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European Journal of Heart Failure 2002 4(6):745-751; doi:10.1016/S1388-9842(02)00163-0
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© 2002 European Society of Cardiology

Effect of aerobic exercise training on inspiratory muscle performance and dyspnoea in patients with chronic heart failure

Nancy Vibarela,b,*, Maurice Hayota, Bertrand Ledermannc, Patrick Messner Pellencc, Michèle Ramonatxoa and Christian Prefauta

a Laboratoire de Physiologie des Interactions, Service Central de Physiologie Clinique, Unité d'Exploration Respiratoire, Centre Hospitalier Arnaud de Villeneuve Montpellier, France
b Laboratoire de la Performance Motrice, Faculté du sport et de l’éducation physique Rue de Vendôme, BP 6237, 45062 Orléans Cedex 2, France
c Service de Cardiologie, Centre Hospitalier Universitaire Nîmes, France

* Corresponding author. Tel.: +33-2-38-49-48-27; fax: +33-2-38-41-72-60. E-maill address: nancy.vibarel{at}univ-orleans.fr

Received October 2, 2000; Revised April 10, 2002; Accepted May 27, 2002


   1. Introduction
Top
 1. Introduction
2. Methods
 3. Results
 4. Conclusion
 References
 
The diminished exercise tolerance of patients with chronic heart failure (CHF) is associated with peripheral muscle fatigue and dyspnoea. Investigations of skeletal muscle in these patients have demonstrated peripheral muscle abnormalities (histochemical and metabolic), including generalised muscle atrophy and a shift from oxidative to glycolytic metabolism, which would explain the symptom of fatigue [1]. It is likely that these intrinsic skeletal muscle changes are not limited to the limb musculature, but are instead generalised [2,3]. Numerous studies have thus focussed on the respiratory muscle abnormalities in these patients: a reduction in strength [4–9]; a decrease in endurance [10,11]; accessory respiratory muscle deoxygenation during exercise [12]; a dramatic increase in diaphragmatic work [2]; and diminished inspiratory muscle performance at exercise [13]. Furthermore, several authors have suggested that, among the mechanisms leading to dyspnoea in patients with CHF, an increase in respiratory muscle activity and/or a weakness of respiratory muscles could be involved [2,3,14]. If respiratory muscles are altered in the same manner as the skeletal muscles, these abnormalities may explain in part the dyspnoea in patients with CHF.

Aerobic exercise training has been shown to partially reverse skeletal muscle abnormalities [15,16], increase maximal exercise performance [17] and improve dyspnoea [18,19]. Mancini et al. [20] showed that selective respiratory muscle training improved respiratory muscle function (endurance and strength), with enhancement of submaximal and maximal exercise capacity and improvement in dyspnoea during activities of daily living in patients with CHF. In the present study, we hypothesised that if aerobic exercise training in patients with CHF improves respiratory muscle function, as it does skeletal muscles, then an increase in respiratory muscle strength and performance should attenuate exertional dyspnoea. Aerobic exercise training may thus improve exercise capacity, with improved inspiratory muscle performance and diminished dyspnoea.

The aim of this study was to investigate the effect of aerobic exercise training on exercise capacity, inspiratory muscle performance (assessed with the tension–time index of the inspiratory muscles) and exertional dyspnoea in patients with CHF.


   2. Methods
Top
 1. Introduction
 2. Methods
3. Results
 4. Conclusion
 References
 
2.1. Subjects
This study was carried out in 10 patients with CHF (eight males and two females). Each subject was informed of the purpose of the study and gave written consent. All patients (51±9 years, 168±9 cm and 72±11 kg) had a history of daily exertional dyspnoea associated with mild to moderate stable CHF [New York Heart Association (NYHA) class II and III] and left ventricular dysfunction at rest of <45% (30±8%), as assessed by isotopic ejection fraction. This dysfunction was due to ischemic or idiopathic dilated cardiomyopathy. All patients were in clinically stable condition, with no worsening of heart failure or change in cardiac medication for the previous 2 months and during the study. Peripheral oedema, ascites and pulmonary crackles were not present at the time of testing. None of the patients had a history of pulmonary disease, myocardial infarction or unstable angina (during the previous 2 months), myocardial ischemia or arrhythmias during exercise, or exercise intolerance for any reason other than fatigue or dyspnoea. None had a history of smoking (past 3 years), or had ever had an implanted pacemaker.

