Exercise Limitation and Pulmonary Rehabilitation in Chronic Obstructive Pulmonary Disease
1992; Elsevier BV; Volume: 67; Issue: 2 Linguagem: Inglês
10.1016/s0025-6196(12)61316-0
ISSN1942-5546
AutoresChristopher O. Olopade, Kenneth C. Beck, Robert W. Viggiano, Bruce A. Staats,
Tópico(s)Cardiovascular and exercise physiology
ResumoImpairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined. Impairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined. Patients with chronic obstructive pulmonary disease (COPD) often have poor tolerance of exercise.1Nery LE Wasserman K French W Oren A Davis JA Contrasting cardiovascular and respiratory responses to exercise in mitral valve and chronic obstructive pulmonary diseases.Chest. 1983; 83: 446-453Crossref PubMed Scopus (87) Google Scholar, 2Pineda H Haas F Axen K Haas A Accuracy of pulmonary function tests in predicting exercise tolerance in chronic obstructive pulmonary disease.Chest. 1984; 86: 564-567Crossref PubMed Scopus (48) Google Scholar The degree of exercise intolerance seems to reflect the severity of the underlying COPD.2Pineda H Haas F Axen K Haas A Accuracy of pulmonary function tests in predicting exercise tolerance in chronic obstructive pulmonary disease.Chest. 1984; 86: 564-567Crossref PubMed Scopus (48) Google Scholar Other factors, however, such as muscle fatigue, malnutrition, and cardiac dysfunction, contribute to the difficulty with exercise in patients with COPD. In the 1950s and early 1960s, the accepted recommendation was to impose exercise limitations for patients with COPD. Because Barach and colleagues3Barach AL Bickerman HA Beck G Advances in the treatment of non-tuberculous pulmonary disease.Bull N Y Acad Med. 1952; 28: 353-384PubMed Google Scholar noted progressive improvement in the ability to walk without dyspnea in patients with COPD who remained active (in contrast to their sedentary counterparts), they suggested that a physiologic response similar to a training effect in athletes may have been produced in such patients. The scientific basis for recommending exercise rehabilitation has only recently been established and, therefore, can only now be recommended. Pierce and co-workers4Pierce AK Taylor HF Archer RK Miller WF Responses to exercise training in patients with emphysema.Arch Intern Med. 1964; 113: 28-36Crossref PubMed Scopus (57) Google Scholar attempted to understand the physiologic processes underlying the improved exercise tolerance in patients with COPD who were active. Nine patients with severe but stable COPD were enrolled in an exercise training program for 3 to 20 weeks after an initial period of acclimatization with treadmill exercise. After the training, the heart rate, respiratory rate, and minute ventilation substantially decreased and the exercise tolerance improved. These investigators, however, were unable to demonstrate any improvement in pulmonary function in these patients. They speculated that a physiologic training effect may have occurred. During the past 2 decades, many investigators have attempted to explain the causes of improved exercise tolerance in active patients with COPD. The approach to rehabilitation in patients with COPD has also dramatically changed; exercise rehabilitation is now commonplace. The numerous proposed reasons for exercise intolerance are discussed in the following material. Impaired lung mechanics is one of the major factors that limit exercise performance in patients with COPD.5Grassino A Gross D Macklem PT Roussos C Zagelbaum G Inspiratory muscle fatigue as a factor limiting exercise.Bull Eur Physiopathol Respir. 1979; 15: 105-110PubMed Google Scholar, 6Jones NL Berman LB Gas exchange in chronic air-flow obstruction.Am Rev Respir Dis. 1984; 129: S81-S83PubMed Google Scholar, 7Rochester DF Arora NS Respiratory muscle failure.Med Clin North Am. May 1983; 67: 573-597PubMed Google Scholar, 8Stubbing DG Pengelly LD Morse JLC Jones NL Pulmonary mechanics during exercise in subjects with chronic airflow obstruction.J Appl Physiol. 