© 2002 American Thoracic Society
Muscle Mass, Not Body Weight, Predicts Outcome in Patients with Chronic Obstructive Pulmonary DiseaseDivision of Pulmonary, Critical Care and Sleep Medicine State University of New York at Buffalo Veterans Administration Medical Center Buffalo, New York It has been known for many years that weight loss and low body weight are common in patients with advanced chronic obstructive pulmonary disease (COPD). Moreover, it has been shown that low body weight is associated with increased mortality independent of lung function in patients with COPD (1, 2). However, unlike starvation in which the predominant body compartment affected is fat, the weight loss of COPD is similar to that of other chronic diseases and preferentially involves the loss of muscle mass. It is this loss of muscle mass, rather than body weight per se, that is likely to be primarily responsible for the observed negative consequences. To the extent that body weight reflects lean body mass, body weight will be a good surrogate marker. But under conditions, such as obesity, in which body weight does not accurately reflect lean body mass, its discriminatory power will diminish markedly. Obesity is extremely common in the western world and is increasing in incidence. Thus, body weight may not be the ideal measure to reflect nutritional status in patients with COPD. For example, body weight and body composition have been measured in 255 patients with COPD (3). Low body weight implying nutritional depletion was defined as a weight less than 90% of ideal body weight and was seen in 89 of 255 patients (35%). A reduction in fat-free mass without a reduction in body weight was seen in 24 of 255 patients (9.4%). A reduction in body weight without a reduction in fat-free mass was seen in 23 of 255 patients (9.0%). Thus, discrepancies between measures of body weight and measures of fat-free mass are not uncommon in this patient population. Reduction in fat-free mass is a better predictor of peak exercise performance than the body mass index (4). Patients with a reduction in fat-free mass have worse health-related quality of life than underweight patients with preserved fat-free mass (5). These results again suggest that it is a reduction in fat-free mass rather than weight per se that affects patients functionally. In this issue of AJRCCM (pp. 809–813), Marquis and colleagues (6) evaluate whether a measure of muscle mass would be a better predictor of mortality than measures of body weight. They measured mid-thigh muscle cross-sectional area by computerized tomography scan and body mass index in 142 patients with COPD enrolled in their pulmonary rehabilitation program. Patients were followed for 41 ± 18 months. During this period, 25 patients died representing a mortality rate of 17.6%. Mean body mass index was essentially normal for this group of patients, whereas mean mid-thigh muscle cross-sectional area was 72% of the normal area. This observation in itself points out the limitations of using body weight for assessing depletion of lean body mass. With multivariate analysis, only mid-thigh muscle cross-sectional area and the FEV1 were significant predictors of mortality. Thus, it is muscle mass and not body weight that is the important physiologic variable. In this study, muscle mass was measured directly by computerized tomography scan. The muscles that were assessed, the proximal muscles of the lower extremity, are particularly affected in patients with COPD (7, 8). Whether similar findings would have been obtained if the investigators had made a global assessment of fat-free mass remains to be determined. This distinction is important. Some methods for assessing fat-free mass are relatively simple and less cumbersome and expensive than a computerized tomography scan and could be more easily used in the clinical arena. The investigators tried to estimate mid-thigh muscle cross-sectional area from simple anthropomorphic measurements. Unfortunately, although this approach has been used successfully in normal subjects, it proved unreliable in this patient population. Patients entering a pulmonary rehabilitation program represented the study population in this study. Whether such patients differ from patients with COPD who do not choose to enter a rehabilitation program needs to be determined. The smoking history of the patients is not clearly stated. Many rehabilitation programs require that patients have successfully quit smoking for a certain period of time before entry in the rehabilitation program. Clearly, continued smoking would be expected to have a significant effect on progression of COPD and mortality, and how this influences muscle mass needs to be determined. In this study, the authors showed a relationship between muscle mass and mortality. Correlation, however, does not prove causation. Thus, we cannot say whether a reduction in muscle mass causes an increase in mortality or whether a reduction in muscle mass is merely a reflection of severity of disease. If a reduction in muscle mass is responsible for the increased mortality, then interventions that successfully increase muscle mass should lead to improvement in mortality. No study addressing this issue has been performed. Several short-term studies have addressed whether interventions that increase muscle mass can lead to improvements in exercise capacity and quality of life. Addition of strength training to a pulmonary rehabilitation program led to significant increases in muscle strength and mass but to no additional increase in exercise capacity or quality of life as compared with that achieved by an endurance exercise program (9). Addition of anabolic steroids to pulmonary rehabilitation resulted in increases in fat-free mass but no additional increase in exercise capacity (10, 11). The mechanisms of muscle atrophy remain to be fully elucidated. In particular, is deconditioning largely or solely responsible for the muscle atrophy or does the disease itself induce systemic effects that promote muscle atrophy? In other clinical models of cachexia, such as cancer, acquired immunodeficiency syndrome, or chronic heart failure, hormonal changes and release of proinflammatory cytokine mediators are believed to be important mechanistically (12). Therapies that address these underlying mechanisms could potentially result in more favorable outcomes than simple reconditioning programs. In summary, this study highlights the significance of changes in body composition in patients with COPD and addresses the most important outcome parameter of all: mortality. It further points out the limitations of using simple measures of body weight to address nutritional status and muscle mass in patients with COPD. REFERENCES
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