scholarly journals Sarcopenia: Aging-Related Loss of Muscle Mass and Function

2019 ◽  
Vol 99 (1) ◽  
pp. 427-511 ◽  
Author(s):  
Lars Larsson ◽  
Hans Degens ◽  
Meishan Li ◽  
Leonardo Salviati ◽  
Young il Lee ◽  
...  
Keyword(s):  
Motor Unit ◽  
Muscle Mass ◽  
Structural Changes ◽  
Neuromuscular Disorders ◽  
Muscle Fibers ◽  
Cost Savings ◽  
The Elderly ◽  
Experimental Models ◽  
And Function ◽  
Qualitative Changes

Sarcopenia is a loss of muscle mass and function in the elderly that reduces mobility, diminishes quality of life, and can lead to fall-related injuries, which require costly hospitalization and extended rehabilitation. This review focuses on the aging-related structural changes and mechanisms at cellular and subcellular levels underlying changes in the individual motor unit: specifically, the perikaryon of the α-motoneuron, its neuromuscular junction(s), and the muscle fibers that it innervates. Loss of muscle mass with aging, which is largely due to the progressive loss of motoneurons, is associated with reduced muscle fiber number and size. Muscle function progressively declines because motoneuron loss is not adequately compensated by reinnervation of muscle fibers by the remaining motoneurons. At the intracellular level, key factors are qualitative changes in posttranslational modifications of muscle proteins and the loss of coordinated control between contractile, mitochondrial, and sarcoplasmic reticulum protein expression. Quantitative and qualitative changes in skeletal muscle during the process of aging also have been implicated in the pathogenesis of acquired and hereditary neuromuscular disorders. In experimental models, specific intervention strategies have shown encouraging results on limiting deterioration of motor unit structure and function under conditions of impaired innervation. Translated to the clinic, if these or similar interventions, by saving muscle and improving mobility, could help alleviate sarcopenia in the elderly, there would be both great humanitarian benefits and large cost savings for health care systems.

scholarly journals The Recent Understanding of the Neurotrophin's Role in Skeletal Muscle Adaptation

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Kunihiro Sakuma ◽  
Akihiko Yamaguchi
Keyword(s):  
Skeletal Muscle ◽  
Neuromuscular Disorders ◽  
Muscle Fibers ◽  
Brain Disorders ◽  
Muscle Adaptation ◽  
Bdnf Mrna ◽  
Pathological Conditions ◽  
Development And Differentiation ◽  
And Function

This paper summarizes the various effects of neurotrophins in skeletal muscle and how these proteins act as potential regulators of the maintenance, function, and regeneration of skeletal muscle fibers. Increasing evidence suggests that this family of neurotrophic factors influence not only the survival and function of innervating motoneurons but also the development and differentiation of myoblasts and muscle fibers. Muscle contractions (e.g., exercise) produce BDNF mRNA and protein in skeletal muscle, and the BDNF seems to play a role in enhancing glucose metabolism and may act for myokine to improve various brain disorders (e.g., Alzheimer's disease and major depression). In adults with neuromuscular disorders, variations in neurotrophin expression are found, and the role of neurotrophins under such conditions is beginning to be elucidated. This paper provides a basis for a better understanding of the role of these factors under such pathological conditions and for treatment of human neuromuscular disease.

scholarly journals Alternative Exercise Technologies to Fight against Sarcopenia at Old Age: A Series of Studies and Review

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Wolfgang Kemmler ◽  
Simon von Stengel
Keyword(s):  
Muscle Mass ◽  
Statistical Power ◽  
The Elderly ◽  
Whole Body ◽  
Elderly Subjects ◽  
Physically Active ◽  
Relevant Effect ◽  
Efficient Alternative ◽  
Physical Limitations ◽  
And Function