1980; 49: 511-515PubMed Google Scholar In patients with severe COPD, expiratory flow may be limited during tidal breathing. One of the strategies adopted by these patients to overcome limitation of expiratory flow (which can curtail exercise) is breathing at a higher end-expiratory lung volume to achieve higher expiratory flows (Fig. 1). This strategy increases the maximal exercise ventilation. The increase in end-expiratory lung volume is associated with expansion of both the thoracic cage and the lung parenchyma—factors that, unfortunately, necessitate an increase in the elastic work of breathing. In addition, at high lung volumes, the diaphragm flattens, and the ribs become horizontally oriented; thus, both the intercostal muscles and the diaphragm are placed in unfavorable mechanical positions (Fig. 2). The ensuing pattern of contraction may cause the diaphragm to act like an expiratory muscle. This response is discernible on examination by inward movement of the costal region (Hoover's sign). Breathing at higher lung volumes decreases the patient's ability to increase tidal volume during exercise; hence, an increase in respiratory frequency is the major remaining means of increasing ventilation (ventilation equals frequency of respiration multiplied by tidal volume). The rapid, shallow pattern of breathing in patients with COPD contrasts with that in normal persons, who typically have an increase in tidal volume before an increase in respiratory frequency with progressive exercise.9Matthews JI Bush BA Ewald FW Exercise responses during incremental and high intensity and low intensity steady state exercise in patients with obstructive lung disease and normal control subjects.Chest. 1989; 96: 11-17Crossref PubMed Scopus (28) Google Scholar Increased resistance to expiratory flow and decreased mechanical advantage of inspiratory muscles at high lung volumes result in an increase in the work or oxygen cost of breathing, which ultimately may lead to fatigue of the inspiratory muscles (diaphragm).Fig. 2Diagram depicting flattening of diaphragm and loss of region of apposition in patient with emphysema. Contraction of flattened diaphragm leads to inward movement of costal region, which is noticeable on physical examination (Hoover's sign).View Large Image Figure ViewerDownload (PPT) Bellemare and Grassino10Bellemare F Grassino A Effect of pressure and timing of contraction on human diaphragm fatigue.J Appl Physiol. 1982; 53: 1190-1195Crossref PubMed Scopus (6) Google Scholar, 11Bellemare F Grassino A Force reserve of the diaphragm in patients with chronic obstructive pulmonary disease.J Appl Physiol. 1983; 55: 8-15PubMed Google Scholar demonstrated the importance of the ratio of inspiration time to total breath duration and the ratio of mean transdiaphragmatic pressure (abdominal pressure minus pleural pressure) generated with each inspiration to maximal transdiaphragmatic pressure as determinants of diaphragmatic endurance in normal volunteers and patients with COPD. They found that when fatigue of the respiratory muscles developed, the tension time index (the product of the ratio of inspiration time to total breath duration and the ratio of mean transdiaphragmatic pressure with each inspiration to maximal transdiaphragmatic pressure) was more than 0.15.10Bellemare F Grassino A Effect of pressure and timing of contraction on human diaphragm fatigue.J Appl Physiol. 1982; 53: 1190-1195Crossref PubMed Scopus (6) Google Scholar, 11Bellemare F Grassino A Force reserve of the diaphragm in patients with chronic obstructive pulmonary disease.J Appl Physiol. 1983; 55: 8-15PubMed Google Scholar Patients with severe COPD have limited ventilatory reserve even at rest and have been shown to have a resting tension time index that approaches 0.15 (normal, 0.02).11Bellemare F Grassino A Force reserve of the diaphragm in patients with chronic obstructive pulmonary disease.J Appl Physiol. 