The vast majority of patients with chronic lung disease (CLD) are limited in their ability to perform daily physical activities because of symptoms that are related to physiologic impairments. These patients typically seek medical attention when the experience of breathlessness interferes with their ability to do certain routine tasks, such as walking, yard work, and housework, and recreational activities such as golf and tennis. Although the mechanisms causing exertional dyspnea are not completely understood, it appears that abnormalities in the mechanics of respiration and in gas exchange are important factors contributing to the difficulty in breathing (1). For example, in chronic obstructive pulmonary disease (COPD), expiratory airflow obstruction can lead to the development of dynamic hyperinflation (i.e., the need to breathe at a higher lung volume to achieve increased ventilation) during even simple tasks (2,3). The consequences of dynamic hyperinflation include shortening of the vertical muscle fibers of the diaphragm as well as an increase in the elastic load due to enhanced recoil of the lung parenchyma. In addition, some patients exhibit oxygen desaturation during activities. Thus, the increased output from the central nervous system (due in part to hypoxemia), ineffective respiratory muscles, and dynamic hyperinflation are mechanisms responsible for breathlessness during exertion in patients with COPD (4).
Patients with CLD typically reduce their physical activities to avoid the unpleasant experience of dyspnea. A more sedentary lifestyle results in deconditioning of the skeletal muscles and promotes a downward spiral of progressive breathlessness. This process is related to a higher level of ventilation being required for a given amount of work in deconditioned muscles. Moreover, Hamilton and colleagues (5) showed that some patients with chronic respiratory disease report that leg fatigue can be the more limiting symptom during cycle ergometry rather than breathlessness. The complaint of leg fatigue or discomfort is most likely due to muscle dysfunction and/or deconditioning as evidenced by the reduced oxidative capacity and lactic acid kinetics during exercise observed in patients with COPD (6).
The underlying CLD, deconditioning, and any disease-related muscle myopathy could cause both dyspnea and leg discomfort during exertion. These unpleasant experiences frequently lead an individual to reduce and even eliminate certain daily tasks and thereby adversely impact quality of life.
WHY SHOULD PATIENTS WITH CLD EXERCISE REGULARLY?
The primary goal of exercise training/pulmonary rehabilitation is to restore the individual patient to the highest possible level of independent function. This can be accomplished by allowing patients to participate in exercise training to reduce their symptoms and to increase their activities. Although the majority of the medical literature in pulmonary rehabilitation deals with patients who have COPD, it is likely that those with other types of CLD, such as interstitial lung disease, asthma, cystic fibrosis, and bronchiectasis, will achieve similar benefits with exercise training.
Numerous randomized, controlled trials have demonstrated reductions in dyspnea and leg discomfort and corresponding improvements in physiologic outcomes as a result of a comprehensive pulmonary rehabilitation program that includes exercise training as a major component (7–15). It is interesting that each of these programs provided different stimuli regarding the frequency, intensity, and duration of exercise training.
Moreover, the apparent mechanisms for the observed reductions in breathlessness and in leg discomfort with exercise training may be due to:
- A physiologic training effect (↓VE and ? HR/work, but no Δ in VO2/work)
- Enhanced mechanical efficiency (↓ VO2/work)
- Psychologic desensitization (↓ dyspnea/work)
A physiologic training effect refers to the salutary effect of exercise on various measurable physiologic responses, especially minute ventilation (VE), oxygen consumption (VO2), the anaerobic, or lactate, threshold, and blood levels of lactic acid. The overall physiologic training responses observed in patients with CLD are similar to changes seen in normal individuals. As a result of exercise training, patients with COPD exhibit a consistent increase in exercise endurance, but do not usually increase peak VO2 as is expected to occur in healthy subjects. Furthermore, whether a physiologic training response is obtained or not in those with CLD may depend on the intensity of the exercise program. For example, Casaburi and coworkers (16) demonstrated substantial physiologic changes in patients with severe COPD after high-intensity training (using a lactic acidosis threshold) compared with low work rate training.
