Abstract
Sarcopenia, broadly defined as the age-related decline in skeletal muscle mass, quality, and function, is associated with chronic low-grade inflammation and an increased likelihood of adverse health outcomes. The regulation of skeletal muscle mass with ageing is complex and necessitates a delicate balance between muscle protein synthesis and degradation. The secretion and transfer of cytokines, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), both discretely and within extracellular vesicles, have emerged as important communication channels between tissues. Some of these factors have been implicated in regulating skeletal muscle mass, function, and pathologies and may be perturbed by excessive adiposity. Indeed, adipose tissue participates in a broad spectrum of inter-organ communication and obesity promotes the accumulation of macrophages, cellular senescence, and the production and secretion of pro-inflammatory factors. Pertinently, age-related sarcopenia has been reported to be more prevalent in obesity; however, such effects are confounded by comorbidities and physical activity level. In this review, we provide evidence that adiposity may exacerbate age-related sarcopenia and outline some emerging concepts of adipose-skeletal muscle communication including the secretion and processing of novel myokines and adipokines and the role of extracellular vesicles in mediating inter-tissue cross talk via lncRNAs and miRNAs in the context of sarcopenia, ageing, and obesity. Further research using advances in proteomics, transcriptomics, and techniques to investigate extracellular vesicles, with an emphasis on translational, longitudinal human studies, is required to better understand the physiological significance of these factors, the impact of obesity upon them, and their potential as therapeutic targets in combating muscle wasting.
Highlights
Beyond middle-age, skeletal muscle mass, and strength decline by 1–2% and 1–5% per year, respectively [1,2,3].GeroScience (2021) 43:85–110Skeletal muscle tissue is the human body’s principle protein bank, and given the absence of a protein pool for storage, it is critical for maintaining protein status via the delicate regulation of its turnover [4, 5]
We present evidence investigating the phenomenon of sarcopenic obesity and discuss the myriad ways that obesity may interact with sarcopenia to the detriment of muscle mass, quality, and function
Here we focus on cytokines which are implicated in adipose-muscle cross talk with emerging significance in the regulation of skeletal muscle mass, namely resistin, IL-15, adiponectin, leptin, lipocalin-2, and myostatin (Fig. 1; Table 1)
Summary
Beyond middle-age, skeletal muscle mass, and strength decline by 1–2% and 1–5% per year, respectively [1,2,3]. While circulating leptin is elevated in animal models of ageing in the absence of obesity [195], it has been reported to decline in elderly adults with severe frailty, but not in community-dwellers [61] This decline may reflect the low abundance of adipose tissue often seen in frail older adults and the diminishing mass of skeletal muscle, which is a significant source of leptin [196,197,198]. In community dwelling older adults, appendicular skeletal muscle mass and thigh muscle cross-sectional area have been negatively associated with plasma leptin concentration, even after adjustments for bodyweight or body fat percentage [62, 63] In these studies, circulating leptin abundance was greater in those presenting with either sarcopenia or obesity, and greater still in individuals presenting with sarcopenic obesity. The subsequent identification and confirmation of differentially regulated adipose-muscle cross talking miRNAs will doubtless present novel potential therapeutic targets for muscle wasting conditions
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