1983; 55: 8-15PubMed Google Scholar With the development of acute respiratory failure, patients may deteriorate from the borderline fatigue zone into the definite fatigue zone (a tension time index that exceeds 0.15).7Rochester DF Arora NS Respiratory muscle failure.Med Clin North Am. May 1983; 67: 573-597PubMed Google Scholar Similar findings have been noted during exercise in patients with COPD. Gas exchange is one of the major functions of the lung. The efficiency of gas exchange is dependent on the balance between alveolar ventilation and pulmonary blood flow (perfusion). In a normal lung, regions with the most ventilation tend to have the most perfusion, and, conversely, poorly ventilated areas receive minimal perfusion. One estimate of the degree of “matching” of ventilation to perfusion is the ratio of physiologic dead space to tidal volume (Vd/Vt). The Vd/Vt is optimal when perfusion is well matched to ventilation. At rest Vd/Vt is normally approximately 0.3—that is, 30% of a given breath is “wasted.” Most of this dead-space ventilation is used to fill the conducting airways. During exercise, the Vd/Vt declines to 0.2 or less.12Wasserman K Van Kessel AL Burton GG Interactions of physiological mechanisms during exercise.J Appl Physiol. 1967; 22: 71-85PubMed Google Scholar In patients with COPD (especially those with emphysema, because of the destruction of the gas-exchanging units), regions of appreciable ventilation-to-perfusion mismatch impair oxygenation of the blood and also elimination of carbon dioxide. At rest, the Vd/Vt is increased as a result of ventilation to poorly perfused alveoli (so-called alveolar dead space). In contrast to the normal decrease in Vd/Vt that occurs during exercise, patients with COPD may experience further increases or lack of decline in Vd/Vt. The high Vd/Vt does not result in hypoxemia but increases the ventilatory requirements of an already overtaxed system. This result causes the ventilatory equivalent for carbon dioxide to be increased;13Jones NL Jones G Edwards RHT Exercise tolerance in chronic airway obstruction.Am Rev Respir Dis. 1971; 103: 477-491PubMed Google Scholar, 14Marcus JH McLean RL Duffell GM Ingram Jr, RH Exercise performance in relation to the pathophysiologic type of chronic obstructive pulmonary disease.Am J Med. 1970; 49: 14-22Abstract Full Text PDF PubMed Scopus (34) Google Scholar together with a reduced maximal voluntary ventilation, these factors contribute to exercise limitation. In addition, hypoxemia may develop in many patients because of perfusion of poorly ventilated alveoli. Pulmonary capillary blood from these regions is not adequately oxygenated, and hypoxemia results when this blood is mixed in the left atrium with normally oxygenated blood. Ventilation-to-perfusion mismatch causes an increase in the oxygen partial pressure difference between alveolar air and arterial blood, which may become worse with exercise. The hypoxemia can be—but is not always—an exercise-limiting factor.6Jones NL Berman LB Gas exchange in chronic air-flow obstruction.Am Rev Respir Dis. 1984; 129: S81-S83PubMed Google Scholar Depending on ventilatory drive, hypoxemia may further stimulate ventilation and hasten exercise limitation. In the past, patients with COPD without coexisting ischemic heart disease or cor pulmonale were not thought to have exercise limitations because of cardiac dysfunction. Nevertheless, studies conducted by Morrison and associates15Morrison DA Adcock K Collins CM Goldman S Caldwell JH Schwarz MI Right ventricular dysfunction and the exercise limitation of chronic obstructive pulmonary disease.J Am Coll Cardiol. 