Sarcopenia

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SARCOPENIA

Sarcopenia, from a Greek word meaning ‘‘poverty of flesh,’’ is the loss of muscle mass and strength caused by normal aging. It is distinct from muscle loss caused by inflammatory disease (cachexia), and from the weight loss and attendant muscle wasting caused by starvation or advanced disease. Compared to young, healthy, physically active young adults, reduced muscle mass and strength are evident in all elderly persons. If the sarcopenia progresses beyond a threshold of functional requirements, it leads to disability and frailty, and this can occur independently of any disease-induced frailty. Of course, a superimposed illness will accelerate the loss of muscle mass, and thus increase the risk of disability, frailty, and death.

There is no absolute level of lean mass, body cell mass, or muscle mass at which one can definitely say that sarcopenia is present. However, it is important to consider two important and generally agreed-upon concepts in relation to lean body mass. First, there is a direct structure-function link between muscle mass and strength—more muscle generally equals greater strength, and vice versa. Second, there is reasonable evidence that there is a limit on how much lean body mass can be lost before death supervenes. The available data, based on patients suffering from starvation, AIDS, and critical illnesses, suggest that loss of more than about 40 percent of baseline lean mass is fatal. Kehayias, et al. (1997) defined baseline lean mass as the mean for adults between twenty and thirty years of age; no healthy elderly adults were found below approximately 70 percent of that standard, and there was a steady decline in body cell mass for both men and women across age groups between the ages of thirty and one hundred.

This decline in body cell mass with age raises the issue of the importance of sarcopenia as an indicator of reduced protein stores for times of stress. During illness, protein is burned for energy in excess of the levels seen in starvation adaptation. Given the anorexia caused by acute illness, endogenous protein stores are crucial in determining the availability of metabolic substrate needed to cope with the illness, and thus the ability to survive it. It is no wonder, then, that elderly, sarcopenic patients fare worse than young, healthy adults for almost all diseases. For this reason, the metabolic significance of sarcopenia in illness should be considered independently of its functional impact during times of better health, as both are important to the survival and well-being of elderly persons.

Prevalence

The prevalence of sarcopenia was studied in the New Mexico Elder Health Survey, which measured appendicular muscle mass by dual-energy X-ray absorptiometry (DXA) in 883 elderly Hispanic and non-Hispanic white men and women. Sarcopenia was defined as a muscle mass two or more standard deviations below the mean for young healthy participants. The prevalence of sarcopenia by this definition increased from between 13 percent and 24 percent of persons under age seventy to over 50 percent of those over eighty years of age. Sarcopenic women had 3.6 times higher rates of disability, and men 4.1 times higher rates, compared to study participants with normal muscle mass.

Kehayias, et al. (1997) found that the quality of the lean body mass, defined as the ratio of cell mass (the metabolically active portion of the body) to lean mass (cell mass plus extracellular water and connective tissue), declined with age. These data suggest that sarcopenia is universal, and indeed this would be consistent with an age-related phenomenon. It also complements the data of Baumgartner, et al., where a cutoff was used to define sarcopenia. Cross-sectional data also indicate that older persons have a lower amount of type II (fast-twitch, glycolytic) fibers in their muscles than young adults, but that type I (slow-twitch, oxidative) fibers are comparable in number.

Structural and functional relationships

As noted earlier, these data all define sarcopenia in terms of its compositional, rather than functional (strength) aspect. However, there are data suggesting that the decline in strength with age exceeds the decline in lean mass. Studies of change in muscle strength over time have shown declines, no change, or gains in strength over periods ranging from four to twenty-five years. A reduction in type II muscle fibers has been shown in some studies, but no change was found in others. In addition to the quantitative decline in muscle with age, there is a qualitative decline, with reduced force production by single fibers from elderly men compared to young men.

Etiology

The etiology of sarcopenia remains unclear, but there are many possible factors involved (see Roubenoff and Hughes, 2000, for a detailed review). These include: (1) loss of alpha motor neurons in the central nervous system with age; (2) change in hormonal milieu in favor of a more catabolic muscle profile, with reductions in growth hormone, testosterone, and estrogen; (3) increased production of catabolic cytokines, especially interleukin-6 and possibly interleukin-1 beta and tumor necrosis factor-alpha, which favor muscle protein breakdown; (4) reduced physical activity, which leads to increased fat accumulation and possibly to resistance to the anabolic effects of insulin, perhaps due to increased tumor necrosis factor production by fat cells; and (5) reduced dietary intake of protein and energy.

