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Muscle erosion, which begins after the age of 50 years, is one of the most important factors of disability in older people, but it may also occur early in life in case of chronic disease [1]. The cumulative decline in muscle mass reaches 40% from 20 to 80 years. The magnitude of this phenomenon as a public health problem is now well established as there has been a lot of epidemiological studies and meta‐analysis focusing on the decrements of strength and muscle mass with advancing age. So, sarcopenia has been recognized as a specific disease with an International Classification of Diseases (ICD) code (M62.84) [2]. The reduction in muscle mass and strength provokes an impaired mobility and increased risk for falls and fall‐related fractures. In addition, muscle loss is associated with a decrease in overall physical activity levels with subsequent metabolic alterations such as obesity, insulin resistance, and a reduction in bone density in older persons. Sedentary individuals, subjects with poor protein intakes, low vitamin D and low testosterone levels, and those suffering from debilitating or inflammatory diseases are at greater risks of sarcopenia. As older person population increases around the world, the involuntary loss of muscle mass with aging will become a major health problem in years to come, from a European prevalence of 10.9 million in 2016 to 18.7 million in 2045 [3].

Sarcopenia is due predominantly to the atrophy of skeletal muscle fibers, mainly type II fibers [4]. This results in a relative elevation in type I fiber density related to a supposed preservation of muscle endurance and a reduction in muscle strength. On a metabolic point of view, muscle size, function, and composition are closely regulated by muscle protein turnover rate. Consequently, the age‐related loss of muscle proteins is a consequence of an imbalance between protein synthesis and degradation rates (Figure 5.1); whereas, basal muscle protein synthesis and breakdown rates appear to be unaffected by age [5, 6], the muscle protein synthetic response to the main anabolic stimuli, i.e. food intake and physical activity, appears to be blunted in older individuals [7–9]. This anabolic resistance is now considered to be a key factor contributing to progressive loss of skeletal muscle mass throughout our lifespan. Other factors such as neurodegenerative processes with loss of alpha motor neurons in the spinal column, dysregulation of anabolic hormone (insulin, growth, and sex hormones) and cytokine productions, modifications in the response to inflammatory events, inadequate nutritional intakes, and sedentarism also participate in muscle loss during aging.

The determinants of sarcopenia include likely both genetic and environmental factors, with a complex series of poorly understood interactions [10]. Likewise it is possible that epigenetic events may influence muscle fiber type evolution [11]. In fact, it is still unknown whether muscle loss of aged people is an inevitable condition of aging per se, or if illnesses, inappropriate nutrition, sedentarism, and other lifestyle habits are major causes of sarcopenia. Currently, as the pathophysiology of sarcopenia is still poorly understood and identified in clinical practice, interventions to either prevent, retard, or reverse this condition are still limited: physical exercise has a positive impact on muscle mass, function, and performance in healthy subjects aged over 60 years with very large variations in response to the dietary supplementation protocols [12–14].

Figure 5.1 Regulation of muscle protein mass.