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* From the Department of Medicine A, Hillel Yaffe Medical Center, Hadera, Israel.
Correspondence to: Paltiel Weiner, MD, Department of Medicine A, Hillel Yaffe Medical Center, Hadera, Israel 38100; e-mail: weiner{at}hillel-yaffe.health.gov.il
| Abstract |
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Methods: Twenty-six patients with COPD (FEV1 38% predicted) were recruited for the study. The patients were randomized into two groups: group 1, 13 patients were assigned to receive specific expiratory muscle training (SEMT) daily, six times a week, each session consisting of 1/2 h of training, for 3 months; and group 2, 13 patients were assigned to be a control group and received training with very low load. Spirometry, respiratory muscle strength and endurance, 6-min walk test, Mahler baseline dyspnea index (before), and the transitional dyspnea index (after) were measured before and after training.
Results: The training-induced changes were significantly greater in the SEMT group than in the control group for the following variables: expiratory muscle strength (from 86 ± 4.1 to 104 ± 4.9 cm H2O, p < 0.005; mean difference from the control group, 24%; 95% confidence interval, 18 to 32%), expiratory muscle endurance (from 57 ± 2.9% to 76 ± 4.0%, p < 0.001; mean difference from the control group, 29%; 95% confidence interval, 21 to 39%), and in the distance walked in 6 min (from 262 ± 38 to 312 ± 47 m, p < 0.05; mean difference from the control group, 14%; 95% confidence interval, 9 to 20%). There was also a small but not significant increase (from 5.1 ± 0.9 to 5.6 ± 0.7, p = 0.14) in the dyspnea index.
Conclusions: The expiratory muscles can be specifically trained with improvement of both strength and endurance in patients with COPD. This improvement is associated with increase in exercise performance and no significant change in the sensation of dyspnea in daily activities.
Key Words: exercise performance expiratory muscle training sensation of dyspnea
| Introduction |
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Surprisingly, there is a paucity of data related to the expiratory muscles (abdominal muscles and the internal intercostal muscles) in patients with COPD. These muscles have been found to be recruited in such patients both at rest and during loaded breathing. The significance of this activation has not been well defined; however, it is considered to be a mechanism that provides the system with functional reserve.7 There are several reports showing that expiratory muscle strength3 8 and endurance9 can be impaired in patients with COPD and therefore decrease functional reserve.
The contraction of the expiratory muscles increases the intrathoracic pressure, diminishes lung volume, and facilitates expiratory flow in the absence of flow limitation. In addition, for cough to be effective, the flow caused by the expiratory muscles should be high.
The expiratory muscles have been specifically trained in several settings. It has been shown that such training tended to enhance expiratory muscle strength, and to improve cough efficacy in severely disabled patients with multiple sclerosis,10 to improve the perception of dyspnea in children with neuromuscular disease,11 and to reduce the sensation of respiratory effort during exercise in healthy subjects.12 When patients with COPD were nonspecifically trained with normocapnic hyperpnea,13 the strength of both inspiratory and expiratory muscle strength were increased, with beneficial effect on exercise performance and quality of life. The effect of specific expiratory muscle training (SEMT) in patients with COPD has not yet been studied. In the present study, we wanted to test the effects of SEMT, not only on the expiratory muscle performance, but also on exercise performance and the sensation of dyspnea in patients with significant COPD.
| Patients and Methods |
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Tests
Spirometry:
FVC and the FEV1 were measured three times on a computerized spirometer (Compact; Vitalograph; Buckingham, England), and the best trial is reported.
6-Minute Walk Test: The distance the patient was able to walk in 6 min was determined in a measured corridor as described by McGavin and coworkers.16 The patients were instructed to walk at their fastest pace and cover the longest possible distance over 6 min under the supervision of a physiotherapist. The test was performed twice, and the best result is reported.
Respiratory Muscle Strength: Respiratory muscle strength was assessed by measuring the maximal inspiratory pressure (PImax) and maximal expiratory pressure (PEmax), at residual volume and total lung capacity, respectively, as previously described by Black and Hyatt.17 The value obtained from the best of at least three efforts, measured at 2-min intervals, was used.
Respiratory Muscle Endurance: To determine inspiratory muscle endurance, a device similar to that proposed by Nickerson and Keens18 was used. Subjects inspired through a two-way Hans-Rudolph valve, the inspiratory port of which was connected to a chamber and plunger to which weights could be added externally. Inspiratory elastic work was then increased by the progressive addition of 25- to 100-g weights at 2-min intervals, as was previously described by Martyn and coworkers,19 until the subjects were exhausted and could no longer inspire. The pressure achieved with the heaviest load (tolerated for at least 60 s) was defined as the peak inspiratory pressure (PImPeak).
To determine expiratory muscle endurance, the subjects inspired through a two-way Hans-Rudolph valve (Hans Rudolph; Kansas City, MO), the inspiratory port of which was open to room air with no load, and the expiratory port was connected to the expiratory port of a threshold muscle trainer (Threshold; HealthScan; Cedar Grove, NJ). The expiratory load was then increased by the progressive addition of 10 to 20 cm H2O (maximal pressure achieved through the increased load) at 2-min intervals until the subjects were exhausted and could no longer continue. Ten to 20 cm H2O were applied in order to get not less than five intervals and not more than seven intervals until exhaustion. The pressure achieved with the highest load (tolerated for at least 60 s) was defined as the peak expiratory pressure (PEmPeak).
