Pulmonary and Critical Care Division, St. Elizabeth’s Medical Center, and Tufts University School of Medicine, Boston, Mass., USA
Summary
Patients suffering from chronic respiratory diseases de-crease their overall physical activity, because any form of exer-cise will often result in worsening dyspnea. The progressive deconditioning associated with inactivity initiates a vicious cycle where dyspnea increases, at ever lower physical demands.
With time, the patients will also adopt a breathing pattern (usually fast and shallow) that is detrimental to overall gas exchange, which may in turn worsen their symptoms. In gener-al, physical reconditioning is a broad therapeutic concept that has unfortunately been equated with simple lower extremity exercise training. In this chapter, I shall review the current knowledge regarding reconditioning in much broader terms.
The effect and role of leg and arm training will be critically analyzed and practical recommendations will be given. Because I also believe it to be important, I shall review the concept of breathing retraining in its broad definition. A word of caution must be raised. The data which forms the basis of our current knowledge in terms of reconditioning, has been obtained from patients with intrinsic lung disease, such as emphysema, bron-chitis, bronchiectasis, cystic fibrosis and acute respiratory fail-ure. Very little is known about reconditioning in patients with pure ‘pump failure’, such as those with degenerative neuro-muscular diseases. There is every reason to believe that, in these patients, physical exercise may worsen rather than improve their overall function and sensation of well being. On the other hand, pure breathing retraining, such as slow deep breathing, could have a more universal application as long as extra loads are not placed on already weakened and
dysfunc-tional respiratory muscles. As will be reviewed in this chapter, patients with symptomatic ‘pump failure’ may benefit more from ventilatory assistance and resting than from further train-ing. This chapter is organized with this in mind.
Physical Reconditioning
General Principles
The short- and long-term effects of systematic exercise conditioning has been the subject of extensive investiga-tion and are addressed in detail in the chapter by Troos-ters T. et al., pp 60–71. However, I shall briefly review the topic as an introduction to the application of these con-cepts to patients with respiratory disease. In normal indi-viduals, participation in an exercise-training program re-sults in several objective changes: (1) there is increased maximal oxygen uptake, primarily due to increases in blood volume, hemoglobin and heart stroke volume with improvement in the peripheral utilization of oxygen;
(2) with specific training there is increase in muscular strength and endurance, primarily, resulting from en-largement of muscle fibers and improved blood and ener-gy supply; (3) better muscle coordination; (4) change in body composition with increased muscle mass and loss of adipose tissue, and (5) improved sensation of well-being.
In patients with obstruction to airflow, participation in a similar program will result in different outcomes
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ing on the severity of the obstruction. Patients with mild-to-moderate disease will, as a rule, manifest the same findings as normals whereas, as we shall discuss later, patients with the severe form will be able to increase exer-cise endurance and improve their sensation of well-being with little if any increase in the maximal oxygen uptake.
Very little is known regarding outcomes different from the specific effects of training on exercise performance in these patients. Similarly, once an effect has been shown, there has been little systematic information regarding the effect of maintenance programs on any of the outcomes, including exercise performance.
In patients with COPD, tolerance to exercise is de-creased. The most important factors thought to contribute to this limitation of exercise in patients with COPD are:
(1) alterations in pulmonary mechanics; (2) abnormal gas exchange; (3) dysfunction of the respiratory muscles;
(4) alterations in cardiac performance; (5) malnutrition, and (6) development of dyspnea. Other factors deserve to be mentioned but are less well characterized. They in-clude: active smoking, abnormal peripheral muscle func-tion and polycythemia. Although the most severe patients cannot exercise to the levels where the training effect is thought to occur (above anaerobic threshold), a large body of evidence supports exercise training as a beneficial ther-apeutic tool useful in helping these patients achieve their full potential.
Physiologic Adaptation to Training
There are several principles that apply to exercise training, and we must understand them in the context of prescribing exercise to patients with severe pulmonary problems. They are: (1) specificity of training; (2) intensi-ty and duration of the exercise load, and (3) detraining effect.
(1) Specificity of training. This principle is based on the observations that programs can be tailored to achieve specific goals and that the training of muscles or muscle groups is beneficial only to the trained muscle.