The most effective physiologic mean to prevent sarcopenia and related muscle malfunction is a physically active lifestyle, or even better, physical exercise. However, due to time constraints, lack of motivation, or physical limitations, a large number of elderly subjects are either unwilling or unable to perform conventional workouts. In this context, two new exercise technologies, whole-body vibration (WBV) and whole-body electromyostimulation (WB-EMS), may exhibit a save, autonomous, and efficient alternative to increase or maintain muscle mass and function. Regarding WB-EMS, the few recent studies indeed demonstrated highly relevant effects of this technology on muscle mass, strength, and power parameters at least in the elderly, with equal or even higher effects compared with conventional resistance exercise. On the contrary, although the majority of studies with elderly subjects confirmed the positive effect of WBV on strength and power parameters, a corresponding relevant effect on muscle mass was not reported. However, well-designed studies with adequate statistical power should focus more intensely on this issue.

scholarly journals An investigation of p53 in skeletal muscle aging

2019 ◽  
Vol 127 (4) ◽  
pp. 1075-1084 ◽  
Author(s):  
Scott M. Ebert ◽  
Jason M. Dierdorff ◽  
David K. Meyerholz ◽  
Steven A. Bullard ◽  
Asma Al-Zougbi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Fibers ◽  
Skeletal Muscle Atrophy ◽  
P53 Expression ◽  
Skeletal Muscle Fibers ◽  
Age Related ◽  
Skeletal Muscle Aging ◽  
And Function

Age-related skeletal muscle atrophy is a very common and serious condition that remains poorly understood at the molecular level. Several lines of evidence have suggested that the tumor suppressor p53 may play a central, causative role in skeletal muscle aging, whereas other, apparently contradictory lines of evidence have suggested that p53 may be critical for normal skeletal muscle function. To help address these issues, we performed an aging study in male muscle-specific p53-knockout mice (p53 mKO mice), which have a lifelong absence of p53 expression in skeletal muscle fibers. We found that the absence of p53 expression in skeletal muscle fibers had no apparent deleterious or beneficial effects on skeletal muscle mass or function under basal conditions up to 6 mo of age, when mice are fully grown and exhibit peak muscle mass and function. Furthermore, at 22 and 25 mo of age, when age-related muscle weakness and atrophy are clearly evident in mice, p53 mKO mice demonstrated no improvement or worsening of skeletal muscle mass or function relative to littermate control mice. At advanced ages, p53 mKO mice began to die prematurely and had an increased incidence of osteosarcoma, precluding analyses of muscle mass and function in very old p53 mKO mice. In light of these results, we conclude that p53 expression in skeletal muscle fibers has minimal if any direct, cell autonomous effect on basal or age-related changes in skeletal muscle mass and function up to at least 22 mo of age. NEW & NOTEWORTHY Previous studies implicated the transcriptional regulator p53 as a potential mediator of age-related skeletal muscle weakness and atrophy. We tested this hypothesis by investigating the effect of aging in muscle-specific p53-knockout mice. Our results strongly suggest that p53 activity within skeletal muscle fibers is not required for age-related skeletal muscle atrophy or weakness.

Techniques of Assessing Muscle Mass and Function (Sarcopenia) for Epidemiological Studies of the Elderly

1995 ◽  
Vol 50A (Special) ◽  
pp. 45-51 ◽  
Author(s):  
W. J. Evans ◽  
Wm. C. Chumlea ◽  
S. S. Guo ◽  
B. Vellas ◽  
Y. Guigoz
Keyword(s):  
Muscle Mass ◽  
The Elderly ◽  
Epidemiological Studies ◽  
And Function

scholarly journals mTORC1 signaling is not essential for the maintenance of muscle mass and function in adult sedentary mice

2019 ◽  
Author(s):  
Alexander S. Ham ◽  
Kathrin Chojnowska ◽  
Lionel A. Tintignac ◽  
Shuo Lin ◽  
Alexander Schmidt ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Ex Vivo ◽  
Morphological Changes ◽  
Muscle Fibers ◽  
Protein Translation ◽  
Muscle Size ◽  
Mtorc1 Signaling ◽  
And Function