2.2. Spirographic measurements
Conventional spirographic measurements were performed on a spirometer (Pulmonet III, Sensormedics, Bilthoven, Netherlands). Forced expiratory volume in 1 s and forced vital capacity were measured. Tiffeneau's ratio (ratio of forced expiratory volume in 1 s/forced vital capacity) was then calculated. The predicted values were those proposed by the European Community of Steel and Coal [21].

2.3. Exercise testing
The exercise test was performed on a bicycle ergometer (Ergometer 990, Bodyguard Jones AS, Sandnes, Norway). During the test, the subjects wore a nose clip and breathed through a low-resistance (0.9 cm H2O l–1 s–1), low-dead-space (50 ml) breathing valve (Warren E. Collins Inc, MA, USA) and large-calibre tubing (3.5 cm). This valve was connected by the expiratory circuit to a breath-by-breath automated exercise metabolic system (CPX, Medical Graphics Corp, MN, USA). Expired gases were analysed for oxygen with a zirconia solid-electrolyte oxygen analyser, and for carbon dioxide with an infrared analyser. Oxygen uptake, carbon dioxide output and respiratory exchange ratio were continuously measured using the CPX. Before each test, the gas analysers were calibrated with two mixtures of gases of known oxygen and carbon dioxide concentration. The data were averaged during the last 20 s of each load over an integral number of breaths. Inspiratory airflow was measured with a Fleish no 3 pneumotachograph (Fleish, Lausanne, Switzerland) placed on the inspiratory line and a differential pressure transducer with a measuring range of ±2 cm H2O (model MP-45, Validyne, CA, USA). Tidal volume was obtained by integration of the flow signal. Heart rate was continuously recorded on a cardioscope (Personal 120, Esaote-Biomedica, Florence, Italy) and an electrocardiogram was periodically recorded.

2.4. Maximal inspiratory and expiratory pressures and mouth occlusion pressure
At rest, maximal inspiratory pressure (PIMAX) and expiratory pressure (PEMAX) at the mouth were measured at functional residual capacity with the Validyne MP-45 transducer (±300 cm H2O) and a model CD 15 carrier demodulator, using the technique of Black and Hyatt [22]. The subjects were asked to make a maximal inspiratory effort against an occluded airway and to maintain maximal pressure for at least 1 s. Repeated measurements were made until three technically satisfactory and reproducible measurements were obtained (variation in PIMAX and PEMAX of <10%). The data reported represent the best values.

At rest and during exercise, mouth occlusion pressure (P0.1) measurement was performed with a silent electromagnetic valve that was closed during expiration and automatically opened approximately 150 ms after the onset of the occluded inspiration. Since closure was silent, the subjects were unable to anticipate which breath was going to be occluded. P0.1 was measured with a Validyne MP-45 transducer (±35 cm H2O) and a model CD 15 carrier demodulator. P0.1 is the pressure developed at the mouth 0.1 s after the beginning of inspiration against an occluded airway and it provides an indirect assessment of neural drive to the respiratory muscles [23].

2.5. Derived parameters
All signals were displayed on a Gould ES 1000 recorder (Gould Instruments, OH, USA). At rest and during exercise, the breathing pattern was determined from an average of 10 respiratory cycles: tidal volume (VT), inspiratory time (TI), and total time of the respiratory cycle (TTOT) were measured. We then calculated respiratory frequency (f), minute ventilation (VE) and the ratio of mean inspiratory time/total time of the respiratory cycle (TI/TTOT), which represents the time fraction during which the inspiratory muscles are in motion (index of the respiratory rhythm).

