Sarcopenia

From Wikipedia, the free encyclopedia

Sarcopenia (from the Greek meaning "poverty of flesh") is the degenerative loss of skeletal muscle mass and strength in senescence. Sarcopenia is the slow loss of muscle mass, strength, and endurance that occurs over time, primarily after the age of 50. Since sarcopenia is marked by an infiltration of fat and excess connective tissue into the muscle mass, simple circumference measures do not provide enough data to determine whether or not an individual is suffering from severe sarcopenia. Sarcopenia is also marked by a decrease in type 2 fiber circumference, but no change in type 1 fiber circumference, and a pathological morphing of muscle structure. Furthermore, sarcopenia is associated with a distinct loss of quiescent satellite cells available for recruitment to repair muscle injury; hence, the ability to repair damaged muscles or respond to nutritional signals is impaired. Extreme muscle loss is often a result of both diminishing anabolic signals, such as growth hormone and testosterone, and promotion of catabolic signals, such as pro-inflammatory cytokines.

Due to the general aging of industrialized populations, sarcopenia is an increasing health concern. For instance, sarcopenia may progress to the extent that older person may lose his or her ability to live independently. Furthermore, 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.

Contents

[edit] Natural history

Strength losses with aging for men and women are relatively similar. They are greater for lower than upper extremity muscles. Maximum attainable strength peaks in mid twenties and declines thereafter. The decline is precipitous after 65 years of age, though few longitudinal studies exist on this topic. An direct assesment of the effects of sarcopenia even in top-physcially fit individuals, can be seen in the age-related decline in Masters athletics (track and field), world-records of muscle intensive sports, such as weight lifting. No substance-free proven olympic weight lifting record has been set by any athlete of any sex or weight class above the age of 31.

[edit] 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.

[edit] Mechanism

At present, the biological mechanisms of sarcopenia are uncertain. What is clear, is that sarcopenia occurs even in the most fit individuals indicating that it is not a consequence of inactivity. Breakdown of neuromuscular junction as as well as age-depent loss of neurons in the spinal cord, are thought to be one of the proximate causes. Possibly, the decreased ability of satellite cells to propagate themselves may be another contributing factor. 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 in the general population, however, even top trained individuals experience sarcopenia. Hormonal factors may be involved, such as decreased levels of sex hormones, growth hormones, and decreased insulin. Vitamin D deficiency has also been found to play a role.

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.

[edit] 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.

[edit] 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.
Languages