Enhanced mechanical efficiency is the beneficial effect of exercise training whereby the same amount of work can be performed at a lower VO2. This may be documented by a lower VO2/work ratio. A lower oxygen requirement would lead to a corresponding reduction in both heart rate and in VE. For example, O’Donnell and colleagues (12,13) and Ramirez-Venegas and coworkers (14) demonstrated that enhanced mechanical efficiency occurred after a moderate-intensity training program in patients with COPD; this mechanism was the presumed explanation for reductions in symptoms after the training program.
Psychologic desensitization may be broadly defined as the reduction or enhanced tolerance of the intensity of breathlessness whatever the stimuli provoking the sensation. Desensitization is the process whereby repeated exposure to the stimulus in graduated steps within a safe environment can gradually decrease the anxiety or fear associated with the stimulus. Consequently, the experience becomes more tolerable or less bothersome (17). If desensitization is achieved as a result of an exercise training program, there will be less dyspnea perceived for the same level of ventilation or work (17,18).
In summary, there is substantial evidence that symptomatic patients with CLD can experience reductions in exertional breathlessness and leg discomfort along with improvements in exercise endurance. Furthermore, patients can also improve their health-related quality of life as a result of an exercise training program (19–22). In 1997, the Joint American College of Chest Physicians/American Association of Cardiovascular 2nd Pulmonary Rehabilitation (ACCP/AACVPR) Guidelines Panel on pulmonary rehabilitation concluded that there was strong evidence that “pulmonary rehabilitation improves health-related quality of life in patients with COPD” (19). In a meta-analysis of 14 studies Lacasse and colleagues (20) reported that there was an overall improvement in health-related quality of life following rehabilitation. Subsequent studies further support to the benefits of exercise training/pulmonary rehabilitation on enhancing health-related quality of life in patients with COPD using generic and disease-specific instruments (21,22).
WHO SHOULD BE REFERRED FOR EXERCISE TRAINING?
Any symptomatic individual with CLD who is motivated to participate in an exercise training program should be referred. There is no absolute age or level of lung dysfunction that should exclude an individual who wants to improve his/her exercise capacity and to reduce symptoms. Referral early in the course of the CLD is encouraged. However, the value of exercise training for those patients with end-stage lung disease requires serious consideration. It is probably more reasonable that such individuals focus their efforts in performance of daily activities rather than cycle ergometry or treadmill walking.
Exercise prescription is based on the principle of “overload” training. Thus, to achieve improvement the muscle must perform more work than usually encountered during daily activities. At the present time there is no optimal or best training regimen.
Published studies and clinical programs of pulmonary rehabilitation vary considerably in the methods of exercise training. The ranges of frequency (once a week to daily), intensity (50% of peak VO2 to maximal tolerated effort), and duration (5–10 minutes as tolerated up to 45 minutes) illustrate the variability. Pulmonary rehabilitation programs may last from 4 to 46 weeks, although most programs are 6 to 8 weeks long. The predominant modes of exercise training are treadmill walking and cycle ergometry.
General guidelines for the mode, frequency, intensity, and duration of exercise training are outlined in the table. Probably the most varied component of the exercise prescription and a somewhat controversial issue is the appropriate intensity of exercise training. Certainly, greater benefits can be expected with the highest possible intensity. For example, both Casaburi and coworkers (16) and Ries and colleagues (7) had patients with COPD train at high workloads and demonstrated substantial physiologic and subjective benefits. However, such programs generally require close supervision and encouragement for patients to maintain such a high training intensity. Of note, Maltais and colleagues (23) showed that 42 patients with moderate to severe COPD could only attain approximately 60% of their peak work load while exercising continuously for a duration of 30 minutes over a 12-week program.
In fact, other investigators have shown that patients with CLD can perform low (exercise of peripheral muscles at home) to moderate (approximately 50% of peak VO2) intensity of exercise training and achieve improved performance and reduced breathlessness (12,14,15,24). As described above, such benefits with low to moderate training are probably due to enhanced mechanical efficiency and/or psychologic desensitization rather than a physiologic training effect.