We calculated TTMUS from the equation: TTMUS=PI/PIMAXxTI/TTOT, where PI is the mean inspiratory pressure developed by the respiratory muscles during inspiration. PI was estimated as follows: PI=5xP0.1xTI [13,24,25], where P0.1 was measured from signals displayed with a paper speed of 100 mm s–1 and with an average of three–five measurements. For the TTMUS equation, PI and TI/TTOT were determined at each workload and PIMAX was measured at rest.

TTMUS is an index of the performance of all the inspiratory muscles. High values of TTMUS correspond to low levels of performance, as shown by Ramonatxo et al. [24]. These authors validated TTMUS in patients with chronic obstructive pulmonary disease at rest by comparison to results obtained using the tension–time index of the diaphragm first described by Bellemare and Grassino [26]. They reported the usefulness of this index during exercise in these patients [27] and in patients with CHF [13].

2.6. Dyspnoea
Dyspnoea was assessed using a visual analogue scale (VAS) [28]. This consisted of 11 diodes laid out in a 15-cm horizontal line standing in front of the patient. The diodes could be switched on via a push button placed on the handlebar. The first diode corresponded to a score of zero and the last diode to 10. The signal was recorded via a numeric card.

With the patient at rest, an investigator read the following standard set of instructions:

Dyspnoea is a sensation of breathlessness experienced during exercise. VAS is a scale that allows patients to locate their breathlessness between two extremes. The left extreme is defined as ‘not at all breathless’ and the right extreme is defined as ‘extremely breathless’. By using the push button, periodically locate your sensation of breathlessness between these two extremes throughout the test. Be careful only to assess the breathless sensation. Please exclude other sensations, such as leg pain or fatigue.

During the exercise test, the investigator asked the patients to locate their sensation of breathlessness at the end of each workload. When a patient experienced an increase in dyspnoea sensation, he or she pressed a push button somewhere to the right of the previously chosen diode. Since the diodes remained illuminated, patients were always aware of their previous assessments.

2.7. Training program
All patients were ambulatory and were trained in hospital in a cardiovascular rehabilitation service. Patients were asked to perform one session of training per day, 3 days per week, over an 8-week period. The target level of training was based on the heart rate corresponding to 70–80% of the peak heart rate recorded before the training program [15,18,19,29,30] (mean 110±23 beats min–1). The training schedule was the same for all of the patients and consisted of a 3-min warm-up followed by 10 min of work and 5 min of active recovery on a stationary bicycle repeated over a 46-min session (3 min of recovery) [31]. During training, heart rate was continuously monitored (Sport Tester PE 3000; Polar Electro, Kemple, Finland). The cardiofrequency meter was set so that subjects would exercise within ±5 beats min–1 of the prescribed intensity. An alarm sounded to remind patients to train within the preselected range. To ensure that training procedures were followed, a cardiologist and an instructor supervised each session.

2.8. Protocol of cardiorespiratory and respiratory muscle assessment
The subjects were all tested in the afternoon before and after the 8-week training period. The subjects first underwent spirometric measurements at rest. They were then seated and, after a period of familiarisation with the experimental equipment (mouthpiece and nose clips), ventilatory and pressure parameters were recorded for 5 min. At least 10 occlusions were performed for each subject, at the rate of two–trhee min–1. After 5 min of rest, PIMAX and PEMAX were measured.

