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Dietary Fibre May Mitigate Sarcopenia Risk: Findings from the NU-AGE Cohort of Older European Adults.
Montiel-Rojas, D, Nilsson, A, Santoro, A, Franceschi, C, Bazzocchi, A, Battista, G, de Groot, LCPGM, Feskens, EJM, Berendsen, A, Pietruszka, B, et al
Nutrients. 2020;(4)
Abstract
Sarcopenia is characterised by a progressive loss of skeletal muscle mass and physical function as well as related metabolic disturbances. While fibre-rich diets can influence metabolic health outcomes, the impact on skeletal muscle mass and function is yet to be determined, and the moderating effects by physical activity (PA) need to be considered. The aim of the present study was to examine links between fibre intake, skeletal muscle mass and physical function in a cohort of older adults from the NU-AGE study. In 981 older adults (71 ± 4 years, 58% female), physical function was assessed using the short-physical performance battery test and handgrip strength. Skeletal muscle mass index (SMI) was derived using dual-energy X-ray absorptiometry (DXA). Dietary fibre intake (FI) was assessed by 7-day food record and PA was objectively determined by accelerometery. General linear models accounting for covariates including PA level, protein intake and metabolic syndrome (MetS) were used. Women above the median FI had significantly higher SMI compared to those below, which remained in fully adjusted models (24.7 ± 0.2% vs. 24.2 ± 0.1%, p = 0.011, η2p = 0.012). In men, the same association was only evident in those without MetS (above median FI: 32.4 ± 0.3% vs. below median FI: 31.3 ± 0.3%, p = 0.005, η2p = 0.035). There was no significant impact of FI on physical function outcomes. The findings from this study suggest a beneficial impact of FI on skeletal muscle mass in older adults. Importantly, this impact is independent of adherence to guidelines for protein intake and PA, which further strengthens the potential role of dietary fibre in preventing sarcopenia. Further experimental work is warranted in order to elucidate the mechanisms underpinning the action of dietary fibre on the regulation of muscle mass.
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Myostatin as a Biomarker of Muscle Wasting and other Pathologies-State of the Art and Knowledge Gaps.
Baczek, J, Silkiewicz, M, Wojszel, ZB
Nutrients. 2020;(8)
Abstract
Sarcopenia is a geriatric syndrome with a significant impact on older patients' quality of life, morbidity and mortality. Despite the new available criteria, its early diagnosis remains difficult, highlighting the necessity of looking for a valid muscle wasting biomarker. Myostatin, a muscle mass negative regulator, is one of the potential candidates. The aim of this work is to point out various factors affecting the potential of myostatin as a biomarker of muscle wasting. Based on the literature review, we can say that recent studies produced conflicting results and revealed a number of potential confounding factors influencing their use in sarcopenia diagnosing. These factors include physiological variables (such as age, sex and physical activity) as well as a variety of disorders (including heart failure, metabolic syndrome, kidney failure and inflammatory diseases) and differences in laboratory measurement methodology. Our conclusion is that although myostatin alone might not prove to be a feasible biomarker, it could become an important part of a recently proposed panel of muscle wasting biomarkers. However, a thorough understanding of the interrelationship of these markers, as well as establishing a valid measurement methodology for myostatin and revising current research data in the light of new criteria of sarcopenia, is needed.
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Sarcopenia in gastric cancer: when the loss costs too much.
Ongaro, E, Buoro, V, Cinausero, M, Caccialanza, R, Turri, A, Fanotto, V, Basile, D, Vitale, MG, Ermacora, P, Cardellino, GG, et al
Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association. 2017;(4):563-572
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Abstract
Sarcopenia is a complex syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength. Malignancy is a major determinant of sarcopenia, and gastric cancer (GC) is among the most common causes of this phenomenon. As sarcopenia is a well-recognized poor prognostic feature in GC and has been associated with worse tolerance of surgical and medical treatments, members of the multidisciplinary team should be aware of the clinical relevance, pathogenic mechanisms, and potential treatments for this syndrome. The importance of sarcopenia is often underestimated in everyday practice and clinical trials, particularly among elderly or fragile patients. As treatment options are improving in all disease stages, deeper knowledge and greater attention to the metabolic balance in GC patients could further increase the benefit of novel therapeutic strategies and dramatically impact on quality of life. In this review, we describe the role of sarcopenia in different phases of GC progression. Our aim is to provide oncologists and surgeons dealing with GC patients with a useful tool for comprehensive assessment and timely management of this potentially life-threatening condition.
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The biology of the metabolic syndrome and aging.
Dominguez, LJ, Barbagallo, M
Current opinion in clinical nutrition and metabolic care. 2016;(1):5-11
Abstract
PURPOSE OF REVIEW Aging of the world population is a major contributor to the growing prevalence of the metabolic syndrome, as older persons are frequently affected by the constellation of cardiovascular and metabolic risk factors that constitute the syndrome. The metabolic syndrome has been related to the increasing prevalence of obesity, which is escalating even among older age groups. The present review covers data on the novel proposed biological mediators of the metabolic syndrome, which are as well linked to the aging process. RECENT FINDINGS Relevant biological mediators of metabolic syndrome and unhealthy aging include sarcopenic obesity, insulin resistance with ectopic fat accumulation, magnesium metabolism alterations, systemic and hypothalamic inflammation, shortening of telomeres length, epigenetics, and circadian rhythm disturbances. SUMMARY Metabolic syndrome is related to increased accumulation of central adiposity and ectopic fat infiltration in the skeletal muscle and the liver, linked to overeating and sedentarism with deleterious consequences in late life. Obesity may be complicated with sarcopenia, which refers to loss of muscle mass, strength, and quality in older populations. Prevention of obesity and metabolic syndrome is a priority through the promotion of healthier lifestyles and policies for sugar and saturated fats, which might be widely implemented.