AbstractBackgroundThe balance between protein synthesis and degradation (proteostasis) is a determining factor for muscle size and function. Signaling via the mammalian target of rapamycin complex 1 (mTORC1) regulates proteostasis in skeletal muscle by affecting protein synthesis and autophagosomal protein degradation. Indeed, genetic inactivation of mTORC1 in developing and growing muscle causes atrophy resulting in a lethal myopathy. However, systemic dampening of mTORC1 signaling by its allosteric inhibitor rapamycin is beneficial at the organismal level and increases lifespan. Whether the beneficial effect of rapamycin comes at the expense of muscle mass and function is yet to be established.MethodsWe conditionally ablated the gene coding for the mTORC1-essential component raptor in muscle fibers of adult mice (iRAmKO). We performed detailed phenotypic and biochemical analyses of iRAmKO mice and compared them with RAmKO mice, which lack raptor in developing muscle fibers. We also used polysome profiling and proteomics to assess protein translation and associated signaling in skeletal muscle of iRAmKO mice.ResultsAnalysis at different time points reveal that, as in RAmKO mice, the proportion of oxidative fibers decreases, but slow-type fibers increase in iRAmKO mice. Nevertheless, no significant decrease in body and muscle mass, or muscle fiber area was detected up to 5 months post-raptor depletion. Similarly, ex vivo muscle force was not significantly reduced in iRAmKO mice. Despite stable muscle size and function, inducible raptor depletion significantly reduced the expression of key components of the translation machinery and overall translation rates.ConclusionsRaptor depletion and hence complete inhibition of mTORC1 signaling in fully-grown muscle leads to metabolic and morphological changes without inducing muscle atrophy even after 5 months. Together, our data indicate that maintenance of muscle size does not require mTORC1 signaling, suggesting that rapamycin treatment is unlikely to negatively affect muscle mass and function.

Mechanisms Regulating Neuromuscular Junction Development and Function and Causes of Muscle Wasting

2015 ◽  
Vol 95 (3) ◽  
pp. 809-852 ◽  
Author(s):  
Lionel A. Tintignac ◽  
Hans-Rudolf Brenner ◽  
Markus A. Rüegg
Keyword(s):  
Neuromuscular Junction ◽  
Muscle Mass ◽  
Motor Neurons ◽  
Structural Changes ◽  
Muscle Wasting ◽  
Chemical Synapse ◽  
Neuromuscular Activity ◽  
Medical Need ◽  
Metabolic Properties ◽  
And Function

The neuromuscular junction is the chemical synapse between motor neurons and skeletal muscle fibers. It is designed to reliably convert the action potential from the presynaptic motor neuron into the contraction of the postsynaptic muscle fiber. Diseases that affect the neuromuscular junction may cause failure of this conversion and result in loss of ambulation and respiration. The loss of motor input also causes muscle wasting as muscle mass is constantly adapted to contractile needs by the balancing of protein synthesis and protein degradation. Finally, neuromuscular activity and muscle mass have a major impact on metabolic properties of the organisms. This review discusses the mechanisms involved in the development and maintenance of the neuromuscular junction, the consequences of and the mechanisms involved in its dysfunction, and its role in maintaining muscle mass during aging. As life expectancy is increasing, loss of muscle mass during aging, called sarcopenia, has emerged as a field of high medical need. Interestingly, aging is also accompanied by structural changes at the neuromuscular junction, suggesting that the mechanisms involved in neuromuscular junction maintenance might be disturbed during aging. In addition, there is now evidence that behavioral paradigms and signaling pathways that are involved in longevity also affect neuromuscular junction stability and sarcopenia.

scholarly journals Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

2010 ◽  
Vol 10 ◽  
pp. 340-349 ◽  
Author(s):  
Emanuele Marzetti ◽  
Giuseppe Privitera ◽  
Vincenzo Simili ◽  
Stephanie E. Wohlgemuth ◽  
Lorenzo Aulisa ◽  
...  
Keyword(s):  
Old Age ◽  
Muscle Mass ◽  
The Elderly ◽  
Cellular Mechanisms ◽  
Age Related ◽  
Tnf Α ◽  
High Prevalence ◽  
Myocyte Apoptosis ◽  
Apoptotic Pathways ◽  
And Function