1987; 9: 1219-1229Abstract Full Text PDF PubMed Scopus (75) Google Scholar and Mahler and colleagues16Mahler DA Brent BN Loke J Zaret BL Matthay RA Right ventricular performance and central circulatory hemodynamics during upright exercise in patients with chronic obstructive pulmonary disease.Am Rev Respir Dis. 1984; 130: 722-729PubMed Google Scholar with use of hemodynamic monitoring and radionuclide studies during exercise have shown that right ventricular dysfunction does occur in some patients during exercise. In these patients, pulmonary artery pressure increased in the setting of normal left ventricular function. The increased pulmonary artery pressure returned to normal or near normal after exercise. In patients with severe COPD, further pulmonary hypertension often develops during exercise and may cause premature termination of exercise. Dyspnea caused by left ventricular dysfunction and that caused by pulmonary disease are sometimes difficult to distinguish clinically. Left ventricular dysfunction is uncommon in patients with COPD in whom such dysfunction is clinically suspected.17Kline LE Crawford MH MacDonald Jr, WJ Schelbert H O'Rourke RA Moser KM Noninvasive assessment of left ventricular performance in patients with chronic obstructive pulmonary disease.Chest. 1977; 72: 558-564Crossref PubMed Scopus (46) Google Scholar In an evaluation of the relationship between right and left ventricular function in patients with varied degrees of severity of COPD, however, Slutsky and colleagues18Slutsky RA Ackerman W Karliner JS Ashburn WL Moser KM Right and left ventricular dysfunction in patients with chronic obstructive lung disease: assessment by first-pass radionuclide angiography.Am J Med. 1980; 68: 197-205Abstract Full Text PDF PubMed Scopus (27) Google Scholar found that left ventricular dysfunction correlated with the decline in right ventricular function only in patients with severe COPD. The results of that study suggested that patients with severe COPD and pulmonary hypertension have worsening of left ventricular function during exercise when right ventricular dysfunction is clearly evident. An increased perception of breathlessness may contribute to exercise limitation in patients with COPD. Woodcock and co-workers19Woodcock AA Johnson MA Geddes DM Breathlessness, alcohol, and opiates (reply to letter to the editor).N Engl J Med. 1982; 306: 1363-1364Crossref PubMed Scopus (51) Google Scholar postulated that the sensation of breathlessness may constitute a greater limitation to exercise than mechanical or cardiovascular factors. They administered a mild depressant of the central nervous system (dihydrocodeine) to patients with severe chronic limitation of airflow and demonstrated a decreased degree of breathlessness and increased exercise tolerance in comparison with the control situation. In some patients with COPD, the control of breathing may be abnormal and may potentially contribute to retention of carbon dioxide. Assessing the ventilatory response to inhaled carbon dioxide is one method of determining the sensitivity of the respiratory drive. The ventilatory response, however, is nonspecific20Dempsey JA CO2 response: stimulus definition and limitations.Chest. 1976; 70: 114-118PubMed Google Scholar because it is influenced by numerous factors, including abnormal pulmonary function and altered acid-base status, both of which are present in patients with COPD. The pressure generated in the first 100 ms when the inspiratory muscles contract during transient occlusion of the airway may be a better measure of respiratory drive.21Murciano D Aubier M Bussi S Derenne J-P Pariente R Milic-Emili J Comparison of esophageal, tracheal, and mouth occlusion pressure in patients with chronic obstructive pulmonary disease during acute respiratory failure.Am Rev Respir Dis. 1982; 126: 837-841PubMed Google Scholar Some studies have shown that this pressure measurement is greater in patients with COPD than in normal subjects, an indication of increased respiratory drive. Some investigators believe that increased respiratory drive in the presence of abnormal pulmonary function is a mechanism for dyspnea in patients with COPD.22Loke J Mahler DA Man SFP Wiedemann HP Matthay RA Exercise impairment in chronic obstructive pulmonary disease.Clin Chest Med. March 1984; 5: 121-143PubMed Google Scholar Depression, anxiety, and inappropriate fear of exercise are prevalent in patients with COPD.23Lustig FM Haas A Castillo R Clinical and rehabilitation regime in patients with chronic obstructive pulmonary disease.Arch Phys Med Rehabil. 