Sarcopenia and Aging

Kamel, Hosam K.

doi:10.1301/nr.2003.may.157-167

Cited by 224 publications

(161 citation statements)

References 81 publications

(103 reference statements)

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“…Sarcopenia can induce muscle weakness and reduced ability to produce rapid force, which are considered to be two of the most common risk factors associated with falls and loss of functional independence in older adults (Taaffe and Marcus 2000;Buchman et al 2007). Sarcopenia can be explained by several physiopathological factors including (a) progressive muscle denervation (Deschenes 2004;Saini et al 2009); (b) alterations in muscle protein turnover, specifically manifested by difficulty to increase protein synthesis (Kumar et al 2009); (c) malnutrition (Doherty 2003); (d) altered expression levels of anabolic hormones (Volpi et al 2004); (e) increased levels of pro-inflammatory cytokines (Kamel 2003); (f) increased oxidative stress (Howard et al 2007); (g) lower physical activity levels (Cesari and Pahor 2008) and (h) diminished number and function of satellite cells in skeletal muscles (Verdijk et al 2007). Concerning the latter, satellite cells are the main contributor to muscle maintenance, growth and repair (Anderson and Wozniak 2004).…”

Section: Sarcopenia In the Elderly: A Common Problemmentioning

confidence: 99%

Genes and the ageing muscle: a review on genetic association studies

Garatachea

Lucía

2011

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Western populations are living longer. Ageing decline in muscle mass and strength (i.e. sarcopenia) is becoming a growing public health problem, as it contributes to the decreased capacity for independent living. It is thus important to determine those genetic factors that interact with ageing and thus modulate functional capacity and skeletal muscle phenotypes in older people. It would be also clinically relevant to identify 'unfavourable' genotypes associated with accelerated sarcopenia. In this review, we summarized published information on the potential associations between some genetic polymorphisms and muscle phenotypes in older people. A special emphasis was placed on those candidate polymorphisms that have been more extensively studied, i.e. angiotensinconverting enzyme (ACE) gene I/D, α-actinin-3 (ACTN3) R577X, and myostatin (MSTN) K153R, among others. Although previous heritability studies have indicated that there is an important genetic contribution to individual variability in muscle phenotypes among old people, published data on specific gene variants are controversial. The ACTN3 R577X polymorphism could influence muscle function in old women, yet there is controversy with regards to which allele (R or X) might play a 'favourable' role. Though more research is needed, up-to-date MSTN genotype is possibly the strongest candidate to explain variance among muscle phenotypes in the elderly. Future studies should take into account the association between muscle phenotypes in this population and complex gene-gene and gene-environment interactions.

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Section: Sarcopenia In the Elderly: A Common Problemmentioning

confidence: 99%

Genes and the ageing muscle: a review on genetic association studies

Garatachea

Lucía

2011

AGE

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“…Aging is associated with a progressive decline in muscle power generating capacity (Runge et al 2004) that contributes to an increased incidence of falls, a decreased independence and reduced quality of life (Kamel 2003;Roubenoff and Hughes 2000). Improvement of muscle function in the older person may alleviate many of these problems.…”

Section: Introductionmentioning

confidence: 99%

Plantaris muscle weakness in old mice: relative contributions of changes in specific force, muscle mass, myofiber cross-sectional area, and number

Ballak

Degens

Busé-Pot

et al. 2014

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The age-related decline in muscle function contributes to the movement limitations in daily life in old age. The age-related loss in muscle force is attributable to loss of myofibers, myofiber atrophy, and a reduction in specific force. The contribution of each of these determinants to muscle weakness in old age is, however, largely unknown. The objective of this study is to determine whether a loss in myofiber number, myofiber atrophy, and a reduction in specific muscle force contribute to the age-related loss of muscle force in 25-month-old mouse. Maximal isometric force of in situ m. plantaris of C57BL/6J male adult (9 months) and old (25 months) mice was determined and related to myofiber number, myofiber size, intramuscular connective tissue content, and proportion of denervated myofibers. Isometric maximal plantaris muscle force was 13 % lower in old than adult mice (0.97±0.05 N vs. 0.84±0.03 N; P<0.05). M. plantaris mass of old mice was not significantly smaller than that of adult mice. There was also no significant myofiber atrophy or myofiber loss. Specific muscle force of old mice was 25 % lower than that of adult mice (0.55±0.05 vs. 0.41± 0.03 N·mm −2 , P<0.01). In addition, with age, the proportion of type IIB myofibers decreased (43.6 vs. 38.4 %, respectively), while the connective tissue content increased (11.6 vs. 16.4 %, respectively). The agerelated reduction in maximal isometric plantaris muscle force in 25-month-old male C57BL/6J mice is mainly attributable to a reduction in specific force, which is for 5 % explicable by an age-related increase in connective tissue, rather than myofiber atrophy and myofiber loss.

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“…Decreased muscle mass and function contribute to the high incidence of accidental falls and resultant injuries observed among the elderly and can compromise quality of life (Kamel 2003). Various factors related to the development of sarcopenia include low levels of physical activity, alterations in hormone balance, loss of neuromuscular function, change in protein metabolism, poor nutrition, disease and trauma (Thomas 2007).…”

Section: Introductionmentioning

confidence: 99%

A novel in vitro model of sarcopenia using BubR1 hypomorphic C2C12 myoblasts

et al. 2015

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Sarcopenia is the age-related loss of skeletal muscle mass and function with adverse outcomes that include physical disability, poor quality of life, and death. The detailed molecular mechanisms remain unknown. An in vitro muscle atrophy model is needed to enable mechanistic studies. To create such a model, we employed BubR1 insufficiency which causes premature ageing in mice. Using C2C12 cells, a recognized in vitro model of the skeletal muscle cell, we obtained the BubR1 hypomorphic C2C12 (C2C12BKD) cells by using shRNA. The resulting C2C12BKD cells displayed several characteristics of the sarcopenic muscle cell. In C2C12BKD cells, formation of myotubes, assessed by analysis of fusion index, was markedly reduced as was the expression of myogenin and MyoD, two marker genes for myogenesis. Moreover, the cells showed increased expression of the muscle-specific ubiquitin ligases Atrogin-1 and MuRF-1, indicating increased protein degradation through the ubiquitin-proteasome dependent proteolytic pathway. These results suggest that C2C12BKD cells are potentially useful as a novel in vitro model of sarcopenia.

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Sarcopenia and Aging

Cited by 224 publications

References 81 publications

Genes and the ageing muscle: a review on genetic association studies

Genes and the ageing muscle: a review on genetic association studies

Plantaris muscle weakness in old mice: relative contributions of changes in specific force, muscle mass, myofiber cross-sectional area, and number

A novel in vitro model of sarcopenia using BubR1 hypomorphic C2C12 myoblasts

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