The decrease in muscle mass and function along with aging is a well-known natural process. However, from as early as about 30 years old the muscle mass and strength begin to physiologically decrease. It may accelerate around the age of 75, but this varies individually, starting as early at 65 or as late at 80 years old. The dynamics of this process depends on many intrinsic and extrinsic factors. These include hormonal changes, co-morbidities with especially chronic heart failure, decreased physical activity, inappropriate protein and caloric intake or their decreased turnover [ , ]. The limited physical activity due to impaired muscle function contributes to a vicious circle, further accelerating atrophy of muscles when they are not stressed by exertion or exercise. The loss of muscle mass, their strength and function is referred to as sarcopenia. The term sarcopenia (from the Greek ‘sarx – the flesh and ‘penia’ – loss) was used for the first time, however, in 1989 by Rosenberg to determine the loss of muscle mass associated with aging [ ]. The process of primary sarcopenia naturally follows chronological aging. It is significantly exacerbated by multiple diseases that usually affect the geriatric population, results in increasing pathological aging and leads to secondary sarcopenia, that is muscle loss when other evident causes are also involved, besides aging [ , ]. According to the present criteria, sarcopenia means loss of muscle mass, muscle strength and/or physical performance [ ]. Sarcopenia affects 5–10% of people over 65 years of age and affects more than 50% of people aged over 80 years, significantly contributing to a decrease in the functional capacity, institutionalization and dependence on third parties [ ]. Sarcopenia is to a certain extent associated with frailty syndrome, and the low muscle mass is a factor increasing mortality [ , ]. Patients with sarcopenia have reduced quality of life (SF-36) in the domain of physical performance, tendency to falls, and in the case of women, dependence when performing domestic tasks was increased [ ]. Due to the aging of the European population, sarcopenia has become a challenge in the field of public health. The number of individuals with sarcopenia in Europe may rise from around 11–20 millions in 2016 to more than 19-32 millions in 2045 (a 64–72% increase), depending on criteria assumed [ ]. In 2016 sarcopenia was classified as a separate disease according to ICD-10 (M62.84) [ ]. The pathophysiological background for sarcopenia includes processes that impair myogenesis and decrease the synthesis of muscle fibers as well as disturbances in the functioning of muscle satellite cells. In particular, a decrease in the amount of fast-twitching myosin type II fibers occurs, conversion of fast- to slow-twitching muscle fibers takes place and infiltration of muscles by fat tissue progresses with age (e.g. myosteatosis) [ ]. Sarcopenia is associated with an imbalance between catabolism and anabolism resulting from decreased levels of anabolic hormones, such as testosterone and adrenal androgens, a decrease in growth hormone secretion leading to a state called somatopause, and a decrease in the secretion of insulin-like growth factor 1. On the other hand, the levels of catabolic hormones increase, and especially in the elderly, unrecognized hyperthyroidism is often observed [ , ]. Chronic inflammation with the participation of cytokines (IL-1, IL-6, TNF-α), as well as myostatin belonging to the myokines family, inhibits the synthesis of muscle tissue and contributes to muscle atrophy [ ]. There is also involvement of a neurogenic background in sarcopenia with synaptic and neuronal degeneration leading to impaired muscle stimulation and atrophy [ ]. Protein-energy malnutrition, especially affecting hospitalized elderly, people living alone and residents of long-term care facilities, is a common external cause that contributes to increased muscle loss [ ]. On the other hand, concomitant obesity can mask sarcopenia, although seemingly normal anthropometric parameters are observed. This is a commonly occurring hidden condition of reduced lean soft tissue in favor of excess adiposity and was called sarcopenic obesity. Although emerging data suggest that obesity may coexist with sarcopenia, one should know that this sarcopenia phenotype cannot be identified without body composition analysis techniques [ ]. The clinical significance of sarcopenic obesity is, however, not clearly established [ ]. Sarcopenic obesity should be considered also in the context of the obesity paradox. This phenomenon means that in some chronic conditions, especially cardiovascular diseases, obese patients exhibit reverse epidemiology, contrary to intuitively expected, and have a better prognosis than would result from the estimated risk related to cardiovascular complications. It is observed, however, in body mass index (BMI) between 25 and 35 kg/m but not beyond that range. It seems that sarcopenic but obese subjects benefit from the obesity paradox [ ]. However, there are also contradictory conclusions, which deny benefits from such a protective function of obesity, stating that the obesity paradox may be a result of survival bias or that normal weight reflects comorbidities, malnutrition, and anabolic deficiency [ ]. Sarcopenia should not be, however, confused with cachexia. Although these conditions have a common hallmark such as loss of muscle mass and strength, they should be considered distinct clinical entities [ ]. Cachexia (from the Greek ‘cacos’ bad and ‘hexis’ having) is characterized by severe body weight loss, including fat and muscle loss, due to an underlying devastating illness [ ]. Contrary to osteoporosis diagnosed on the basis of widely recognized and applied criteria, the importance of sarcopenia, which inevitably although slowly, weakens the efficiency of the musculoskeletal system, is still underappreciated. Deterioration of the physical performance is basically caused by loss of the muscle weight and function. However, there is a known unfavorable relationship between a decrease in the lean body mass in older men and loss of bone density that aggravates osteoporosis, increasing risk of fractures [ ]. This is explained by the hypothesis of decrease in osteogenic activity due to either minor mechanical stimulation imposed on the bone by reduced muscles or decreased mechanical stimuli due to lower physical activity in the case of sarcopenia [ ]. It is also discussed whether sarcopenia and osteoporosis should be considered as one or two separate diseases; in fact many studies support the idea of a “bone-muscle unit” with bone and muscle mutually interacting via secreted cytokines [ ]. The muscle component of this complex entity is however underappreciated. The reason why sarcopenia is under-diagnosed is, among others, associated with low awareness of this problem. Screening tests are not widely popular or used in the geriatric population. When the approach to this commonly neglected health issue has been changed it may prolong independence of the elderly through preventive actions including nutritional supplementation, as well as appropriate physical exercises [ , ]. It can also be mentioned that increased risk of falls and pathological fractures, as well as impaired functionality associated with sarcopenia, increases healthcare costs, which could be reduced by appropriate prevention.
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