Sarcopenia and Its Implications for the Elderly{

European Journal of Clinical Nutrition (2000) 54, Suppl 3, S40±S47 ß 2000 Macmillan Publishers Ltd All rights reserved 0954±3007/00 $15.00 www.nature.com/ejcn Sarcopenia and its implications for the elderly{ R Roubenoff1* 1Nutrition, Exercise Physiology, and Sarcopenia (NEPS) Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tuffs University, Boston, MA, USA Sarcopenia is the loss of muscle mass and strength with age. Sarcopenia is a part of normal aging, and occurs even in master athletes, although it is clearly accelerated by physical inactivity. Sarcopenia contributes to disability, reduced ability to cope with the stress of a major illness, and to mortality in the elderly. The etiology of sarcopenia is unclear, but several important factors have been identi®ed. These include loss of alpha motor neurons, decline in muscle cell contractility, and several potential humoral factors, such as androgen and estrogen withdrawal and increase in production of catabolic cytokines. Treatment of sarcopenia with progressive resistance training is safe and effective, but dissemination of this technique to the general population has yet to occur. As the number of elderly persons increases exponentially in the new century, a public health approach to prevention and treatment of sarcopenia, based on increasing physical activity at all ages, will be crucial to avoiding an epidemic of disability in the future. Descriptors: aging; sarcopenia European Journal of Clinical Nutrition (2000) 54, S40±S47 De®ning sarcopenia hypertrophy, at least in the ®rst few months of training. For example, Figure 2 shows the strength and vastus lateralis Sarcopenia is the loss of muscle mass and strength caused area (measured by CT scan) lost over a 12 y follow-up by aging (Rosenberg, 1989). It is distinct from muscle loss period in seven healthy men, and the amount gained during (cachexia) caused by in¯ammatory disease, or from the a 12 week period of intensive resistance training (Frontera weight loss and attendant muscle wasting caused by starva- et al, 2000). It is clear that there is hysteresis in this system: tion or advanced disease (Roubenoff et al, 1997a). As be®ts the decline and the regain occur at vastly different rates. a truly age-driven phenomenon, it is universal with Thus, de®ning sarcopenia solely on compositional terms advanced age. That is, reduced muscle mass and strength may be useful and attractive for research purposes, but it are evident in all elderly persons compared to young, may be simplistic in explaining functional changes caused healthy, physically active young adults. If the sarcopenia by treatment of sarcopenia. progresses beyond a threshold of functional requirements, it Second, there is reasonable evidence that there is a limit leads to disability and frailty, and this can occur indepen- on how much lean body mass can be lost before death dently of any disease-induced frailty (Figure 1). Of course, supervenes. The available data, based on starvation superimposed illness will accelerate the loss of muscle (Winick, 1979), AIDS patients (Kotler et al, 1989), and mass, and thus increase the risk of disability, frailty, and critical illness (Tellado et al, 1989), suggest that loss of death. more than about 40% of baseline lean mass is fatal. There is no absolute level of lean mass, body cell mass, `Baseline' is a slippery concept here, because again abso- or muscle mass at which one can de®nitely say that lute mass is not explanatory Ð basketball players do not sarcopenia is present. Such a de®nition would be an necessarily outlive jockeys Ð but rather the amount of loss important advance. In reaching such a de®nition, one as a function of the baseline mass that the individual started should consider two important and generally agreed-upon with. Reference Man and Woman are one benchmark, concepts in relation to lean body mass. First, there is a based on a few cadaver studies in generally healthy persons direct structure ± function link between muscle mass and (Ellis, 1990). Kehayias et al (1997) de®ned baseline as the strength, in that more muscle generally equals greater mean for adults aged 20 ± 30 y; no healthy subjects were strength and vice versa. However, the function de®ning found below approximately 70% of that standard, and there the relationship between muscle loss and strength loss is was a steady decline in body cell mass for both men and not the same as that applying to muscle and strength gain. women across age groups between 30 and 100 y (Figure 3). Pharmacologic interventions such as growth hormone or The latter point also raises the issue of the importance of testosterone, which increase lean mass (and evidently sarcopenia as an indicator of reduced protein stores for muscle mass as well) do not alter strength much, while times of stress. It is well accepted that during illness, progressive resistance training, which causes large