The traditional approach to exercise training in patients with CLD is to emphasize sustained or continuous effort. To examine an alternative approach, Coppoolse and coworkers (25) compared the responses between continuous and interval (alternating 1 minute at 90% and 2 minutes at 45% of the peak work rate) training over 8 weeks in patients with severe COPD. The continuous training group achieved significant increases in peak VO2 and decreases in lactic acid production during submaximal exercise, whereas the interval-training group had an increase in peak work rate and a decrease in leg pain. In general, this study supports the principle of specificity of training, i.e., training effects derived from an exercise program, are specific to the exercise performed and the muscles involved. In other words, continuous training primarily benefits endurance, whereas interval training enhances speed.
However, for most patients the primary objective of participating in an exercise program is to be able to do an activity for a longer time period rather than at a higher intensity. Moreover, in a study of patients with coronary artery disease adherence to training during the first year was better in a group who exercised at a low intensity compared with a high-intensity group (26).
How much exercise is enough? In those with CLD most, if not all, patients are deconditioned. Therefore, any training program will improve exercise endurance and reduce dyspnea. Although “more is better,” the exercise prescription must consider the motivation and compliance of the individual patient, particularly if some or all of the training sessions are unsupervised. Certainly, the benefits of exercise training have been shown to occur in a variety of patients with CLD including COPD, interstitial lung disease, asthma, and cystic fibrosis (27,28).
Many patients with CLD have muscle weakness and/or atrophy of the upper and lower extremities. Resistance training can promote muscle growth and strength in normal subjects as well as in patients with COPD. For example, Simpson and coworkers (29) reported that 8 weeks of strength training produced increases in muscle strength and in submaximal exercise tolerance in patients with COPD.
Bernard and colleagues (30) examined the benefits of strength training when combined with aerobic training versus aerobic training alone in patients with moderate to severe COPD over a 12-week period. The strength-training regimen included three sets of 8 to 10 repetitions of four weight lifting exercises; aerobic training consisted of three weekly 30-minute sessions of cycle ergometry. The investigators found that strength training was performed safely by the patients with COPD. Although the changes in peak exercise work rate, the 6-minute walking distance, and quality of life were comparable between the two groups, the addition of strength training to aerobic exercise was associated with significantly greater increases in muscle strength and mass.
Despite the limited number of published studies, it is reasonable to recommend that resistance training be incorporated into a comprehensive pulmonary rehabilitation program (31). Patients should be encouraged to coordinate breathing with the movement of the extremities. For example, inspiration should take place during motion of the extremities away from the body (e.g., overhead press), whereas expiration should occur when the motion is toward the thorax.
HOW SHOULD PATIENTS MONITOR THEIR EXERCISE TRAINING?
The traditional method in healthy individuals has been to use a target heart rate (HR) to regulate/monitor the intensity. Yet, patients with COPD are limited by the mechanics of breathing, oxygen desaturation, or dyspnea rather than cardiovascular factors. An alternative approach is to use dyspnea ratings as a target just as ratings of perceived exertion (RPE) have been used as a guide for intensity of effort in healthy persons and in those with cardiac disease. Horowitz and colleagues (32) have shown that dyspnea ratings on the 0 to 10 category-ratio scale obtained from an incremental exercise test can be used to achieve a desired intensity; accuracy was better at a higher exercise level (approximately 80% of peak VO2) compared with a lower intensity (approximately 50% of peak VO2). Moreover, Mejia and coworkers (33) reported that patients with symptomatic COPD could use dyspnea ratings as well as HR as a target to accurately produce an expected exercise intensity (approximately 75% of peak VO2) for 10 minutes of submaximal exertion.
The advantages of using dyspnea as a target for monitoring exercise training intensity are: 1) the process is simple and easy for most patients to learn to apply; 2) the use of a scale to rate the severity of breathlessness enables the patient to accept a certain level of physical exertion rather than stopping at the onset of dyspnea; and 3) the patient can continuously monitor his/her dyspnea/exercise intensity and does not need to stop to “check the pulse” if using the HR as a guide. Practice sessions may also be required for some patients to learn and to receive feedback in order to improve their ability to use the scale.