Treatment of sarcopenia

While both cardiopulmonary fitness and muscle strength are important determinants of functional capacity; in frail, elderly persons with advanced sarcopenia, muscle weakness may be more limiting than aerobic fitness. Weakness in turn leads to further disuse, as people avoid activities that are uncomfortable. Thus, reduced physical activity follows loss of muscle mass, and then accelerates it by removing the trophic stimulus of the activity. The improved survival and reduced disability of elderly athletes who remain physically active suggest that such a vicious cycle is avoidable under some circumstances. More importantly, perhaps, the ability to reverse these changes with progressive resistance training (PRT) suggests that they are modifiable effects of aging.

Many studies have now documented that exercise training can reverse sarcopenia, and that people who retain a high level of physical activity throughout their lives maintain a higher level of physical functioning and live longer. In addition, physical activity is one of the few factors that are within the control of nearly everyone, and it does not require pharmacological treatment. Moreover, Fiatarone, et al. have shown that it is never too late to begin strength training, and that even frail, elderly, nursing home patients in their nineties retain the plasticity of muscle in response to training. The effectiveness of strength training is clear, and the effect can be obtained in as little as eight weeks with training two to three times per week. Strength training can be done with low-tech, relatively low-cost equipment in the home, or in congregate settings such as gyms or senior centers. In addition, strength training can be used safely in people with arthritis, coronary artery disease, heart failure, and renal failure. The difficulty with strength training is translating it into an effective public health intervention on a large scale. This requires training an adequate number of exercise leaders who can, in turn, train others. This is a serious impediment to application of this therapy.

Ronenn Roubenoff

See also Andropause; Deconditioning; Exercise; Frailty.

BIBLIOGRAPHY

Baumgartner, R. N.; Koehler, K. M.; Gallagher, D.; Romero, L.; Heymsfield, S. B.; Ross, R. R.; Garry, P. J.; and Lindeman, R. D. ‘‘Epidemiology of Sarcopenia among the Elderly in New Mexico.’’ American Journal of Epidemiology 147 (1998): 755–763.

Fiatarone, M. A.; O’Neill, E. F.; Ryan, N. D.; Clements, K. M.; Solares, G. R.; Nelson, M. E.; Roberts, S. B.; Kehayias, J. J.; Lipsitz, L. A.; and Evans, W. J. ‘‘Exercise Training and Nutritional Supplementation for Physical Frailty in Very Elderly People.’’ New England Journal of Medicine 330 (1994): 1769–1775.

Frontera, W. R.; Hughes, V. A.; Fielding, R. A.; Fiatarone, M. A.; Evans, W. J.; and Roubenoff, R. ‘‘Aging of Skeletal Muscle: A 12-Year Longitudinal Study.’’ Journal of Applied Physiology 88 (2000): 1321–1326.

Kallman, D. A.; Plato, C. C.; and Tobin, J. D. ‘‘The Role of Muscle Loss in the Age-Related Decline of Grip Strength: Cross-Sectional and Longitudinal Perspectives.’’ Journal of Gerontology 45 (1990): M82–M88.

Kehayias, J. J.; Fiatarone, M. F.; Zhuang, H.; and Roubenoff, R. ‘‘Total Body Potassium and Body Fat: Relevance to Aging.’’ American Journal of Clinical Nutrition 66 (1997): 904–910.

Poehlman, E. T.; Toth, M. J.; and Gardner, A. W. ‘‘Changes in Energy Balance and Body Composition at Menopause: A Controlled Longitudinal Study.’’ Annual of Internal Medicine 123 (1995): 673–675.

Roubenoff, R.; Harris, T. B.; Abad, L. W.; Wilson, P. W. F.; Dallal, G. E.; and Dinarello, C. A. ‘‘Monocyte Cytokine Production in an Elderly Population: Effect of Age and Inflammation.’’ Journal of Gerontology 53A (1998): M20–M26.