scholarly journals Inactivity and Skeletal Muscle Metabolism: A Vicious Cycle in Old Age

2020 ◽  
Vol 21 (2) ◽  
pp. 592 ◽  
Author(s):  
Elena Rezuş ◽  
Alexandra Burlui ◽  
Anca Cardoneanu ◽  
Ciprian Rezuş ◽  
Cătălin Codreanu ◽  
...  

Aging is an inevitable and gradually progressive process affecting all organs and systems. The musculoskeletal system makes no exception, elderly exhibit an increased risk of sarcopenia (low muscle mass),dynapenia (declining muscle strength), and subsequent disability. Whereas in recent years the subject of skeletal muscle metabolic decline in the elderly has been gathering interest amongst researchers, as well as medical professionals, there are many challenges yet to be solved in order to counteract the effects of aging on muscle function efficiently. Noteworthy, it has been shown that aging individuals exhibit a decline in skeletal muscle metabolism, a phenomenon which may be linked to a number of predisposing (risk) factors such as telomere attrition, epigenetic changes, mitochondrial dysfunction, sedentary behavior (leading to body composition alterations), age-related low-grade systemic inflammation (inflammaging), hormonal imbalance, as well as a hypoproteic diet (unable to counterbalance the repercussions of the age-related increase in skeletal muscle catabolism). The present review aims to discuss the relationship between old age and muscle wasting in an effort to highlight the modifications in skeletal muscle metabolism associated with aging and physical activity.

2014 ◽  
pp. 683-691 ◽  
Author(s):  
A. ZEMBROŃ-ŁACNY ◽  
W. DZIUBEK ◽  
Ł. ROGOWSKI ◽  
E. SKORUPKA ◽  
G. DĄBROWSKA

According to European Working Group on Sarcopenia in Older People (EWGSOP) sarcopenia includes both a loss of muscle strength and a decline in functional quality in addition to the loss of muscle protein mass. In order to develop strategies to prevent and treat sarcopenia, the risk factors and causes of sarcopenia must be identified. Age-related muscle loss is characterized by the contribution of multiple factors, and there is growing evidence for a prominent role of low-grade chronic inflammation in sarcopenia. The elderly who are less physically active are more likely to have lower skeletal muscle mass and strength and are at increased risk of developing sarcopenia. Resistance training added to aerobic exercise or high-intensity interval training promote numerous changes in skeletal muscle, many of which may help to prevent or reverse sarcopenia. In this review, we provided current information on definition and monitoring, molecular mechanisms, and physical intervention to counteract sarcopenia.


2016 ◽  
Vol 36 (1) ◽  
pp. 129-156 ◽  
Author(s):  
Brandon J.F. Gheller ◽  
Emily S. Riddle ◽  
Melinda R. Lem ◽  
Anna E. Thalacker-Mercer

1994 ◽  
Vol 30 (2) ◽  
pp. 171-185 ◽  
Author(s):  
O. Pastoris ◽  
M. Dossena ◽  
R. Arnaboldi ◽  
A. Gorini ◽  
R.F. Villa

2016 ◽  
Vol 229 (2) ◽  
pp. R67-R81 ◽  
Author(s):  
Mark E Cleasby ◽  
Pauline M Jamieson ◽  
Philip J Atherton

Insulin resistance (IR) in skeletal muscle is a key defect mediating the link between obesity and type 2 diabetes, a disease that typically affects people in later life. Sarcopenia (age-related loss of muscle mass and quality) is a risk factor for a number of frailty-related conditions that occur in the elderly. In addition, a syndrome of ‘sarcopenic obesity’ (SO) is now increasingly recognised, which is common in older people and is applied to individuals that simultaneously show obesity, IR and sarcopenia. Such individuals are at an increased risk of adverse health events compared with those who are obese or sarcopenic alone. However, there are no licenced treatments for sarcopenia or SO, the syndrome is poorly defined clinically and the mechanisms that might explain a common aetiology are not yet well characterised. In this review, we detail the nature and extent of the clinical syndrome, highlight some of the key physiological processes that are dysregulated and discuss some candidate molecular pathways that could be implicated in both metabolic and anabolic defects in skeletal muscle, with an eye towards future therapeutic options. In particular, the potential roles of Akt/mammalian target of rapamycin signalling, AMP-activated protein kinase, myostatin, urocortins and vitamin D are discussed.


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