Additional therapeutic strategies have been and are currently being evaluated for potential use to enhance the exercise training process. These include unloading the respiratory muscles with noninvasive ventilatory assistance using pressure support (34) or proportional assist ventilation (35) during actual training, nutritional support to supplement the benefits of aerobic and resistance training (36), and the possible use of anabolic hormones in conjunction with training to optimize the response of the muscles to training (37).
A final but important issue is payment for an individual’s participation in a comprehensive pulmonary rehabilitation program. Although there is an abundance of scientific evidence to support the benefits of exercise training, at the present time reimbursement for pulmonary rehabilitation is not generally supported by insurance companies or the Health Care Finance Agency. Currently, there are organizational efforts underway to convince third-party payors to cover pulmonary rehabilitation (similar to existing reimbursement for cardiac rehabilitation).
1. O’Donnell DE. Exertional breathlessness in chronic respiratory disease. In: Mahler DA, ed. Dyspnea. Lung Biology in Health and Disease. Volume 111. New York: Marcel Dekker 1998: 97–148.
2. O’Donnell DE, Webb KA. Exertional breathlessness in patients with chronic airflow limitation: the role of lung hyperinflation. Am Rev Respir Dis. 1993; 148: 1351–1357.
3. Marin JM, Carrizo SJ, Gascon M, et al. Inspiratory capacity, dynamic hyperinflation, breathlessness, and exercise performance during the 6-minute-walk test in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2001; 163: 1395–1399
4. Mahler DA. Dyspnea in chronic obstructive pulmonary disease. Monaldi Arch Chest Dis. 1998; 53: 669–671.
5. Hamilton AL, Killian KJ, Summers E, et al. Muscle strength, symptom intensity, and exercise capacity of patients with cardiorespiratory disorders. Am J Respir Crit Care Med. 1996; 152: 2021–2031.
6. Maltais F, Simard A, Simard C, et al. Oxidative capacity of the skeletal muscle and lactic acid kinetics during exercise in normal subjects and in patients with COPD. Am J Respir Crit Care Med. 1996; 153: 288–293.
7. Ries AL, Kaplan RM, Limberg TM. Effects of pulmonary rehabilitation on physiologic and psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med. 1995; 122: 823–832.
8. Readon J, Award E, Normandin E, et al. The effect of comprehensive outpatient pulmonary rehabilitation on dyspnea. Chest. 1994; 105: 1046–1052.
9. Goldstein RS, Gort EH, Stubbing D, et al. Randomized controlled trial of respiratory rehabilitation. Lancet. 1994; 344: 1394–1397.
10. Strijbos JH, Koeter GH, Meinesz AF. Home care rehabilitation and perception of dyspnea in chronic obstructive pulmonary disease (COPD) patients. Chest. 1990; 97: 109S–110S.
11. O’Neill PA, Dodds M, Phillips B, et al. Regular exercise and reduction of breathlessness in patients with cystic fibrosis. Br J Dis Chest. 1987; 81: 62–69.
12. O’Donnell DE, McGuire M, Samis L, et al. The impact of exercise reconditioning on breathlessness in severe chronic airflow limitation. Am J Respir Crit Care Med. 1995; 152: 2005–2013.
13. O’Donnell DE, McGuire M, Samis L, et al. General exercise training
improves ventilatory and peripheral muscle strength and endurance in chronic airflow limitation. Am J Respir Crit Care Med. 1998; 157: 1489–1497.
14. Ramirez-Venegas A, Ward JL, Olmstead EM, et al. Effect of exercise training
on dyspnea measures in patients with chronic obstructive pulmonary disease. J Cardiopulmonary Rehabil. 1997; 17: 103–109.
15. Carrieri-Kohlman V, Gormley JM, Douglas MK, et al Exercise training
decreases dyspnea and the distress and anxiety associated with it. Chest. 1996; 110: 1526–1535.
16. Casaburi R, Porszasz J, Burns MR, et al. Physiologic benefits of exercise training
in rehabilitation of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1997; 155: 1541–1551.