gluconeogenesis increases in importance, while ketogenesis increases in strength, can do so with little evident muscle is relatively suppressed, so that protein is burned for energy in excess of the levels seen in starvation adaptation. Given *Correspondence: R Roubenoff, Nutrition, NEPS Laboratory, Human the anorexia caused by acute illness, and by the iatrogenic Nutrition Research Center on Aging, 711 Washington Street, Boston, MA limitation on dietary intake that often obtains in hospitals, 02111, USA. endogenous protein stores are crucial in determining the E-mail: [email protected] availability of metabolic substrate to cope with the illness, {The contents of this publication do not necessarily re¯ect the views or and thus the ability to survive it. Therefore, it is no wonder policies of the US Department of Agriculture nor does mention of trade names, commercial products, or organizations imply endorsement by the that elderly, sarcopenic patients fare worse than young, US Government. healthy adults for almost all diseases. Tellado et al (1989) Sarcopenia R Roubenoff S41 Figure 1 Relationship between sarcopenia, frailty, and medical out- comes. (From Roubenoff & Harris, 1997c). have shown that measurement of body cell mass was the only independent determinant of survival in intensive care unit patients in multivariate analysis, removing the signi®- cance of univariate predictors such as albumin, age, and even diagnosis. Thus, the metabolic signi®cance of sarcopenia in illness should be considered independently of its Figure 3 Body cell mass, measured as total body potassium (TBK) functional impact during times of better health, as both are per kg body weight, as a function of age in a cross-sectional study (from important to the survival and well-being of elderly persons. Kehayias et al, 1997). Data are expressed as a percentage of the reference 20 ± 30-y-old groups for men (s) and women (6) separately. (From Kehayias et al, 1997). Epidemiology of sarcopenia muscle mass 2 or more standard deviations below the There in one population-based study of the prevalence of mean for young healthy participants in the Rosetta Study, sarcopenia with advancing age. Data are available from the a large cross-sectional study of body composition in New New Mexico Elder Health Survey, by Baumgartner et al York. The prevalence of sarcopenia by this de®nition (1998), who measured appendicular muscle mass by dual- increased from 13 ± 24% of persons under age 70 to over energy X-ray absorptiometry (DXA) in 883 elderly Hispa- 50% of those over age 80 y. nic and non-Hispanic White men and women. The subjects Kehayias et al (1997) found that the quality of the lean were selected randomly from the Health Care Financing body mass, de®ned as the ratio of cell mass (measured by Administration (HCFA) Medicare listing for Bernalillo whole body potassium counting) to lean mass (measured by County, New Mexico. A total of 2200 subjects were hydrodensitometry or neutron activation), declined with sampled; 534 had died, moved, could not be contacted, or age in a cross sectional analysis. These data suggest that were ineligible. Of the 1666 eligible subjects contacted, sarcopenia is universal, and indeed this would be consistent 1130 (67.8%) completed the home interview and 883 with an age-related phenomenon, and complement the data (53%) underwent DXA. Sarcopenia was de®ned as a of Baumgartner et al, where a cutoff was used to de®ne Figure 2 Change in strength and vastus lateralis area (measured by CT scan) over a 12 y follow-up period in 7 healthy men, and the amount gained during a 12 week period of intensive resistance training in the same men. (From Frontera et al, 2000). European Journal of Clinical Nutrition Sarcopenia R Roubenoff S42 sarcopenia. Gallagher et al (1997) have shown that the ®bers. The capillary=®ber ratio was also signi®cantly cross-sectional change in appendicular muscle mass mea- reduced (1.39 vs 1.08, P < 0.05). These data indicate that sured by DXA parallels the decline in total body cell mass longitudinal change in the amount of muscle is strongly measured by total body potassium (TBK), the reference linked to change in strength in healthy elderly men. method for this compartment. Cross-sectional studies of muscle ®ber distribution have suggested that the loss of muscle is largely con®ned to type II ®bers, the fast twitch Impact of sarcopenia cells that are most responsible for strength and anaerobic, short-term movements (Lexell, 1995). There is a strong direct relationship between muscle mass However, one cannot easily come to conclusions about and strength. Thus, sarcopenic persons are weaker than the phenomenology of sarcopenia based on cross-sectional persons with normal muscle mass. In reality, there may be a data. Longitudinal data are harder to come by, but a few feedback loop between muscle mass and function that can studies do exist.

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