1972; 53: 315-322PubMed Google Scholar Excitement or exertion results in increased respiratory rate and minute ventilation, leading to increased work of breathing and worsening of the sensation of breathlessness. A vicious cycle is thus created. Patients with COPD who have incapacitating psychosocial problems (such as severe depression or anxiety) respond less favorably to rehabilitation programs than do patients without such problems.24Agle DP Baum GL Chester EH Wendt M Multidiscipline treatment of chronic pulmonary insufficiency. 1. Psychologic aspects of rehabilitation.Psychosom Med. 1973; 35: 41-49PubMed Google Scholar In addition, patients with well-established psychosocial skills exhibit positive responses to group psychotherapy.25Pattison EM Rhodes RJ Dudley DL Response to group treatment in patients with severe chronic lung disease.Int J Group Psychother. 1971; 21: 214-225PubMed Google Scholar The contribution of psychologic factors to exercise limitation in COPD is considerable and must not be overlooked in a comprehensive rehabilitation program. The overall incidence of malnutrition in patients with COPD is unknown. In a group of hospitalized patients with COPD, however, the prevalence of nutritional depletion determined by anthropographic measurements and a body weight less than 90% of ideal was 50%.26Driver AG McAlevy MT Smith JL Nutritional assessment of patients with chronic obstructive pulmonary disease and acute respiratory failure.Chest. 1982; 82: 568-571Crossref PubMed Scopus (78) Google Scholar, 27Hunter AMB Carey MA Larsh HW The nutritional status of patients with chronic obstructive pulmonary disease.Am Rev Respir Dis. 1981; 124: 376-381PubMed Google Scholar Poor nutritional status also correlates with suboptimal pulmonary function in patients with emphysema28Lopes J Russell DM Whitwell J Jeejeebhoy KN Skeletal muscle function in malnutrition.Am J Clin Nutr. 1982; 36: 602-610PubMed Google Scholar, 29Openbrier DR Irwin MM Rogers RM Gottlieb GP Dauber JH Van Thiel DH Pennock BE Nutritional status and lung function in patients with emphysema and chronic bronchitis.Chest. 1983; 83: 17-22Crossref PubMed Scopus (115) Google Scholar and has been shown to be an independent risk factor for poor survival.30Wilson DO Rogers RM Wright EC Anthonisen NR Body weight in chronic obstructive pulmonary disease.Am Rev Respir Dis. 1989; 139: 1435-1438Crossref PubMed Scopus (428) Google Scholar Proposed causes of malnutrition include interference with gastrointestinal function by medications (such as theophylline and corticosteroids), vascular congestion of the gut caused by cor pulmonale, catabolic effects of corticosteroids, gastric distention from aerophagia, and high metabolic rate. Patients with emphysema, in particular, have a higher than normal metabolic rate as a result of their increased oxygen consumption during breathing.31Roussos C Campbell EJM Respiratory muscle energetics.in: Fishman AP Macklem PT Mead J Geiger SR Handbook of Physiology. Section 3: The Respiratory System. Vol 3. American Physiological Society, Bethesda, Maryland1986: 481-509Google Scholar Dyspnea and arterial de-saturation while eating may also cause decreased dietary intake in some patients.32Brown SE Casciari RJ Light RW Arterial oxygen saturation during meals in patients with severe chronic obstructive pulmonary disease.South Med J. 1983; 76: 194-198Crossref PubMed Scopus (24) Google Scholar Ultimately, the malnutrition may interfere with ventilatory muscle strength and exercise performance. In addition, malnutrition may predispose the patient with COPD to frequent infections