17. Wolpe J. The systematic desensitization treatment of neurosis. J Nerv Ment Dis. 1961; 132: 189–203.
18. Haas F, Salazar-Schicchi J, Axen K. Desensitization to dyspnea in chronic obstructive pulmonary disease. In: Casaburi R, Petty TL, eds. Principles and Practice of Pulmonary Rehabilitation. Philadelphia: Saunders, 1993: 241–251.
19. Joint ACCP/AACVPR evidence-based guidelines on pulmonary rehabilitation. Chest. 1997; 112: 1363–1396.
20. Lacasse Y, Guyatt GH, Goldstein RG. The components of a respiratory rehabilitation program: a systematic overview. Chest. 1997; 111: 1077–1088.
21. Wedzicha JA, Bestall JC, Garrod R, et al.. Randomized controlled trial of pulmonary rehabilitation in patients with severe chronic obstructive pulmonary disease, stratified with the MRC dyspnoea scale. Eur Repir J. 1998; 12: 363–369.
22. Boueri FMV, Bucher-Bartelson BL, Glenn KA, et al. Quality of life measured with a generic instrument (Short Form-36) improves following pulmonary rehabilitation in patients with COPD. Chest. 2001; 119: 77–84.
23. Maltais F, LeBlanc P, Jobin J, et al. Intensity of training and physiologic adaptation in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1997; 155: 555–561.
24. Clark CJ, Cochrane L, Mackay E. Low intensity peripheral muscle conditioning improves exercise tolerance and breathlessness in COPD. Eur Respir J. 1996; 9: 2590–2596.
25. Coppoolse R, Schols AMWJ, Baarends EM, et al. Interval versus continuous training in patients with severe COPD: a randomized clinical trial. Eur Respir J. 1999; 14: 258–263.
26. Lee JY, Jensen BE, Oberman A, et al. Adherence in the training levels comparison trial. Med Sci Sports Exerc. 1996; 28: 47–52.
27. Foster S, Thomas HM. Pulmonary rehabilitation in lung disease other than chronic obstructive pulmonary disease. Am Rev Respir Dis. 1990; 141: 601–604.
28. Wietze de Jong PT, Grevink RG, Roorda RJ, et al. Effect of a home exercise training
programin patients with cystic fibrosis. Chest. 1994; 105: 463–468.
29. Simpson K, Killian K, McCartney N, et al. Randomised controlled trial of weightlifting exercise inn patients with chronic airflow limitation. Thorax. 1992; 47: 70–75.
30. Bernard S, Whittom F, LeBlanc P, et al. Aerobic and strength training in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1999; 159: 896–901.
31. Casaburi R. Special considerations for exercise training
. In: ACSM’s Resource Manual for Guidelines for Exercise Testing and Prescription, 4th
Edition. Philadelphia: Lippincott Williams & Wilkins; 2001: 346–352.
32. Horowitz MB, Littenberg B, Mahler DA. Dyspnea ratings for prescribing exercise intensity in patients with chronic obstructive pulmonary disease. Chest. 1996; 109: 1169–1175.
33. Mejia R, Ward J, Lentine T, Mahler DA. Target dyspnea ratings predict expected oxygen consumption as well as target heart rate values. Am J Respir Crit Care Med. 1999; 159: 1485–1489.
34. Maltais F, Reissmann H, Gottfried SB. Pressure support reduces inspiratory effort and dyspnea during exercise in chronic airflow obstruction. Am J Respir Crit Care Med. 1995; 151: 1027–1033.
35. Bianchi L, Foglio K, Pagani M, et al. Effects of proportional assist ventilation on exercise tolerance in COPD patients with chronic hypercapnia. Eur Respir J. 1998; 11: 422–427.
36. Schols AMWP, Soeters PB, Mostert R, et al. Physiologic effects of nutritional support and anabolic steroids in patients with chronic obstructive pulmonary disease: a placebo controlled randomized trial. Am J Respir Crit Care Med. 1995; 152: 1268–1274.
37. Ferreira IM, Verreschi IT, Nery LE, et al. The influence of 6 months of oral anabolic steroids on body mass and respiratory muscles in undernourished COPD patients. Chest. 1998; 114: 19–28.