Hurrah for the increasing longevity: feasible strategies to counteract age-related loss of skeletal muscle mass

2015 ◽  
Vol 25 (1) ◽  
pp. 1-2 ◽  
Author(s):  
L. Holm ◽  
A. P. Jespersen ◽  
D. S. Nielsen ◽  
M. B. Frøst ◽  
S. Reitelseder ◽  
...  
2021 ◽  
Vol 22 (6) ◽  
pp. 3032
Author(s):  
Anna Picca ◽  
Riccardo Calvani

Sarcopenia involves a progressive age‐related decline of skeletal muscle mass and strength/function [...]


2020 ◽  
Vol 67 (1.2) ◽  
pp. 151-157 ◽  
Author(s):  
Michiko Sato ◽  
Teruhiro Morishita ◽  
Takafumi Katayama ◽  
Shigeko Satomura ◽  
Hiroko Okuno ◽  
...  

2018 ◽  
pp. 1-3
Author(s):  
B.C. Clark

Sarcopenia was originally conceptualized as the age-related loss of skeletal muscle mass. Over the ensuing decades, the conceptual definition of sarcopenia has changed to represent a condition in older adults that is characterized by declining muscle mass and function, with “function” most commonly conceived as muscle weakness and/or impaired physical performance (e.g., slow gait speed). Findings over the past 15-years, however, have demonstrated that changes in grip and leg extensor strength are not primarily due to muscle atrophy per se, and that to a large extent, are reflective of declines in the integrity of the nervous system. This article briefly summarizes findings relating to the complex neuromuscular mechanisms that contribute to reductions in muscle function associated with advancing age, and the implications of these findings on the development of effective therapies.


2009 ◽  
Vol 106 (6) ◽  
pp. 2040-2048 ◽  
Author(s):  
René Koopman ◽  
Luc J. C. van Loon

Aging is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk of developing chronic metabolic disease. The age-related loss of skeletal muscle mass is attributed to a disruption in the regulation of skeletal muscle protein turnover, resulting in an imbalance between muscle protein synthesis and degradation. As basal (fasting) muscle protein synthesis rates do not seem to differ substantially between the young and elderly, many research groups have started to focus on the muscle protein synthetic response to the main anabolic stimuli, i.e., food intake and physical activity. Recent studies suggest that the muscle protein synthetic response to food intake is blunted in the elderly. The latter is now believed to represent a key factor responsible for the age-related decline in skeletal muscle mass. Physical activity and/or exercise stimulate postexercise muscle protein accretion in both the young and elderly. However, the latter largely depends on the timed administration of amino acids and/or protein before, during, and/or after exercise. Prolonged resistance type exercise training represents an effective therapeutic strategy to augment skeletal muscle mass and improve functional performance in the elderly. The latter shows that the ability of the muscle protein synthetic machinery to respond to anabolic stimuli is preserved up to very old age. Research is warranted to elucidate the interaction between nutrition, exercise, and the skeletal muscle adaptive response. The latter is needed to define more effective strategies that will maximize the therapeutic benefits of lifestyle intervention in the elderly.


2021 ◽  
Author(s):  
Yoshihito Sakai ◽  
Norimitsu Wakao ◽  
Hiroki Matsui ◽  
Tsuyoshi Watanabe ◽  
Hiroki Iida ◽  
...  

Abstract Although the prevalence and the associated burden of LBP increase with age, research on LBP has primarily focused on young people and adults, and little attention has been given to the elderly population. Chronic inflammation is well-known as senescence associated secretory phenotype (SASP), which produces numerous proinflammatory cytokines leading to age-related inflammation. We enrolled 203 patients with an average age of 79.0 years, with non-specific CLBP; the patients were compared with age- and sex-matched controls without CLBP using a propensity score-matched analysis. We performed laboratory analysis, radiographic evaluations for global spinal parameter and lumbar degeneration assessment, and body composition analysis using whole-body dual-energy X-ray absorptiometry. We observed a higher red blood cell distribution width (RDW), as well as a lower skeletal muscle mass index and a higher fat mass in patients with CLBP. Moreover, patients with geriatric CLBP had significantly lower lumbar lordosis, and higher sagittal vertical axis was correlated with lower muscle mass in the extremities and trunk, independent of lumbar degeneration. Geriatric CLBP is associated with senescence. RDW, which is an index of aging, was high among elderly patients with CLBP. Furthermore, geriatric patients with CLBP often have age-related skeletal muscle mass reduction and spinal sagittal malalignment.


2002 ◽  
Vol 22 (3) ◽  
pp. 169-172 ◽  
Author(s):  
Jun Sugawara ◽  
Motohiko Miyachi ◽  
Kerrie L. Moreau ◽  
Frank A. Dinenno ◽  
Christopher A. DeSouza ◽  
...  

Author(s):  
José A. Morais

Sarcopenia is a progressive and inevitable loss of skeletal muscle mass and strength associated with ageing that places older adults at high risk for adverse health outcomes. Up to of 15% of older adults suffer negative healthcare consequences because of sarcopenia. Furthermore, it is responsible for two to four times greater risk of disability. Expert groups have proposed clinical oriented criteria based on gait speed <0.8 m/s and low handgrip strength before performing muscle mass assessment. Multiple aetiologies are implicated in the development of sarcopenia including age-related, lifestyle, neurodegeneration, hormonal, and inflammation factors. Resistance exercise training and higher than recommended protein intake are two accessible means to counteract sarcopenia. Hormonal interventions, despite amelioration in muscle and fat masses, have not led to significant gains in function. Sarcopenia shares many features with frailty and can be considered as one of its underlying mechanisms.


Gerontology ◽  
2016 ◽  
Vol 63 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Sophie Joanisse ◽  
Joshua P. Nederveen ◽  
Tim Snijders ◽  
Bryon R. McKay ◽  
Gianni Parise

Sarcopenia is the age-related loss of skeletal muscle mass and strength. Ultimately, sarcopenia results in the loss of independence, which imposes a large financial burden on healthcare systems worldwide. A critical facet of sarcopenia is the diminished ability for aged muscle to regenerate, repair and remodel. Over the years, research has focused on elucidating underlying mechanisms of sarcopenia and the impaired ability of muscle to respond to stimuli with aging. Muscle-specific stem cells, termed satellite cells (SC), play an important role in maintaining muscle health throughout the lifespan. It is well established that SC are essential in skeletal muscle regeneration, and it has been hypothesized that a reduction and/or dysregulation of the SC pool, may contribute to accelerated loss of skeletal muscle mass that is observed with advancing age. The preservation of skeletal muscle tissue and its ability to respond to stimuli may be impacted by reduced SC content and impaired function observed with aging. Aging is also associated with a reduction in capillarization of skeletal muscle. We have recently demonstrated that the distance between type II fibre-associated SC and capillaries is greater in older compared to younger adults. The greater distance between SC and capillaries in older adults may contribute to the dysregulation in SC activation ultimately impairing muscle's ability to remodel and, in extreme circumstances, regenerate. This viewpoint will highlight the importance of optimal SC activation in addition to skeletal muscle capillarization to maximize the regenerative potential of skeletal muscle in older adults.


2019 ◽  
Vol 127 (4) ◽  
pp. 1075-1084 ◽  
Author(s):  
Scott M. Ebert ◽  
Jason M. Dierdorff ◽  
David K. Meyerholz ◽  
Steven A. Bullard ◽  
Asma Al-Zougbi ◽  
...  

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.


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