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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
| Abstract |
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Study objective: To investigate the relationship between ß2-agonist consumption and the score of perception of dyspnea, in mild asthmatics, and the relationship between the effect of specific inspiratory muscle training (SIMT) on the score of perception of dyspnea and ß2-agonist consumption in "high perceivers."
Methods: Daily ß2-agonist consumption was assessed during a 4-week run-in period in 82 patients with mild asthma. Patients with a mean ß2-agonist consumption of > 1 puff/d ("high consumers") then were randomized into two groups: one group of patients received SIMT for 3 months; the other group of patients was assigned as a control group and received sham training. Inspiratory muscle strength and perception of dyspnea were assessed before patients entered the study, following the 4-week run-in period, and after completing the training period.
Results: Following the 4-week run-in period, 23 high-consumer patients (mean [± SEM] ß2-agonist consumption, 2.7 ± 0.4 puffs/d) were detected. The mean Borg score during breathing against resistance was significantly higher (p < 0.05) in the patients with high ß2-agonist consumption than in the subjects with low mean ß2-agonist consumption. Following SIMT, the mean maximal inspiratory pressure increased significantly from 94.1 ± 5.1 to 109.7 ± 5.2 cm H2O (p < 0.005) in the training group. The increase in inspiratory muscle strength was associated with a statistically significant decrease in the mean Borg score during breathing against resistance (p < 0.05) as well as in the mean daily ß2-agonist consumption.
Conclusions: We have shown that patients with mild asthma, who have a high ß2-agonist consumption, have a higher perception of dyspnea than those with normal consumption. In addition, SIMT was associated with a decrease in perception of dyspnea and a decrease in ß2-agonist consumption.
Key Words: high consumption of inhaled ß2-agonists inspiratory muscle training perception of dyspnea
| Introduction |
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The perception of airway obstruction is blunted in many patients with asthma.1 4 5 6 8 Such a decreased perception of dyspnea may result in undertreatment of asthma, delay modification in treatment,9 and even may predispose patients to fatal asthma attacks.10 On the other hand, some patients who are "high perceivers" become very distressed with relatively minor changes in bronchoconstriction,1 and may use ß2-agonists unnecessarily.
Studies investigating dyspnea suggest that, at least in part, it is perceived by the patient as respiratory muscle effort.11 12 In addition, a number of studies have been carried out in order to correlate dyspnea and respiratory muscle performance. It is well documented that the degree of breathlessness subjectively reported by the patients is related to the activity and strength of the inspiratory muscles.13 14
In the present study, ß2-agonist consumption was used to detect patients who are "high consumers" among patients with mild asthma. The mean score of perception of dyspnea was also high in these patients. Then the effect of specific inspiratory muscle training (SIMT) on the score of perception of dyspnea and ß2-agonist consumption was investigated in those patients who were high perceivers.
| Materials and Methods |
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Study Design
All patients were studied during a 4-week run-in period and were
required to be compliant with the recording of prebronchodilator
consumption morning peak expiratory flow rates (PEFRs) and daily
ß2-agonist consumption in a diary card. The
information on the diary card was verified by a respiratory therapist
daily by phone and once weekly by a personal visit. Patients with
recorded PEFR < 80% of their best value were excluded from the
study.
After the 4-week run-in period, the study subjects were separated into
two groups: one group of patients had a mean
ß2-agonist consumption of > 1 puff/d (high
consumers); the other group had a mean
ß2-agonist consumption of
1 puff/d (normal
consumers). The groups were defined arbitrarily before the study
began. Inspiratory muscle strength and perception of dyspnea
then were measured. The subjects who were high consumers comprised the
study group and were randomized into two groups: one group received
SIMT (group A) for 3 months; the other group was assigned to be a
control group and received sham training (group B).
ß2-agonist consumption again was recorded in
diary cards during the last 4 weeks of the training. Patients again
were told to take ß2-agonists only when needed
and were not told that the aim of the training was to reduce
ß2-agonist consumption. Inspiratory muscle
strength and perception of dyspnea then were measured once again. In
all the patients, we performed several practice tests before the
baseline value was recorded in order to correct possible training and
learning effects. All the data were collected by the same person, who
was blinded to the training group designation, as were the patients
themselves, who were also blinded to the mode of treatment.
Tests
Spirometry:
The FVC and the FEV1 were measured
three times on a computerized spirometer (Compact; Vitalograph;
Buckingham England), and the best trial is reported. Bronchodilators
were withheld 12 h before spirometry testing.
Inspiratory Muscle Strength: Inspiratory muscle strength was assessed by measuring the maximal inspiratory pressure (PImax) at residual volume (RV), as previously described by Black and Hyatt.16 The value obtained from the best of at least three efforts was used.
Perception of Dyspnea: The sensation of dyspnea was measured while the subject breathed through a device similar to that proposed by Nickerson and Keens.17 Subjects inhaled through a two-way valve (Hans-Rudolph; Fridengen, Germany), the inspiratory port of which was connected to a chamber and plunger to which weights could be added externally. The subjects breathed against progressive resistance, at 1-min intervals, in order to achieve a mouth pressure (Pm) of 0 (no resistance), 5, 10, 20, and 30 cm H2O. After breathing for 1 min in each inspiratory load, in a protocol similar to the one that has been described previously by Kikuchi et al,10 the subjects rated the sensation of difficulty in breathing (dyspnea) using a modified Borg scale.18 This scale is a linear scale of numbers ranking the magnitude of difficulty in breathing, ranging from 0 (none) to 10 (maximal).