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Exercise as a remedy for sarcopenia.
Landi, F, Marzetti, E, Martone, AM, Bernabei, R, Onder, G
Current opinion in clinical nutrition and metabolic care. 2014;(1):25-31
Abstract
PURPOSE OF REVIEW Although prolongation of life is a significant public health aim, at the same time the extended life should involve preservation of the capacity to live independently. Consequently, the identification of cost-effectiveness interventions to prevent frailty is one of the most important public health challenges. In the present review, we present the available evidence regarding the impact of physical exercise on the components of frailty syndrome and, in particular, as a remedy for sarcopenia. RECENT FINDINGS Resistance exercise training is more effective in increasing muscle mass and strength, whereas endurance exercises training is superior for maintaining and improving maximum aerobic power. Based on these evidences, recommendations for adult and frail older people should include a balanced program of both endurance and strength exercises, performed on a regular schedule (at least 3 days a week). SUMMARY Regular exercise is the only strategy found to consistently prevent frailty and improve sarcopenia and physical function in older adults. Physical exercises increase aerobic capacity, muscle strength and endurance, by ameliorating aerobic conditioning and/or strength. In older patients, exercise and physical activity produce at least the same beneficial effects observed in younger individuals.
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Sex hormones and sarcopenia in older persons.
Maggio, M, Lauretani, F, Ceda, GP
Current opinion in clinical nutrition and metabolic care. 2013;(1):3-13
Abstract
PURPOSE OF REVIEW Sarcopenia is a geriatric syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength with a risk of adverse outcomes such as physical disability, poor quality of life, and death. Sarcopenia is a multifactorial process involving the decline of androgens, including dehydroepiandrosterone sulphate (DHEAS) and testosterone. The aim of this review is to highlight the effects of DHEAS and testosterone treatment to counteract sarcopenia, especially in older men. RECENT FINDINGS DHEAS and, more importantly, testosterone treatment are associated with increased muscle mass, whereas the effects on muscle function and physical performance are less clear. The results of recent randomized placebo controlled trials with DHEAS in older men and women and testosterone in men with mobility limitation are discussed. The novel current and future scenarios to attenuate the detrimental effects and to optimize the efficacy of sex hormone treatment are also addressed. SUMMARY DHEAS and testosterone are important options in the armamentarium of sarcopenia treatment in older men. Future studies are needed to address new approaches by using selective compounds, targeting the correct form and dosage, tailoring the correct patient to treat, and taking into account the multifactorial origin and the new definition of sarcopenia.
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Posttransplant sarcopenia: an underrecognized early consequence of liver transplantation.
Dasarathy, S
Digestive diseases and sciences. 2013;(11):3103-11
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Abstract
Liver transplantation is believed to reverse the clinical and metabolic abnormalities of cirrhosis. Reduced skeletal muscle mass or sarcopenia contributes to increased mortality and adverse consequences of cirrhosis. Failure of reversal of sarcopenia of cirrhosis after liver transplantation is not well recognized. Six temporally, geographically, and methodologically distinct follow-up studies in 304 cirrhotics reported conflicting data on changes in indirect measures of skeletal muscle mass after transplantation. Distinct measures of body composition but not skeletal muscle mass were used and did not focus on the clinical consequences of sarcopenia after transplantation. A number of studies reported an initial rapid postoperative loss of lean mass followed by incomplete recovery with a maximum follow-up of 2 years. Posttransplant sarcopenia may be responsible for metabolic syndrome and impaired quality of life after liver transplantation. Potential reasons for failure to reverse sarcopenia after liver transplantation include use of immunosuppressive agents [mammalian target of rapamycin (mTOR) and calcineurin inhibitors] that impair skeletal muscle growth and protein accretion. Repeated hospitalizations, posttransplant infections, and renal failure also contribute to posttransplant sarcopenia. Finally, recovery from muscle deconditioning is limited by lack of systematic nutritional and physical-activity-based interventions to improve muscle mass. Despite the compelling data on sarcopenia before liver transplantation, the impact of posttransplant sarcopenia on clinical outcomes is not known. There is a compelling need for studies to examine the mechanisms and consequences of sarcopenia post liver transplantation to permit development of therapies to prevent and reverse this disorder.
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Sarcopenia: characteristics, mechanisms and functional significance.
Narici, MV, Maffulli, N
British medical bulletin. 2010;:139-59
Abstract
Sarcopenia reflects a progressive withdrawal of anabolism and an increased catabolism, along with a reduced muscle regeneration capacity. Muscle force and power decline more than muscle dimensions: older muscle is intrinsically weak. Sarcopenic obesity (SO) among the elderly corroborates to the loss of muscle mass increasing the risk of metabolic syndrome development. Recent studies on the musculoskeletal adaptations with ageing and key papers on the mechanisms of muscle wasting, its functional repercussions and on SO are included. Neuropathic, hormonal, immunological, nutritional and physical activity factors contribute to sarcopenia. Selective fast fibre atrophy, loss of motor units and an increase in hybrid fibres are typical findings of ageing. Satellite cell number decreases reducing muscle regeneration capacity. SO promotes further muscle wasting and increases risk of metabolic syndrome development. The proportion of fast to slow fibres seems maintained in old age. In elderly humans, nuclear domain is maintained constant. Basal protein synthesis and breakdown show little changes in old age. Instead, blunting of the anabolic response to feeding and exercise and of the antiproteolytic effect of insulin is observed. Further understanding of the mechanisms of sarcopenia requires disentangling of the effects of ageing alone from those of disuse and disease. The causes of the greater anabolic resistance to feeding and exercise of elderly women need elucidating. The enhancement of muscle regeneration via satellite cell activation via the MAPK/notch molecular pathways seems particularly promising.