Utilization of high resistance, low repetition stimulus increases muscle strength (weight lifting), whereas low resistance, high repetition routines increase muscle en-durance. Strength training is achieved by increasing myo-fibrils in certain muscle fibers whereas endurance training increases the number of capillaries and mitochondrial content in the trained muscles.
The training is specific to the trained muscle. Clausen et al. [1] trained subjects in their arms and legs and observed that the decreased heart rate observed for arm muscle training could not be transferred to the leg group
and vice versa. Davies and Sargeant [2] showed that if training was completed for one leg, the beneficial effect could not be transferred to exercise involving the un-trained leg. Belman and Kendregan [3] confirmed these findings in patients with COPD. They examined the effect of 6 weeks of training in 8 patients who only trained their arms and 7 patients who only trained their legs. They observed improved exercise only for the exercise for which the patients trained. Interestingly, they failed to see any changes in muscle enzyme content of biopsies taken before and after the exercise training program [3].
(2) Intensity, frequency and duration of the exercise load. These factors profoundly affect the degree of the training effect. Athletes will usually train at maximal or near maximal levels in order to rapidly achieve the desired effects. On the other hand, middle age nonathletes may require less intense exercise. Siegel et al. [4] showed that training sessions of 30 min close to 3 times a week for 15 weeks significantly improved maximal oxygen uptake if the heart rate was raised over 80% of the predicted max-imal rate. In patients with chronic lung disease, the issue of exercise intensity and duration has been studied by dif-ferent authors, as we shall review later, but it would appear that the larger the number of sessions and the more intense (as a function of maximal performance), the better the results.
In their work, Belman and Kendregan [3] exercised patients at 30% of maximal and after 6 weeks of 4 times weekly training where the load was increased as tolerated, they observed significant improvement in endurance time in 9 of the 15 patients. It is possible that the relatively low training level (30% of maximal) may help explain why 6 of their patients failed to increase the endurance time. In contrast, Niederman et al. [5] started the exercise at 50%
of maximal cycle ergometer level and increased its inten-sity on a weekly basis and observed endurance improve-ment in most patients. In a very interesting study, Clark et al. [6] randomized 16 patients with COPD to a control group and 32 other patients to a daily training program lasting 12 weeks. The patients had moderate airflow obstruction (FEV1 of 1.7 B 0.3 liters). Training of the patients included isotonic endurance exercises of upper and lower extremity, and isokinetic muscle strength. After the 12 weeks, the patients in the exercise group improved their exercise endurance without worsening of dyspnea.
The patients also increased their walked distance. This study is important because it raised the question whether moderate intensity strength training may induce benefi-cial changes similar or additive to those already described for classical endurance training.
Belman
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Other authors have used higher starting exercise levels and have achieved a better endurance effect [7–11].
The best study in this regard is that of Casaburi et al.
[11] who studied 19 patients with moderate COPD (mean B SD FEV1 of 1.8 B 0.53 liters) who could achieve anaer-obic threshold, before and after randomly assigned train-ing at low intensity (50% of maximal) or high intensity (80% of maximal) exercise. The authors showed that the high intensity training program was more effective than the low intensity one. They also observed a decrease in ventilatory requirement for exercise after training, that was proportional to the drop in lactate at a given work rate. Using a different study design, Puente-Maestu et al.
[12] randomized 35 patients with COPD (FEV1 of 1.09 B 0.17 liters) to either supervised training on a treadmill or to self-monitored walking program. Both groups trained four times a week. As expected, the intensity of training was different for the two groups (35 B 10 vs. 70 B 22 W).
The mean endurance time at submaximal workload (70%
of maximal pretraining workload ) increased more in the supervised group when compared with the usual care one.
It seems that training is achieved if the intensity of exercise is higher than of minimal, and that the intensity of training can be increased as tolerated. In other words, any exercise is better than none, and indeed good results have been shown even for patients with minimal exercise performance when tested [9, 12]. However, more exercise induces larger changes [11, 12].
The number of exercise sessions is also a matter of debate [3, 13]. As shown in table 1, in general as the num-ber of sessions is increased, so is the change in observed endurance time. Since stopping the exercise results in a loss of the training effect, the optimal plan should involve an intense training phase and a maintenance phase. This latter part is very difficult to implement and results in the frequently observed failure to maintain and preserve the beneficial effects achieved through the training. Unfortu-nately, there is no study in any respiratory disease that has addressed this important issue.
