Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Abstract

Sarcopenic obesity is defined as a multifactorial disease in aging with decreased body muscle, decreased muscle strength, decreased independence, increased fat mass, due to decreased physical activity, changes in adipokines and myokines, and decreased satellite cells. People with sarcopenic obesity cause harmful changes in myokines and adipokines. These changes are due to a decrease interleukin-10 (IL-10), interleukin-15 (IL-15), insulin-like growth factor hormone (IGF-1), irisin, leukemia inhibitory factor (LIF), fibroblast growth factor-21 (FGF-21), adiponectin, and apelin. While factors such as myostatin, leptin, interleukin-6 (IL-6), interleukin-8 (IL-8), and resistin increase. The consequences of these changes are an increase in inflammatory factors, increased degradation of muscle proteins, increased fat mass, and decreased muscle tissue, which exacerbates sarcopenia obesity. In contrast, exercise, especially strength training, reverses this process, which includes increasing muscle protein synthesis, increasing myogenesis, increasing mitochondrial biogenesis, increasing brown fat, reducing white fat, reducing inflammatory factors, and reducing muscle atrophy. Since some people with chronic diseases are not able to do high-intensity strength training, exercises with blood flow restriction (BFR) are newly recommended. Numerous studies have shown that low-intensity BFR training produces the same increase in hypertrophy and muscle strength such as high-intensity strength training. Therefore, it seems that exercise interventions with BFR can be an effective way to prevent the exacerbation of sarcopenia obesity. However, due to limited studies on adipokines and exercises with BFR in people with sarcopenic obesity, more research is needed.

Effect of Exercise Training on Body Composition and Inflammatory Cytokine Levels in Overweight and Obese Individuals: A Systematic Review and Network Meta-Analysis

“…Secondly, CT is superior to AE and RT in improving muscle protein synthesis and myocellular quality ( 78 ). Moreover, exercise promotes the production of skeletal muscles and the release of muscle-derived cytokines (such as IL-6), which play significant anti-inflammatory and metabolic functions ( 79 ). Thirdly, Inflammatory monocytes (CD14+CD16+) are highly “proinflammatory”, and are potent producers of inflammatory proteins ( 80 ).…”

Exercise-induced signaling pathways to counteracting cardiac apoptotic processes

“…FOXO family consists of four members (FOXO1, FOXO3, FOXO4, and FOXO6) whose activity is inhibited by insulin signaling and growth factor ( Webb and Brunet, 2014 ; Alizadeh Pahlavani, 2022a ; Alizadeh Pahlavani, 2022b ). FOXO acts as a pro-apoptotic agent through the expression of proteins such as Bim, BAD, Bnip3, FasL, and TRAIL in the apoptotic internal and external pathways.…”

Organokines, Sarcopenia, and Metabolic Repercussions: The Vicious Cycle and the Interplay with Exercise

“…Interleukin-6 (IL-6) is a dual organokine, as it is secreted by both myocyte and adipocyte. IL-6 is directly related to BMI by acting on adipocytes and is increased in individuals with insulin resistance, obesity, and T2DM [ 10 , 25 , 81 , 82 ]. IL-6, as a myokine, acts by regulating satellite cells leading to skeletal muscle hypertrophy.…”

“…Physical exercise, in addition to improving lipid parameters by reducing cardiovascular risk, as well as mediating oxidative stress, might have a direct and significant impact on the prevention of sarcopenia since there is a release of myokines that promote muscle mass index preservation through a cross-link with the other organokines. However, physical inactivity leads to a lack of production of these myokines and causes the opposite effect, such as atrophy and other metabolic functions that will be explored throughout this study [ 10 ].…”