Dyspnea: Dyspnea in daily activities was assessed with the Mahler baseline dyspnea index (BDI) and by the transition dyspnea index (TDI), following training.20
Training Protocol
Subjects in both groups trained daily, six times a week, each session consisting of 1/2 h. The subjects received SEMT with a threshold inspiratory muscle trainer (Threshold; HealthScan). The subjects started breathing through the expiratory port of the threshold muscle trainer at a resistance equal to 15% of their PEmax for 1 week. The resistance was then increased incrementally, 5 to 10% each session, to reach 60% of their baseline PEmax at the end of the first month. SEMT was then continued at 60% of the PEmax, adjusted weekly to the new PEmax achieved. Lung volume was not monitored throughout the training, although it is likely that the end-expiratory lung volume increased during the training. Patients in the control group trained with the same device, but with a fixed resistance of 7 cm H2O. The training was performed under the supervision of a physiotherapist twice weekly, and the patients were encouraged to train by daily phone calls.
Data Analysis
The results are expressed as mean ± SEM. Comparisons of lung function, respiratory muscle strength and endurance, the 6-min walk test, and rating of dyspnea within and between the two groups were carried out using two-way, repeated measures, analysis of variance. Post hoc analysis was performed using the Student Newman-Keuls test.
| Results |
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Spirometry
Mean baseline FEV1 and FVC were similar in the training group and in the control group (Table 1)
. Following the SEMT period, there was no significant change in the FEV1 or FVC either in the training group or in the control group.
Blood Gas Analysis
Following the SEMT period, there were no significant changes in the blood gas values either in the training group or in the control group.
Respiratory Muscle Strength and Respiratory Muscle Endurance
Before the training period, there was no difference in PImax, PEmax, PImPeak, or PEmPeak between the training group and the control group. Following the SEMT period, there was a statistically significant increase of 21% in the PEmax (from 86 ± 4.1 to 104 ± 4.9 cm H2O, p < 0.005) in the training group but not in the control group. The PImax remained unchanged following the training period, in both groups, emphasizing the specificity of the training (Fig 1
).
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| Discussion |
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Besides airflow obstruction, many other features are present in patients with COPD, and one of these is respiratory muscle weakness. Although inspiratory muscle weakness is more pronounced than the expiratory muscle weakness in patients with COPD,1 there are several reports showing that the expiratory muscle strength is impaired in most patients with significant COPD.3 9 26 While the inspiratory muscle weakness is usually considered to be caused by hyperinflation placing the inspiratory muscles at a mechanical disadvantage, the expiratory muscles partake in the generalized muscle weakness observed in patients with COPD.27 In addition to the expiratory muscle weakness, it was recently shown that the endurance of the expiratory muscles is decreased in patients with COPD.9 This decrease was related to the severity of airflow obstruction and to the decrease of the strength of different muscle groups. These investigators have used both the incremental loading test and the constant submaximal load test for measuring the expiratory muscle endurance. We are using the incremental loading test to assess the endurance and not the measurement of the time breathing against a constant submaximal load, because it allows the subject to learn a breathing strategy, is not influenced by learning or choice of breathing, and is reproducible.19
There is, therefore, a rationale for hypothesizing that the impairment of the expiratory muscle performance would have clinically relevant implications. The decreased expiratory muscle performance was associated with reduced exercise tolerance and reduced quality of life in patients with COPD.27 In addition, it is well documented that failure to cough efficiently is associated with expiratory muscle weakness.28
Several studies have shown that specific inspiratory muscle training may diminish the sensation of respiratory effort,29 increase the capacity to walk, and improve the quality of life in patients with COPD.30 It has also been shown13 that training both inspiratory and expiratory muscles by normocapnic hyperpnea results in improved exercise performance, health-related quality of life, and dyspnea in daily activities.
The expiratory muscles were specifically trained in our patients with an increase in exercise performance. In previous settings other than COPD, expiratory muscle training tended to improve cough efficacy,10 improve the perception of dyspnea in children with neuromuscular disease,11 and reduce the sensation of respiratory effort during exercise in healthy subjects.12 Therefore, if the decreased expiratory muscle performance is associated with reduced exercise tolerance in patients with COPD, it is rational to assume that in the trained subjects the increased expiratory muscle strength and endurance contributed to the improved performance at the end of the study. Since no other general exercise training was applied in our protocol, the improvement of the exercise performance should be attributed to the SEMT.
As for all types of muscle training, the training stimulus should be adequate to induce the appropriate physiologic response.31 In our group of patients, the training load induced significant and adequate increase in the expiratory muscle performance. Cough efficiency was not evaluated in the present study. In addition, the present study is limited by the fact that it was performed only in normocapneic patients, with no comparison with other forms of training. However, the significant increase in the 6-minute walk test results in our study is encouraging, may suggest a better daily activities handling, and therefore SEMT may be considered in individual patients with COPD.
| Footnotes |
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Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: permissions{at}chestnet.org)
Received for publication July 22, 2002. Accepted for publication February 11, 2003.
| References |
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