Abstract
Sarcopenia, the age-related loss of skeletal muscle mass and function, is becoming more prevalent as the lifespan continues to increase in most populations. As sarcopenia is highly disabling, being associated with increased risk of dependence, falls, fractures, weakness, disability, and death, development of approaches to its prevention and treatment are required. Androgens are the main physiologic anabolic steroid hormones and normal testosterone levels are necessary for a range of developmental and biological processes, including maintenance of muscle mass. Testosterone concentrations decline as age increase, suggesting that low plasma testosterone levels can cause or accelerate muscle- and age-related diseases, as sarcopenia. Currently, there is increasing interest on the anabolic properties of testosterone for therapeutic use in muscle diseases including sarcopenia. However, the pathophysiological mechanisms underlying this muscle syndrome and its relationship with plasma level of androgens are not completely understood. This review discusses the recent findings regarding sarcopenia, the intrinsic, and extrinsic mechanisms involved in the onset and progression of this disease and the treatment approaches that have been developed based on testosterone deficiency and their implications.
Highlights
In healthy young adults, the skeletal muscle mass comprises approximately 60% of total body mass
On the contrary, regarding total muscle mass, age-related loss in total body muscle mass was greater in the male than female subjects, independent of change in stature, and can be clearly observed after approximately age 45. These results indicate that age-related loss of skeletal muscle mass is greater in the lower than upper body in both men and women [16]
The authors hypothesized that the consequences of the mitochondrial dysfunction that they observed in the Sod1−/ − mice, which included elevated apoptotic potential; decrease in myonuclear number per millimeter of fiber length; and alterations in neuromuscular junction histology and contractility, occur in the skeletal muscle of aging humans, and that mitochondrial dysfunction is an important factor in the pathophysiology of sarcopenia
Summary
The skeletal muscle mass comprises approximately 60% of total body mass. The authors hypothesized that the consequences of the mitochondrial dysfunction that they observed in the Sod1−/ − mice, which included elevated apoptotic potential; decrease in myonuclear number per millimeter of fiber length; and alterations in neuromuscular junction histology and contractility, occur in the skeletal muscle of aging humans, and that mitochondrial dysfunction is an important factor in the pathophysiology of sarcopenia.
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