2315.7 per person compared to individuals without sarcopenia.ConclusionSarcopenia places considerable economic burden on the US healthcare system. The ethnic disparity and economic burden associated with sarcopenia warrant further investigation.

New insights into the pathogenesis and treatment of sarcopenia in chronic heart failure.

Sarcopenia is an age-related geriatric syndrome that is characterized by a progressive loss of muscle mass, strength and function. Chronic heart failure (CHF), the final stage of various cardiovascular diseases, may be closely correlated with the occurrence of sarcopenia. Accumulating evidence has demonstrated that CHF can promote the development of sarcopenia through multiple pathophysiological mechanisms, including malnutrition, inflammation, hormonal changes, oxidative stress, autophagy, and apoptosis. Additionally, CHF can aggravate the adverse outcomes associated with sarcopenia, including falls, osteoporosis, frailty, cachexia, hospitalization, and mortality. Sarcopenia and CHF are mutually interacting clinical syndromes. Patients with these two syndromes seem to endure a double burden, with no particularly effective way to hinder their progression. However, the combination of physical exercise, nutritional supplements, and drug therapy may counteract the development of these maladies. In this review, we will summarize the latest progress in the pathogenesis and treatment of sarcopenia in patients with CHF.

The Impact of Dairy Protein Intake on Muscle Mass, Muscle Strength, and Physical Performance in Middle-Aged to Older Adults with or without Existing Sarcopenia: A Systematic Review and Meta-Analysis.

Sarcopenia is an age-related condition associated with a progressive loss of muscle mass and strength. Insufficient protein intake is a risk factor for sarcopenia. Protein supplementation is suggested to improve muscle anabolism and function in younger and older adults. Dairy products are a good source of high-quality proteins. This review evaluates the effectiveness of dairy proteins on functions associated with sarcopenia in middle-aged and older adults. Randomized controlled trials were identified using PubMed, CINAHL/EBSCO, and Web of Science databases (last search: 10 May 2017) and were quality assessed. The results of appendicular muscle mass and muscle strength of handgrip and leg press were pooled using a random-effects model. The analysis of the Short Physical Performance Battery is presented in narrative form. Adverse events and tolerability of dairy protein supplementation were considered as secondary outcomes. Fourteen studies involving 1424 participants aged between 61 and 81 y met the inclusion criteria. Dairy protein significantly increased appendicular muscle mass (0.13 kg; 95% CI: 0.01, 0.26 kg; P=0.04); however, it had no effect on improvement in handgrip (0.84 kg; 95% CI: -0.24, 1.93 kg; P=0.13) or leg press (0.37 kg; 95% CI: -4.79, 5.53 kg; P=0.89). The effect of dairy protein on the Short Physical Performance Battery was inconclusive. Nine studies reported the dairy protein to be well tolerated with no serious adverse events. Although future high-quality research is required to establish the optimal type of dairy protein, the present systematic review provides evidence of the beneficial effect of dairy protein as a potential nutrition strategy to improve appendicular muscle mass in middle-aged and older adults.

Low Lean Mass and Sarcopenia in Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis

Background. Chronic obstructive pulmonary disease (COPD) is associated with a progressive loss of muscle mass and function. However, there is an unmet need to define and to standardize methods to estimate the prevalence of sarcopenia in COPD patients. Therefore, we performed a systematic review and meta-analysis of the prevalence of this extra-pulmonary manifestation in patients with COPD. Methods. We searched Embase, Medline (Ovid), CINAHL (EBSCO), Web of Science, Scopus and Google Scholar for studies published until July 2017, assessing lean mass or sarcopenia in COPD patients. Interventional studies, in vitro experiments, protocols or reviews and meta-analyses were excluded. The main outcome was the prevalence of sarcopenia and low lean mass. Risk of bias was assessed by the Hoy scale. We used random-effects models and assessed heterogeneity (I2) by X² test. PROSPERO, registration number CRD42018095480. Findings. 3,915 articles were initially identified, and 253 were unique articles. From 27 articles included in this systematic review, 24 were meta-analyzed (n=13.009). The prevalence of sarcopenia in patients with COPD was 25.7% (95%CI: 12.9-44.8%; I²=88%). Low lean mass based on a low fat free mass index was present in 23.4% (95%CI: 18.6-29.0; I² =96%) of COPD patients, whereas the prevalence of a low appendicular skeletal muscle index was 31.0% (95%CI: 28.0-34.2; I²=65%). Interpretation. Sarcopenia and low lean mass are frequently observed in COPD patients with varying prevalence. Heterogeneity was considerable as a result of wide range of operational definitions, cut-offs, and methods used to diagnose sarcopenia. Assessment of sarcopenia in COPD patients should integrate standardized tests of muscle mass and muscle function. Funding: There was no funding source related to the execution of this study. Declaration of Interest: The authors have no conflicts of interest to declare.