Training Protocol: Subjects in both groups trained daily for a period of 3 months, six times a week, with each session consisting of 0.5 h of training. The subjects received SIMT with a threshold inspiratory muscle trainer (Threshold Inspiratory Muscle Trainer; Healthscan; Cedar Grove, NJ). The subjects started breathing at a resistance level equal to 15% of their PImax for 1 week. The resistance then was increased incrementally, 5 to 10% each session, to reach 60% of their PImax at the end of the first month. SIMT then was continued for the next 2 months at 60% of their PImax and was adjusted every week to the new PImax achieved. Patients in group B received sham training with the same device but trained with no resistance.
Data Analysis
The results are expressed as the mean ± SEM. Correlations were
assessed by calculating Spearman correlation coefficients. Comparisons
of lung function inspiratory muscle strength and dyspnea score were
carried out using the two-way, repeated-measures analysis of variance.
| Results |
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Following the 4-week run-in period, the remaining 76 subjects were
separated into two groups: one group comprised 23 patients (15 men and
8 women) with a mean ß2-agonist consumption of
> 1 puff/d (defined as high consumers; mean ± SEM, 2.7 ± 0.4
puffs/d); the other group comprised 53 patients with a low mean
ß2-agonist consumption of
1 puff/d (mean
± SEM, 0.4 ± 0.1 puffs/d) who were excluded from the next stage of
the study. There were no differences between the groups in age,
baseline FEV1 values, or PImax (Table 1
).
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The Borg scores of individual patients during breathing with resistance to create a Pm of 20 cm H2O are shown in Figure 1 . We have chosen the value of 20 cm H2O, as did Kikuchi et al,10 because this is a moderate load that may be encountered daily by asthmatic patients. The mean score for the patients with high ß2-agonist consumption was significantly higher than that for the normal consumers (4.3 ± 0.4 vs 3.1 ± 0.2, respectively; p < 0.01).
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| Discussion |
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The perception of dyspnea is critical, but it presents a paradox to patients with airway obstruction. On one hand, it limits daily activity and impairs quality of life, but, on the other hand, it provides a warning of deterioration.
It has been shown that there is a close relationship between the sensation of breathlessness and respiratory muscle force both in healthy subjects and in patients with COPD who have severe lung function impairment.11 12 13 19 The respiratory muscles, like other skeletal muscles, can be trained,20 21 resulting in significant improvement in respiratory muscle performance. This increase in respiratory muscle performance was associated with a decrease in the sensation of breathlessness in patients who had COPD with a pretraining respiratory muscle weakness.19
Patients with asthma usually are assumed to have normal respiratory muscle performance. Although asthma patients are exposed to airway obstruction and hyperinflation, which by itself adversely affects the inspiratory muscles by forcing them to operate in an inefficient part of the force-length relationship, these conditions are probably opposed by the training effect of breathing through increased airway resistance. However, it already has been demonstrated, in healthy subjects with normal respiratory muscle performance, that the perceived magnitude of added ventilatory loads can be reduced by resistive training that is aimed at increasing inspiratory muscle strength.22 In another study,1 Burdon and colleagues have found that asthmatic subjects who frequently develop acute airflow obstruction acquire a degree of tolerance that reduces the perception of dyspnea.
In a previous study performed by us,23 inspiratory muscle training resulted in a decrease in ß2-agonist consumption in patients with moderate asthma. The perception of dyspnea was not measured in this study.
Many factors may be responsible for the considerable variations in the perception of dyspnea for any particular degree of airflow obstruction in asthmatic patients; the efficiency and performance of the inspiratory muscles, the length-tension relationship of the system, the cooperation of the various muscle groups in generating force, the frequency and timing of force generation, and the variation in the psychological response.24 25
It has been shown already that temporal adaptation is responsible for some of the variability in breathlessness experienced by asthmatic subjects.1 Patients with prolonged exposure to airflow obstruction were less breathless for any given reduction in FEV1 than those with normal FEV1. The asthmatic patients in our training group passed two processes that might contribute to the decrease in their perception of breathlessness and decreased ß2-agonist consumption: (1) temporal adaptation by the exposure to increased airway resistance that might mimic airflow obstruction; and (2) inspiratory muscle training that increased the inspiratory muscle strength known to reduce the perceived magnitude of breathlessness, at least in healthy subjects.
A decreased perception of breathlessness is potentially dangerous in patients with asthma, because the severity of an exacerbation of asthma may be underestimated. On the other hand, high perception carries with it the possibility of a decrease in quality of life and the usage of unnecessary, and sometimes dangerous, ß2-agonists.
Our study shows that even in patients with mild asthma there is a wide variation in the magnitude of the sensation of dyspnea. Those who are high perceivers also consume relatively high doses of ß2-agonists. SIMT seems to reduce both the perception of dyspnea and ß2-agonist consumption. We believe that SIMT is safe, at least in patients with mild asthma, without producing the possible result of an exaggerated ablation of the perception of dyspnea. The clinical significance of our short-term study is not yet clear and needs to be elucidated in long-term follow-up studies in asthmatic patients.
| Footnotes |
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Received for publication February 2, 1999. Accepted for publication October 21, 1999.
| References |
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