Multifactorial Mechanism of Sarcopenia and Sarcopenic Obesity. Role of Physical Exercise, Microbiota and Myokines

Abstract

Obesity and ageing place a tremendous strain on the global healthcare system. Age-related sarcopenia is characterized by decreased muscular strength, decreased muscle quantity, quality, and decreased functional performance. Sarcopenic obesity (SO) is a condition that combines sarcopenia and obesity and has a substantial influence on the older adults’ health. Because of the complicated pathophysiology, there are disagreements and challenges in identifying and diagnosing SO. Recently, it has become clear that dysbiosis may play a role in the onset and progression of sarcopenia and SO. Skeletal muscle secretes myokines during contraction, which play an important role in controlling muscle growth, function, and metabolic balance. Myokine dysfunction can cause and aggravate obesity, sarcopenia, and SO. The only ways to prevent and slow the progression of sarcopenia, particularly sarcopenic obesity, are physical activity and correct nutritional support. While exercise cannot completely prevent sarcopenia and age-related loss in muscular function, it can certainly delay development and slow down the rate of sarcopenia. The purpose of this review was to discuss potential pathways to muscle deterioration in obese individuals. We also want to present the current understanding of the role of various factors, including microbiota and myokines, in the process of sarcopenia and SO.

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

“…FGF-21 and its receptors such as β-Klotho, FGFR1b, FGFR1c, and FGFR4 are strongly increased in muscle under catabolic conditions ( 61 ). In addition, FGF-21 enhances myoblast differentiation and acts through the FGF-21/SIRT1/AMPK/PGC-1α axis to convert anaerobic myofibers to aerobic ( 11 , 13 ) ( Figure 1 ). FGF-21, as an anti-inflammatory agent, stimulates the oxidation of fatty acids, the production of ketone bodies, and inhibits lipogenesis ( 63 ).…”

“…FGF-21, as an anti-inflammatory agent, stimulates the oxidation of fatty acids, the production of ketone bodies, and inhibits lipogenesis ( 63 ). FGF-21 is a major regulator of brown fat differentiation by increasing the expression of UCP1 and PGC-1α and thus generates heat in adipose tissue and skeletal muscle ( 11 , 64 ). In confirmation of this, a study reported that suppression of FGF-21 prevents white adipose tissue from turning brown.…”

“…Muscle-derived FGF-21 plays an important role in aging and obese, and a positive correlation has been found in serum FGF-21 levels and sarcopenia and obese. Thus, sarcopenia and sarcopenic obesity may be associated with FGF-21 disorder ( 11 , 13 , 67 – 69 ). In this regard, a study identified FGF-21 as potential therapeutic targets associated with PGC-1α for aging and age-related diseases ( 65 ).…”

“…In addition, after exercise intervention, sarcopenic obesity biomarkers such as weight loss and lean mass gain improved in the exercise group ( 10 ). A combination of resistance and aerobic exercise has also been reported to effectively reduce sarcopenic obesity and related biomarkers ( 8 , 10 , 11 ). Another study reported that after 24 sessions of resistance training with blood flow restriction (BFR), a 12% increase in muscle cross-section and an 8% increase in lateral extensor muscle thickness were observed in 90-year-olds.…”

Insulin and cancer: a tangled web

“…Sarcopenic (loss of muscle mass, often associated with ageing) obesity is the concept that an individual can be meet clinical definitions of obesity (BMI > 30 kg/m 2 ) and simultaneously exhibit skeletal muscle wasting [ 68 , 69 ]. Sarcopenic skeletal muscles are known to be insulin resistant even in the setting of low whole-body fat stores [ 70 ], and considering that skeletal muscle is a primary site of both insulin action and glucose uptake/storage [ 71–75 ], sarcopenia contributes significantly to systemic metabolic syndrome [ 76 ].…”