(3) Detraining effect. This principle is based on obser-vations that the effect achieved by training is lost after the exercise is stopped. Saltin et al. [14] showed that bed rest in normal subjects resulted in a significant decrease in maximal oxygen uptake within 21 days of resting. It took between 10 and 50 days for the values to return to those seen before resting. Keens et al. [15] examined ventilatory muscle endurance after training in normal subjects who had undergone ventilatory muscle training. Within 1 month of having stopped training, the subjects had lost
Table 1. Number of sessions of exercise in these studies that summa-rized the improvement in exercise endurance
Author Sessions Endurance change, %
45 50
Epstein 19 30
Make 12 12
the training effect that they had achieved. Therefore, it seems important to continue to train, but the minimum practical and effective timing of maintenance training remains to be determined.
Our exercise program is based on the data and con-cepts developed above. Patients are exercised at 70% of the maximal work achieved in a test day. This work is increased on a weekly basis as tolerated by the patient. We aim to complete 24 sessions. This is achieved in the out-patient setting by sessions held three times weekly. In con-trast, the program may be completed quicker if the patient is in the hospital, because the sessions are completed on a daily basis. Each session lasts 30 min if tolerated by the patient, otherwise it is begun as tolerated by the patient and no further load is provided until the patient can com-plete the 30 min of the session. A close communication exists between the person in charge of the training and the rehabilitation planning team. In those settings where met-abolic measurements are not possible, the use of the per-ception of dyspnea using a Borg visual analog scale can substitute a target work rate. This has been shown in a study of 15 patients by Horowitz et al. [16]. It is appealing to use dyspnea and not heart rate as the target to train patients with lung disease, as breathlessness constitutes their most important complaint.
Lower Extremity Exercise
A large number of studies have shown that the inclu-sion of leg exercise in the training of patients with lung disease is beneficial [18–21]. Cockcroft et al. [22] ran-domized 39 dyspneic patients younger than 70 years and not on oxygen to a treatment group that spent 6 weeks in a rehabilitation center, where they underwent gradual en-durance exercise training, and a control group that re-ceived medical care but was given no special advice to exercise. The control group served as such for 4 months and was then admitted to the rehabilitation center for 6 weeks. Just like the treated patients, they were instructed
Cockroft
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Table 2. Controlled studies of rehabilitation with exercise in patients with COPD
Author Patients Duration Results
18 T daily, 16 weeks ↑ 12 MW, VO2
16 C – no change
Sinclair 17 T daily, 40 weeks ↑ FVC, ↑ 12 MW
16 C – no change
O’Donnell 23 T daily, 8 weeks ↑ FVC, ↑ 12 MW
↓ dyspnea
13 C – no change
Reardon 10 T 2!/week, 6 weeks ↓ dyspnea
10 C – no change
Ries 57 T daily, 8 weeks ↑ exercise capacity
↓ dyspnea
↑ self efficacy 62 C daily, 8 weeks
education
no change
Wijkstra 28 T daily, 12 weeks at home
↑ exercise capacity
↑ quality of life
15 C – no change
Goldstein 45 T daily, 24 weeks ↑ 6MWD VO2
↓ dyspnea, ↓ S.O.B.
44 C none, 24 weeks no change
Guell 30 T daily, 12 weeks ↑ 6MWD
↓ dyspnea, ↑ QoL
30 C usual care no change
T = Treated; C = controls; 12 MW = 12-min walk distance;
6MWD = 6-min walk distance; FVC = forced vital capacity; VO2 = peak oxygen uptake.
to exercise at home afterward. Both groups were similar at baseline. After rehabilitation, only 2 of the 16 control patients manifested improvement in dyspnea and cough, whereas 16 of the 18 patients included in the treatment group manifested improvement in these symptoms. More importantly, the treated patients showed significant im-provement in the 12-min walk and in the peak oxygen uptake when compared with the controls. In a different setting, Sinclair and Ingram [33] randomized 33 patients with chronic bronchitis and dyspnea to two groups. The 17 patients in the treatment group exercised by climbing up and down on two 24-cm steps twice daily. The exercise time was increased to tolerance. The patients exercised at home and were evaluated by the treatment team weekly.