of the respiratory tract and bacterial colonization of the airway through reduced secretory IgA, increased bacterial adherence, and decreased bacterial clearance.33Askanazi J Weissman C Rosenbaum SH Hyman AI Milic-Emili J Kinney JM Nutrition and the respiratory system.Crit Care Med. 1982; 10: 163-172Crossref PubMed Scopus (124) Google Scholar, 34Wilson DO Rogers RM Sanders MH Pennock BE Reilly JJ Nutritional intervention in malnourished patients with emphysema.Am Rev Respir Dis. 1986; 134: 672-677PubMed Google Scholar Arora and Rochester35Arora NS Rochester DF Respiratory muscle strength and maximal voluntary ventilation in undernourished patients.Am Rev Respir Dis. 1982; 126: 5-8PubMed Google Scholar reported substantial decreases in respiratory muscle strength and maximal voluntary ventilation that were proportional to the degree of weight loss in nutritionally depleted normal volunteers. Similar changes most likely occur in undernourished patients with COPD because of their high ventilatory requirements. Physical conditioning increases the ability to perform work. In a group of well-trained athletes, the imposition of strict bed rest or inactivity for 10 days to 2 months resulted in a deconditioned state characterized by the physiologic changes of a decrease in maximal oxygen uptake,36Convertino V Hung J Goldwater D DeBusk RF Cardiovascular responses to exercise in middle-aged men after 10 days of bedrest.Circulation. 1982; 65: 134-140Crossref PubMed Scopus (103) Google Scholar, 37Martin III, WH Coyle EF Bloomfield SA Ehsani AA Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume.J Am Coll Cardiol. 1986; 7: 982-989Abstract Full Text PDF PubMed Scopus (113) Google Scholar, 38Saltin B Blomqvist G Mitchell JH Johnson Jr, RL Wildenthal K Chapman CB Response to exercise after bed rest and after training: a longitudinal study of adaptive changes in oxygen transport and body composition.Circulation. 1968; 38: VIIl-VII55Google Scholar an increased response of the heart rate and the blood pressure to exercise,36Convertino V Hung J Goldwater D DeBusk RF Cardiovascular responses to exercise in middle-aged men after 10 days of bedrest.Circulation. 1982; 65: 134-140Crossref PubMed Scopus (103) Google Scholar, 37Martin III, WH Coyle EF Bloomfield SA Ehsani AA Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume.J Am Coll Cardiol. 1986; 7: 982-989Abstract Full Text PDF PubMed Scopus (113) Google Scholar, 38Saltin B Blomqvist G Mitchell JH Johnson Jr, RL Wildenthal K Chapman CB Response to exercise after bed rest and after training: a longitudinal study of adaptive changes in oxygen transport and body composition.Circulation. 1968; 38: VIIl-VII55Google Scholar a posture-dependent reduction in stroke volume,36Convertino V Hung J Goldwater D DeBusk RF Cardiovascular responses to exercise in middle-aged men after 10 days of bedrest.Circulation. 1982; 65: 134-140Crossref PubMed Scopus (103) Google Scholar, 38Saltin B Blomqvist G Mitchell JH Johnson Jr, RL Wildenthal K Chapman CB Response to exercise after bed rest and after training: a longitudinal study of adaptive changes in oxygen transport and body composition.Circulation. 1968; 38: VIIl-VII55Google Scholar and a reduction in size of the left ventricle.37Martin III, WH Coyle EF Bloomfield SA Ehsani AA Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume.J Am Coll Cardiol. 1986; 7: 982-989Abstract Full Text PDF PubMed Scopus (113) Google Scholar Exercise intolerance sometimes forces patients with severe COPD to adopt a sedentary life-style, which results in deconditioning. Depending on the degree of inactivity, physical deconditioning (in conjunction with the other factors previously discussed in this review) contributes considerably to exercise intolerance in patients with COPD. In recent years, exercise training has become the focus of many cardiac rehabilitation programs. Cardiovascular and peripheral muscle training responses have been achieved through rehabilitation after both myocardial infarction and a cardiac surgical procedure.39Erdman RAM Duivenvoorden HJ Verhage F Kazemier M Hugenholtz PG Predictability of beneficial effects in cardiac rehabilitation: a randomized clinical trial of psychosocial variables.J Cardiopulmonary Rehabil. 