RESPONSE: DEFINING EXERCISE CAPACITY, EXERCISE PERFORMANCE, AND A SEDENTARY LIFESTYLE

Dear Editor-in-Chief: The difficulty that White and Fulcher express in accepting our data may lie in a misinterpretation of the terminology and testing procedures used by exercise physiologists to define exercise status. Exercise capacity. The two critical measures of exercise capacity are maximal oxygen uptake and the lactate threshold (3,9). These measures can be precisely quantified according to well-accepted criteria (6) and were found to be normal in our study. Therefore, the claim that we “did not give the data” to support our finding is untrue. We suspect that they are confusing “exercise capacity” with “exercise performance” where the time taken to complete a given task or total work completed may be used as measures. Although no one denies that “exercise performance” is impaired in CFS, obtaining a useful index of performance in sedentary individuals is notoriously difficult (7,8) and almost impossible where there is a strong element of unexplained fatigue. Sedentary. “Sedentary” (2,11) is used to define normal, healthy individuals not engaged in regular, structured physical activity and normative population data abound to describe the exercise capacity of such individuals (1,5). The majority of individuals (> 70%) in Western societies can be categorized as “sedentary,” and their exercise capacity is appropriate to meet the demands of this lifestyle. Therefore, it is misleading to state, “patients with CFS were ...at least as deconditioned as sedentary healthy controls.” Gender. Comparisons of exercise status between subject groups that include members of both genders, whether the numbers in each group are the same or not, are meaningless. All normative population data (1,5), describing the exercise status of sedentary individuals, are routinely stratified on a gender basis. Exercise and CFS. Although it is well accepted that an appropriate graded exercise program will increase the exercise capacity of sedentary individuals, the central issue is whether CFS patients have a loss of normal, sedentary exercise capacity, which then requires correction. Our study (10) provided no evidence of a reduction in exercise capacity and, therefore, there is no physiological basis for instituting an exercise-training program. We feel that much of the confusion that White and Fulcher find between our study and those of other authors resides in the definitions used and the exercise tests employed. From our reading, much of the exercise testing in CFS patients has been directed at exercise performance. Hence, the widely reported reductions in maximal heart rate, ventilation, workload, and peak oxygen uptake are not unexpected. They almost certainly reflect the outcome of symptom-limited protocols where tests were terminated prematurely by unexplained fatigue rather than a reduced exercise capacity, an opinion shared by Fischler et al. (4). We found (10) that the “metabolic engine” of CFS patients was not different from that expected in healthy sedentary individuals of a similar age and gender. Therefore, the cause of their fatigue, which severely reduces exercise performance and results in extreme postexercise exhaustion, must be sought elsewhere. Charli Sargent, B App Sci, B Sc (Hons) Garry Scroop, MD, PhD

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