Sarcopenia and exercise: challenges in the era of aging
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Sarcopenia, characterized by the loss of muscle mass and strength due to aging, impacts the functional independence and quality of life of older adults. It is linked to the pathophysiology of various chronic diseases, including cardiovascular diseases, diabetes, and obesity, beyond mere muscle loss. Sarcopenia also is linked to cognitive decline, which impacts the healthy lifespan of older adults. Therefore, preventing and managing sarcopenia is crucial for maintaining muscle health, as well as for managing chronic diseases, supporting cognitive function, and promoting overall health.
Sarcopenia diagnosis involves complex physiological and clinical processes. European criteria define sarcopenia with a muscle mass index below 7.0 kg/m2 for men and 5.5 kg/m2 for women, including muscle strength and physical performance assessments. Grip strength standards are below 30 kg for men and 20 kg for women. Asian criteria recommend a muscle mass standard with grip strength below 26 kg for men and 18 kg for women. Existing diagnostic criteria measure muscle mass, strength, and physical function but might not entirely reflect the physiological changes linked to aging. A simple decline in muscle mass does not necessarily equate to the same level of functional impairment across all older adults, and the relationship between muscle strength and functional performance is more complex. Evaluating the relationship between sarcopenia and cognitive decline necessitates a comprehensive understanding of these interrelated factors. This understanding is essential for developing effective interventions to address both muscle degradation and cognitive impairment in the aging population.
The pathophysiology of sarcopenia is multidimensional and closely linked to physiological and metabolic changes associated with aging. Aging reduces both the size and number of muscle fibers while increasing the proportion of fat and connective tissue within muscles. These changes impair the contractile function of muscle fibers, leading to a decline in muscle strength. Furthermore, chronic increases in inflammatory mediators and insulin resistance disrupt muscle metabolism, accelerating the progression of sarcopenia. Muscles, stimulated by insulin, are major sites for glucose processing and are significant components of basal metabolic rate, directly and indirectly affecting bone density. Muscles also produce myokines, which influence various tissues and store essential amino acids for protein synthesis. Aging causes selective atrophy of type II muscle fibers, resulting in decreased maximal strength and impaired physical performance. The complexity of this pathophysiology is further compounded by decreased mitochondrial function within muscles and increased oxidative stress, with links to endothelial dysfunction and cognitive decline, suggesting that sarcopenia impacts not just physical but also cognitive functions.
Exercise plays a crucial role in the prevention and treatment of sarcopenia. Resistance training is effective in promoting muscle protein synthesis and maintaining muscle fiber size and function, thus slowing the progression of sarcopenia. Exercise also improves insulin sensitivity and suppresses the production of inflammatory mediators, enhancing the metabolic health of muscles. These effects, along with improved neuromuscular control, enhance the functional performance of muscles. For older adults, tailored exercise programs are necessary and should be designed considering individual health status and capabilities. Resistance training has been identified as the most effective method for maintaining muscle mass, with recommendations for engaging in exercise at least 2–3 times per week. Exercise programs should be designed and supervised by professionals to maximize effectiveness, significantly enhancing the functional independence of elderly individuals with sarcopenia, as reported in various studies.
There are several mechanisms by which beneficial exercise effects inhibit the progression of sarcopenia and promote muscle health. It activates pathways for protein synthesis within muscles, increases synthesis rates, and reduces fat accumulation within muscle fibers, improving their physical properties and contributing to strength enhancement. Exercise stimulates mitochondrial biogenesis, reduces oxidative stress to optimize muscle fiber function, decreases inflammation, enhances insulin sensitivity, and promotes neuromuscular activation, all contributing to improved muscle strength and function. Additionally, exercise stimulates the secretion of neurotrophic factors such as brain-derived neurotrophic factor, contributing to neuroplasticity and neuroprotection, thus potentially enhancing cognitive function. It improves cerebrospinal fluid circulation, promoting brain health and acting on the complex interactions between physical health and cognitive function.
Future research should focus on understanding and managing sarcopenia through exercise. Firstly, it is necessary to better understand the factors that induce and exacerbate sarcopenia, as well as to elucidate the long-term effects and interactions between sarcopenia and exercise throughout life. Secondly, improving the accuracy of sarcopenia diagnosis and prediction is needed, alongside developing assessment tools to identify high-risk elderly individuals and establishing precise criteria for evaluating and identifying responses to sarcopenia treatments. Thirdly, studies targeting diverse populations are needed to evaluate the effectiveness of personalized exercise programs, proposing new paradigms for the prevention and treatment of sarcopenia.
In conclusion, the prevention and management of sarcopenia and cognitive function are essential for maintaining and improving the healthy lifespan of older adults. Exercise plays a pivotal role in preventing and improving sarcopenia and cognitive functions, necessitating diverse clinical and physiological research on the effects of exercise for healthy aging.
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CONFLICT OF INTEREST
No potential conflict of interest relevant to this article was reported.