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Review
. 2020 Jan 16;21(2):592.
doi: 10.3390/ijms21020592.

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

Elena Rezuş  1 , Alexandra Burlui  1 , Anca Cardoneanu  1 , Ciprian Rezuş  2 , Cătălin Codreanu  3 , Mirela Pârvu  4 , Gabriela Rusu Zota  5 , Bogdan Ionel Tamba  6
Affiliations
Review

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

Elena Rezuş et al. Int J Mol Sci. .

Abstract

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.

Keywords: adipokine; aging; anabolism; catabolism; exercise; inflammation; muscle mitochondria; myokine; sarcopenia; sedentary lifestyle.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Associated with age-related sarcopenia.
Figure 2
Figure 2
Epigenetic changes, enzymes involved, skeletal muscle expression, and metabolic consequences. DNMT: DNA methyltransferase; TET: ten-eleven translocation; AID: activation-induced cytidine deaminase; APOBEC: apolipoprotein B mRNA editing enzyme component 1; BER: base excision repair; GNAT: Gcn5-related N-acetyltransferase; CBP: Creb-binding protein; HDAC: histone deacetylase (after [40]).
Figure 3
Figure 3
Skeletal muscle mitochondria [56].
Figure 4
Figure 4
Size-dependent imbalance between pro-inflammatory adipokines (such as leptin, visfatin, adipsin, resistin, interleukin-6 (IL-6), IL-1β, and tumor necrosis factor α (TNFα)) and anti-inflammatory adipokines (adiponectin, omentin, visceral adipose tissue-derived serine protease inhibitor (vaspin), secreted frizzled-related protein 5 (SFRP5), and IL-10) [79,80,85].
Figure 5
Figure 5
Hormonal changes and their impact on skeletal muscles.
See this image and copyright information in PMC

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