1986; 6: 206-210Crossref Scopus (69) Google Scholar, 40Froelicher V Jensen D Genter F Sullivan M McKirnan MD Witztum K Scharf J Strong ML Ashburn W A randomized trial of exercise training in patients with coronary heart disease.JAMA. 1984; 252: 1291-1297Crossref PubMed Scopus (132) Google Scholar, 41Hedbäck BEL Perk J Engvall J Areskog N-H Cardiac rehabilitation after coronary artery bypass grafting: effects on exercise performance and risk factors.Arch Phys Med Rehabil. 1990; 71: 1069-1073PubMed Google Scholar In contrast to the success in training cardiac patients, numerous studies with various designs during the past 25 years have shown that exercise training only modestly improves tolerance in patients with COPD.4Pierce AK Taylor HF Archer RK Miller WF Responses to exercise training in patients with emphysema.Arch Intern Med. 1964; 113: 28-36Crossref PubMed Scopus (57) Google Scholar, 42Belman MJ Kendregan BA Exercise training fails to increase skeletal muscle enzymes in patients with chronic obstructive pulmonary disease.Am Rev Respir Dis. 1981; 123: 256-261PubMed Google Scholar, 43Busch AJ McClements JD Effects of a supervised home exercise program on patients with severe chronic obstructive pulmonary disease.Phys Ther. 1988; 68: 469-474PubMed Google Scholar, 44Carter R Nicotra B Clark L Zinkgraf S Williams J Peavler M Fields S Berry J Exercise conditioning in the rehabilitation of patients with chronic obstructive pulmonary disease.Arch Phys Med Rehabil. 1988; 69: 118-122PubMed Google Scholar, 45Cockcroft AE Saunders MJ Berry G Randomised controlled trial of rehabilitation in chronic respiratory disability.Thorax. 1981; 36: 200-203Crossref PubMed Scopus (135) Google Scholar, 46Daly J Cooper C Casaburi R Burns M Chang R Wasserman K Exercise training as a mediator of increased exercise performance in COPD patients undergoing rehabilitation (abstract).Am Rev Respir Dis. 1989; 139: A331Google Scholar, 47Foster S Lopez D Thomas III, HM Pulmonary rehabilitation in COPD patients with elevated PCO2.Am Rev Respir Dis. 1988; 138: 1519-1523Crossref PubMed Scopus (53) Google Scholar, 48Hughes RL Davison R Limitations of exercise reconditioning in COLD.Chest. 1983; 83: 241-249Crossref PubMed Scopus (22) Google Scholar, 49Moser KM Bokinsky GE Savage RT Archibald CJ Hansen PR Results of a comprehensive rehabilitation program: physiologic and functional effects on patients with chronic obstructive pulmonary disease.Arch Intern Med. 1980; 140: 1596-1601Crossref PubMed Scopus (48) Google Scholar, 50Mungall IPF Hainsworth R An objective assessment of the value of exercise training to patients with chronic obstructive airways disease.Q J Med. 1980; 49: 77-85PubMed Google Scholar, 51Nicholas JJ Gilbert R Gabe R Auchincloss Jr, JH Evaluation of an exercise therapy program for patients with chronic obstructive pulmonary disease.Am Rev Respir Dis. 1970; 102: 1-9PubMed Google Scholar, 52Paez PN Phillipson EA Masangkay M Sproule BJ The physiologic basis of training patients with emphysema.Am Rev Respir Dis. 1967; 95: 944-953PubMed Google Scholar, 53Petty TL Nett LM Finigan MM Brink GA Corsello PR A comprehensive care program for chronic airway obstruction: methods and preliminary evaluation of symptomatic and functional improvement.Ann Intern Med. 1969; 70: 1109-1120Crossref PubMed Scopus (104) Google Scholar, 54Sinclair DJM Ingram CG Controlled trial of supervised exercise training in chronic bronchitis.Br Med J. 1980; 280: 519-521Crossref PubMed Scopus (87) Google Scholar The results of some of these studies are summarized in Table 1. Few studies showed improvement in pulmona
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