Sarcopenia, the age-related decline in muscle mass and function, represents a significant health issue due to the high prevalence of frailty and disability associated with this condition. Nevertheless, the cellular mechanisms responsible for the loss of muscle mass in old age are still largely unknown. An altered regulation of myocyte apoptosis has recently emerged as a possible contributor to the pathogenesis of sarcopenia. Studies in animal models have shown that the severity of skeletal muscle apoptosis increases over the course of aging and correlates with the degree of muscle mass and strength decline. Several apoptotic pathways are operative in aged muscles, with the mitochondria- and TNF-α-mediated pathways likely being the most relevant to sarcopenia. However, despite the growing number of studies on the subject, a definite mechanistic link between myocyte apoptosis and age-related muscle atrophy has not yet been established. Furthermore, the evidence on the role played by apoptosis in human sarcopenia is still sparse. Clearly, further research is required to better define the involvement of myocyte apoptosis in the pathogenesis of muscle loss at advanced age. This knowledge will likely help in the design of more effective therapeutic strategies to preserve muscle mass into old age, thus fostering independence of the elderly population and reducing the socioeconomic burden associated with sarcopenia.

The role of attenuated redox and heat shock protein responses in the age-related decline in skeletal muscle mass and function

2017 ◽  
Vol 61 (3) ◽  
pp. 339-348 ◽  
Author(s):  
Anne McArdle ◽  
Malcolm J. Jackson
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Muscle Mass ◽  
Stress Responses ◽  
Redox Regulation ◽  
Experimental Models ◽  
Age Related ◽  
Shock Proteins ◽  
And Function

The loss of muscle mass and weakness that accompanies ageing is a major contributor to physical frailty and loss of independence in older people. A failure of muscle to adapt to physiological stresses such as exercise is seen with ageing and disruption of redox regulated processes and stress responses are recognized to play important roles in theses deficits. The role of redox regulation in control of specific stress responses, including the generation of heat shock proteins (HSPs) by muscle appears to be particularly important and affected by ageing. Transgenic and knockout studies in experimental models in which redox and HSP responses were modified have demonstrated the importance of these processes in maintenance of muscle mass and function during ageing. New data also indicate the potential of these processes to interact with and influence ageing in other tissues. In particular the roles of redox signalling and HSPs in regulation of inflammatory pathways appears important in their impact on organismal ageing. This review will briefly indicate the importance of this area and demonstrate how an understanding of the manner in which redox and stress responses interact and how they may be controlled offers considerable promise as an approach to ameliorate the major functional consequences of ageing of skeletal muscle (and potentially other tissues) in man.

scholarly journals PERBANDINGAN KEKUATAN OTOT DAN MASSA OTOT ANTARA WANITA LANSIA AKTIF DAN TIDAK AKTIF BEROLAHRAGA

2021 ◽  
Vol 4 (1) ◽  
pp. 9
Author(s):  
Della Hestia Suyanto ◽  
Cindra Paskaria ◽  
Decky Gunawan
Keyword(s):  
Muscle Strength ◽  
Muscle Mass ◽  
Elderly Women ◽  
The Elderly ◽  
Normal Function ◽  
Research Subjects ◽  
Sports Activity ◽  
Cross Sectional ◽  
Cross Sectional Design ◽  
And Function

is a process of slowly losing the tissue's ability to maintain normal function and causing changes in muscle structure and function. A decrease in strength and muscle mass is a problem that often found in the elderly. Exercise is one of the factors that affect strength and muscle mass. The objective of the research is to compare the strength and muscle mass in elderly women who act and not actively exercise. This study is an observational analytic study with a cross-sectional design analyzed by an independent T-test. The research subjects were taken by purposive sampling, 20 elderly women aged over 60 years who met the inclusion and exclusion criteria were assessed for sports activity, muscle strength, and muscle mass so that it is obtained a sample of 13 elderly who are actively exercising and 7 elderly who are not actively exercising. Handheld muscle strength research data was measured using a handgrip dynamometer, muscle mass was measured using the Bioimpedance Analysis (BIA) method, and exercise habits were taken from the modification of the Baecke Physical Activity questionnaire. The results show that the elderly who were active in exercising with a mean score of muscle strength (10.59 ± 3.62) and muscle mass (34.22 ± 4.62) were higher than those who did not exercise (6.51 ± 3.42) and (29.81 ± 3.39) with p-values of 0.020 and 0.0125. There is a difference between strength and muscle mass in elderly women who are active and not actively exercising.

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