Sarcopenia

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Editor-in-Chief: Angela Botts, M.D., Beth Israel Deaconess Medical Center Geriatric Medicine [1]


Introduction

Sarcopenia (from the Greek meaning "poverty of flesh") is the degenerative loss of skeletal muscle mass and strength in senescence. About a third of muscle mass is lost in old age. This loss of mass reduces the performance of muscles. Due to the increasing number of elderly people, sarcopenia is an increasing health issue in the developed world. The level of sarcopenia can be so severe that it prevents an elderly person from living an independent life and they require constant assistance and care. Sarcopenia is an important independent predictor of disability in population-based studies, linked to poor balance, gait speed, falls, and fractures.

Sarcopenia can be thought of as analogous to "osteoporosis", which is the age-related loss of bone. The combination of osteoporosis and sarcopenia results in the significant frailty often seen in the elderly population.

Natural history

Strength losses with aging are similar for men and women on a relative bases. They are greater for lower than upper extremity muscles. Strength generally peaks in mid twenties and declines thereafter. The decline is precipitous after 65 years of age, though few longitudinal studies exist on this topic.

Diagnosis

Making the clinical diagnosis of sarcopenia is difficult for the following reasons. There is no absolute level of lean mass, body cell mass, or muscle mass for comparison. There is no generally accepted clinical test to diagnose sarcopenia. Finally, there is no accepted threshold of functional decline at which sarcopenia is implied.

Mechanism

The biological mechanism of sarcopenia appears to be in the decreased ability of satellite cells to propagate themselves. Satellite cells are required to fuse into skeletal muscle fibers, and help in settings where repair and regeneration are required. Therefore aging muscle loses its ability to respond to anabolic stimuli, such as insulin, growth hormone, and amino acids. Catabolic stimuli may also play a role: the inflammatory IL-6, IL1-Ra, and TNF-alpha are elevated in elderly people with significant sarcopenia. Many anabolic stimuli are withdrawn in the elderly population. Decreased protein intake in the elderly plays a role: 1/3 of men over the age of 60 eat less than the RDA of 0.8 g/kg. A decline in exercise, a potent stimulus to protein synthesis, also contributes. Hormonal factors may be involved, such as decreased levels of sex hormones, growth hormones, and decreased insulin.

Depleted muscles atrophy and are replaced by connective tissue, though the mechanism in sarcopenia may be different than that seen in other settings of "muscle atrophy", since in younger individuals there is not an obvious problem with the satellite cells. Type II muscle fibers atrophy more so than type I.

Management

Possible therapeutic strategies include increased protein intake and aggressive resistance-based exercise programs, but long-term randomized controlled trials are needed to evaluate the efficacy of these modalities. Hormonal supplementation may help if levels are low. Countermeasures should have the goals of maintaining adequate total body mass and protein intake. Physical activity incorporating resistance training is probably the most effective countermeasure to sarcopenia.

References

  • Roubenoff R, Hughes VA. (2000) Sarcopenia: Current Concepts. J Gerontol 55A, M716-M724.
  • Lynch, G.S. (2004). Tackling Australia's future health problems: developing strategies to combat sarcopenia--age-related muscle wasting and weakness. Journal of Internal Medicine. 34 (5), 294-296.
  • Edström, E., Ulfhake, B. (2005). Sarcopenia is not due to lack of regenerative drive in senescent skeletal muscle. Aging Cell. 4 (2), 65-77.
  • Fujita S & Volpi E (2006). Branched-Chain Amino Acids: Metabolism, Physiological Function, and Application: Session III. Amino Acids and Muscle Loss with Aging. Journal of Nutrition, 136:277S-280S.


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