Immunobiology of Inherited Muscular Dystrophies.

The immune response to acute muscle damage is important for normal repair. However, in chronic diseases such as many muscular dystrophies, the immune response can amplify pathology and play a major role in determining disease severity. Muscular dystrophies are inheritable diseases that vary tremendously in severity, but share the progressive loss of muscle mass and function that can be debilitating and lethal. Mutations in diverse genes cause muscular dystrophy, including genes that encode proteins that maintain membrane strength, participate in membrane repair, or are components of the extracellular matrix or the nuclear envelope. In this article, we explore the hypothesis that an important feature of many muscular dystrophies is an immune response adapted to acute, infrequent muscle damage that is misapplied in the context of chronic injury. We discuss the involvement of the immune system in the most common muscular dystrophy, Duchenne muscular dystrophy, and show that the immune system influences muscle death and fibrosis as disease progresses. We then present information on immune cell function in other muscular dystrophies and show that for many muscular dystrophies, release of cytosolic proteins into the extracellular space may provide an initial signal, leading to an immune response that is typically dominated by macrophages, neutrophils, helper T-lymphocytes, and cytotoxic T-lymphocytes. Although those features are similar in many muscular dystrophies, each muscular dystrophy shows distinguishing features in the magnitude and type of inflammatory response. These differences indicate that there are disease-specific immunomodulatory molecules that determine response to muscle cell damage caused by diverse genetic mutations. © 2018 American Physiological Society. Compr Physiol 8:1313-1356, 2018.

Prevalence of sarcopenia and 9-year mortality in nursing home residents

Sarcopenia is a progressive loss of muscle mass, strength, and function. It is linked to functional decline, and secondary to this, to nursing home admission. To look into the prevalence of sarcopenia in a nursing home population and to gain insight into the relation of sarcopenia with mortality in this cohort. A longitudinal cohort follow-up started in October 2007 in 52 nursing homes in Belgium. Following data were procured: anthropometrics (weight/length), body composition (muscle mass through bio-impedance absorptiometry, BIA), functional status (Katz), nutritional status (mini-nutritional assessment-short form, MNA), and a number of laboratory parameters. In total, 745 residents were included. Mean age was 84.6 ± 7.2years. Mean follow-up time was 1632 ± 1026days. In total, 17% had severe sarcopenia, 45% had moderate sarcopenia, and 38% had no sarcopenia. Following items were significant (p < 0.05) on univariate analysis with mortality as outcome: sarcopenia, gender, BMI, skeletal muscle mass, age, MNA, and functional level. In multivariate analysis, only MNA, skeletal muscle mass, and age were still significant. Odds ratio for skeletal muscle mass was 1.171 for the highest percentile group, 2.277 for the middle percentile group, and 4.842 for the lowest percentile group. The prevalence of sarcopenia was higher than in comparative literature, for which there are a few hypotheses. Cut-off values for sarcopenia using BIA for specific cohorts need to be re-evaluated. It seems to remain useful to screen for muscle mass in institutionalized elderly, because there is a clear and significant correlation with long-term mortality.

The impact of protein support on weight loss, sarcopenia and quality of life after sleeve gastrectomy

Rationale: Today, laparoscopic sleeve gastrectomy (LSG) is the most common bariatric procedure all around the world. Sarcopenia refers to the progressive loss of muscle mass and power. After LSG, sarcopenia can be seen due to decreased protein intake. In this study, the effects of protein supplementation after LSG on weight loss, muscle metabolism and quality of life was evaluated.

Skeletal muscle in aged mice reveals extensive transformation of muscle gene expression

BackgroundAging leads to decreased skeletal muscle function in mammals and is associated with a progressive loss of muscle mass, quality and strength. Age-related muscle loss (sarcopenia) is an important health problem associated with the aged population.ResultsWe investigated the alteration of genome-wide transcription in mouse skeletal muscle tissue (rectus femoris muscle) during aging using a high-throughput sequencing technique. Analysis revealed significant transcriptional changes between skeletal muscles of mice at 3 (young group) and 24 (old group) months of age. Specifically, genes associated with energy metabolism, cell proliferation, muscle myosin isoforms, as well as immune functions were found to be altered. We observed several interesting gene expression changes in the elderly, many of which have not been reported before.ConclusionsThose data expand our understanding of the various compensatory mechanisms that can occur with age, and further will assist in the development of methods to prevent and attenuate adverse outcomes of aging.