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.

Highlights

  • After the fifth decade of life, several changes in the body accelerate, including decreased mobility, increased muscle weakness, decreased muscle strength, increased adipose tissue, increased risk of falling and increased bone fragility, these factors are known as sarcopenia (1)

  • This study showed that resistance exercise activates Jun N-terminal kinases (JNK)/SMAD signaling for overload-induced muscle hypertrophy in aging mammalian (127) (Figure 1)

  • The Ras/Raf/ERK pathway and the Akt/mTOR/p70S6K axis are activated by INSULIN-LIKE GROWTH FACTOR-I (IGF-I), which can increase muscle cell proliferation, differentiation, and survival and prevent muscle atrophy (1)

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Summary

Hamed Alizadeh Pahlavani*

Specialty section: This article was submitted to Endocrinology of Aging, a section of the journal Frontiers in Endocrinology. People with sarcopenic obesity cause harmful changes in myokines and adipokines These changes are due to a decrease interleukin-10 (IL-10), interleukin-15 (IL15), 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. Numerous studies have shown that low-intensity BFR training produces the same increase in hypertrophy and muscle strength such as high-intensity strength training It seems that exercise interventions with BFR can be an effective way to prevent the exacerbation of sarcopenia obesity.

INTRODUCTION
MYOKINES AFFECTING SARCOPENIC OBESITY
ADIPOKINES AFFECTING SARCOPENIC OBESITY
THE EFFECT OF RESISTANCE AND ENDURANCE TRAINING ON SARCOPENIC OBESITY
Findings
CONCLUSION
Full Text
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