The control group did not exercise but were all reassessed after 6 months. There were no changes in the degree of airflow obstruction in either group. Similarly, there was
no improvement in strength of the quadriceps, the minute ventilation and heart rate. In contrast, the 12-min walk test significantly increased in the patients that were trained. These two studies are particularly important in that they were well designed and used randomization in the assignment of patients to the specific treatment groups. O’Donnell et al. [24] compared breathlessness, 6-min walking distance and cycle ergometer work, between two age-matched groups of patients with moderate COPD. The endurance exercise trained group (n = 23) achieved significant reduction in dyspnea scores, and increased the distance walked as well as the cycle ergome-try work, when compared to the control group (n = 13).
This trial is important in that it not only documented increased endurance, but for the first time evaluated the patient’s perception of dyspnea which is the most proble-matic symptom and the one leading to physical limita-tion.
Since those initial studies, several randomized trials have documented the beneficial effect of lower extremity exercise [25–27]. Perhaps the most important one is the study by Ries et al. [27]. In this study, 119 patients were randomized to an education support group (n = 62) or to a similar educational program with the addition of 3 times weekly walking exercise for 8 weeks (n = 57). At 2 months and still seen at 4, 6 and 12 months, the patient who exer-cised manifested increased exercise endurance, less dys-pnea with exercise and with activity of daily living and statistically not significant increase in survival. More recently, Guell et al. [28] randomized 60 patients with moderate degree of COPD (FEV1 of 35 B 14% predicted) to either usual care without supervised exercise or pulmo-nary rehabilitation. Pulmopulmo-nary rehabilitation included 3 months of five 30-min sessions every week of cycle ergom-etry, starting at 50% of the maximal load achieved during a baseline evaluation. The workload was progressively increased as tolerated. After 2 years, the 30 patients ran-domized to exercise not only manifested significant favor-able differences compared with usual care in the distance walked over 6 min, but also in dyspnea and in the emotion component of the disease-specific Chronic Respiratory Questionnaire. These landmark studies have established the pivotal role of exercise in the proven benefit of pulmo-nary rehabilitation. The results of the most important studies are summarized in table 2.
Numerous studies using patients as their own controls have shown similar results, with significant increases in exercise endurance. The mechanism by which this im-provement occurs remains a matter of debate. Several studies, including those of Paez et al. [21] and Mohsenifar
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et al. [7] have demonstrated a decrease in heart rate at a similar work level, a hallmark of a training effect for the specific exercise. This is perhaps related to a decrease in exercise lactate level as suggested by Woolf and Suero [29]. More recent evidence in support of a training effect is provided by the study of Casaburi et al. [11]. In their group of trained patients with COPD, they showed a reduction in exercise lactic acidosis and ventilation after patients were trained. Furthermore, the reduction was proportional to the intensity of the training. There was a 12% decrease in the lactic acidosis rise in patients trained with the low work rate (50% of maximum) and 32%
decrease in the ones trained with the high work rate (80%
of maximum). In both groups there were significant decreases in heart rate after training. Other studies have failed to document either an increase in maximum O2 uptake, a decrease in heart rate or lactate at similar work level. The most important study in this group is the one by Belman and Kendregan [3] which failed to show a de-crease in heart rate at the same workload as represented by the VO2. These authors went further and analyzed muscle biopsies oxidative enzyme content before and after training. They observed no change in this parameter.
Interestingly, 9 of the treated patients improved their exercise endurance. As stated previously, it is possible that this study used too low a training effort since training was started at 30% of the maximum achieved during their testing. That this may be so is supported by two studies from one same group [30, 31]. They first showed that muscle biopsies from the legs of patients with COPD had decreased content of oxidative enzymes in their mito-chondria [30]. Subsequently, and extremely important for those that believe in the physiologic training, the mito-chondrial enzymatic content significantly increased after exercise training [31]. In that same group of patients they also documented a delay of onset of the lactase threshold after training.
The evidence therefore indicates that patients with COPD can be trained to a level that produces physiologic changes consistent with improved muscle performance.
Two studies addressed the issue of whether patients with the most severe COPD can undergo exercise
Two studies addressed the issue of whether patients with the most severe COPD can undergo exercise