© 2003 American Thoracic Society
Limitation to Exercise Tolerance in Chronic Obstructive Pulmonary DiseaseLook to the Muscles of AmbulationRehabilitation Clinical Trials Center Harbor-UCLA Research and Education Institute Torrance, California I just love physiologic research. I'll take it over evidence-based studies anytime. In this issue of AJRCCM (pp. 425–430), the article by Saey and coworkers (1) is a perfect case in point. For years, we've struggled to understand how exercise training improves exercise tolerance in patients with severe chronic obstructive pulmonary disease (COPD). The evidence couldn't be any clearer that rehabilitative training improves exercise tolerance; a large number of randomized trials can now be cited. An evidence-based document (2) and a meta-analysis (3) have proclaimed it as a fact. Now along comes this small, cleverly designed study that doesn't even feature a training intervention. Yet it shines like a beacon in the darkness to illuminate the truth. We can now understand why a training intervention should be successful in most patients. The physiologic rationale for the practice of pulmonary rehabilitation is now rock solid. It has been a long road. As recently as the late 1980s, exercise training was proclaimed to yield only psychological benefits (4); its main effect was to relieve unrealistic fears of dyspnea (5). Patients with severe disease were presumed to have a ventilatory limitation to exercise—that is, exercise was limited by intolerable dyspnea before the muscles of ambulation were stressed very much. A corollary of this theory was that improving function of the exercising muscle would be of no benefit. Besides, the thinking went, the ventilatory limitation precluded work rates capable of yielding the physiologic training effect necessary to improve muscle function. In other words, exercise above the critical training intensity was impossible. It took a while to chip away at the precepts of this theory. Physiologically based studies with effort-independent outcome measures clearly demonstrated that a physiologic training effect could be achieved at work rates that these patients could sustain. Lower circulating lactate levels at a given level of exercise (6) and higher levels of aerobic enzymes in the trained muscles (7) were unmistakable proof of better muscle function. This is apparently possible because the muscles of ambulation of most patients with COPD function so poorly (because of deconditioning and perhaps because of a COPD-specific myopathy) (8) that the critical training intensity is extraordinarily low. The second step was to show that improving function of the muscles of ambulation has a salutary effect on exercise tolerance. Can improving the function of the exercising muscles relieve ventilatory limitation? Ventilatory limitation to exercise occurs because the ventilatory requirement for exercise is abnormally high and because the level of ventilation that the patient can sustain is abnormally low. It was postulated (9) and then demonstrated (6) that because lactic acidosis stimulates ventilation, a training program would yield a lower ventilatory requirement in proportion to the reduction in lactic acidosis engendered by a given level of exercise. This finding led to the suggestion that only patients who are shown to be capable of sustaining an elevated lactate level during exercise should be subjected to high-intensity rehabilitative training programs (10). However, this concept did not hold water; patients with severe disease were shown to derive clear benefits from rigorous exercise programs whether or not they were able to raise circulating lactate levels substantially (11). A paradigm shift was needed. The concept that the exercise tolerance of severe COPD patient was limited only by the ventilation that they could sustain slowly started to be challenged. A large study asserted that, subjectively, patients with COPD were often limited in their exercise tolerance by leg discomfort as well as by dyspnea (12). Furthermore, exercise tolerance was found to be poorly correlated with measures of lung function (e.g., FEV1) and better correlated with leg muscle mass or cross-sectional area (13). Muscle strength was found to be a good predictor of exercise tolerance as well (14). The study of Saey and coworkers provides more than correlative information. An objective method of determining whether an exercise task yields fatigue of the muscles of ambulation was employed. In a group of 18 patients with severe COPD (average FEV1 was 29% predicted), half met their definition of contractile fatigue at the end of a constant work rate cycle ergometer test to exhaustion. Does this mean that this subgroup is limited in their exercise tolerance by their muscles of ambulation? This was by no means apparent because these patients also met the traditional measure of ventilatory limitation: Peak ventilation during exercise averaged 97% of the maximum voluntary ventilation. The clincher was that when the ventilatory limitation was relieved by a bronchodilator that yielded an FEV1 that averaged 15% higher than did placebo, exercise tolerance was not improved in the subgroup that exhibited contractile fatigue. Clearly, these patients were limited in their exercise tolerance by fatigue of their muscles of ambulation. Can we use this information to improve our selection of patients who are more likely to benefit from a program of exercise training? Probably not—at least not yet. The technique to determine contractile fatigue used by Saey and coworkers is technically demanding, probably specific to the type of exercise task employed and likely too variable to allow its use to select individual subjects. It is better to use these results to spur rededication to establishing strategies aimed at improving the function of the muscles of ambulation in all patients with COPD. Exercise intolerance is often the chief complaint of these patients and is frequently the major source of debility. Exercise training will likely remain the most effective way to improve exercise tolerance, and methods to improve the effectiveness of rehabilitative exercise programs should be explored. Searches should also be conducted for pharmacologic agents capable of improving muscle endurance. Physiologic principles should guide the design of experiments to evaluate these therapeutic advances. Acknowledgments R.C. has no declared conflict of interest. REFERENCES
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