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|dc.identifier.isbn||0065-2598 / 2214-8019 (electronic)||-|
|dc.description.abstract||Skeletal muscle contractions power human body movements and are important for maintaining stability. Skeletal muscle tissue accounts for about half of the human body mass and, in addition to its power-generating role, is a crucial factor in maintaining homeostasis. Given its central role in human mobility and metabolic function, any impairment in the contractile, material, and metabolic properties of skeletal muscle has an adverse effect on human health. Aging is related to a progressive loss of muscle mass, quality, and strength, a condition known as sarcopenia. Although this term is applied clinically to denote loss of muscle mass, it is often used to explain both some cellular processes (denervation, mitochondrial dysfunction, inflammatory and hormonal alterations) and some outcomes, such as reduced muscle strength, mobility, and function, a higher risk of falls, and decreased energy requirements (Fig. 12.1). Von Haeling et al.  have estimated its prevalence at 5–13% for the elderly population aged 60–70 years and at 11–50% for those aged 80 years or above. Lean muscle mass generally contributes up to 50% of total body weight in young adults, but decreases with aging to approximately 25% around 75–80 years of age. At the muscle fiber level, sarcopenia is described by specific type II muscle fiber atrophy, fiber necrosis, and fiber-type grouping. Several probable mechanisms of age-related muscle atrophy have been reported. Agerelated muscle loss is due to losses in the size and number of muscle fibers, possibly resulted from a multi-factorial process that includes physical activity level, nutrient intake, hormonal changes, metabolic homeostasis, oxidative stress, and lifespan. The specific contribution of each of these factors is unknown but there is growing evidence that the disruption of several positive regulators of muscle hypertrophy such as Akt and serum response factor (SRF) are an important feature in the progression of sarcopenia [2, 3]. Some studies demonstrated a functional defect in autophagy- and myostatin-dependent signaling in sarcopenic muscle [4–6]. In contrast, many researchers have failed to identify age-related increases in the levels of common negative regulators, such as atrophy gene-1 (atrogin-1), nuclear factorkappaB (NF-κB) and calpain, in senescent mammalian muscles [2, 3, 7].||en_US|
|dc.title||Chapter 12 The Role of Nutrition in Attenuating Age-Related Skeletal Muscle Atrophy||-|
|Appears in Collections:||Nutrition|
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