The patients then performed an incremental exercise test on a calibrated cycle ergometer in the sitting position. Resting measurements were obtained for 5 min at rest on the cycle ergometer. This was followed by a 3-min, 20-W warm-up and the workload was then increased by 10 W every 90 s until exhaustion. All patients were vigorously encouraged to perform maximal exercise until they felt unable to continue or they reached their maximal oxygen uptake. For each workload, a period of 90 s was needed to obtain all measurements of respiratory gas exchanges, breathing pattern, P0.1 and dyspnoea. To ensure that maximal oxygen uptake was attained, at least three of the following four criteria had to be met: (1) stability of heart rate at a value close to the theoretical maximal heart rate; (2) stability of oxygen uptake despite the increase in workload; (3) respiratory ratio >1.10; and (4) the inability to maintain the required pedalling rate (50 rev min–1) despite maximal effort and verbal encouragement. If one of three points was not observed, we considered the maximal oxygen uptake to be symptom-limited oxygen uptake. All patients stopped exercise because of fatigue or dyspnoea, or both.

2.9. Statistics
The values are reported as mean±standard deviation (S.D.). The data at rest and maximal exercise were compared before and after exercise training using a paired Student's t-test or a Wilcoxon signed rank test when variables were non-parametric. Exercise data were compared at the same workload (20, 30, 40, 50 and 60 W) before and after exercise training, using a two-way analysis of variance (ANOVA) for repeated measures or a Friedman's test when variables were non-parametric. Post hoc pairwise multiple comparisons were made using the Student–Newman–Kreuls method. A P value <0.05 was considered statistically significant.


   3. Results
Top
 1. Introduction
 2. Methods
 3. Results
4. Conclusion
 References
 
3.1. Spirometric parameters
The spirometric data are listed in Table 1. There was no statistical difference for forced expiratory volume in 1 s, forced vital capacity or Tiffeneau's ratio between pre- and post-training.


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  		Table 1 Spirometric parameters at rest in patients with CHF, before and after exercise training

 
3.2. Gas exchanges and cardiorespiratory parameters
At rest, no significant difference was found for heart rate, minute ventilation, tidal volume, respiratory frequency, TI/TTOT, oxygen uptake and carbon dioxide output between pre- and post-training. At maximal exercise, heart rate, minute ventilation, tidal volume, respiratory frequency, and TI/TTOT were not significantly different pre- and post-training. In contrast, maximal workload (P<0.05), maximal oxygen uptake (P<0.01) and maximal carbon dioxide output (P<0.05) were significantly higher post-training compared with pre-training. The results are summarised in Table 2.


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  		Table 2 Gas exchanges and cardiorespiratory parameters at rest and with maximal exercise, before and after exercise training, in patients with CHF

 
During exercise, 20, 30, 40, 50, and 60 W were the workloads reached by all patients with CHF before exercise training. At comparable workloads, minute ventilation (at 30, 40, 60 W) was lower at post-training (Fig. 1). In contrast, TI/TTOT was comparable at each workload before and after training (Fig. 2).


Figure 1
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  		Fig. 1 Minute ventilation at comparable submaximal and maximal workloads before and after exercise training in patients with chronic heart failure. The circles represent the workloads reached by all patients before ({circ}) and after (bullet) training. The triangles represent the means of the maximal workloads before ({triangleup}) and after ({blacktriangleup}) training. For this value, the S.D. on the horizontal axis represents the inter-subject variability of the maximal workload. *P<0.05; ns, not significant at comparable pre- and post-training workload; NS, not significant at maximal workload before and after training. The values are expressed as mean±S.D.

 


Figure 2
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  		Fig. 2 Ratio of mean inspiratory time to total time of the respiratory cycle (TI/TTOT) at comparable submaximal and maximal workloads before and after exercise training in patients with chronic heart failure. The circles represent the workloads reached by all patients before ({circ}) and after (bullet) training. The triangles represent the means of the maximal workloads before ({triangleup}) and after ({blacktriangleup}) training. For this value, the S.D. on the horizontal axis represents the inter-subject variability of the maximal workload. ns, not significant at comparable pre- and post-training workload; NS, not significant at maximal workload before and after training. The values are expressed as mean±S.D.

 
3.3. Respiratory muscle parameters
At rest, PIMAX and PEMAX were not significantly higher post-training as compared with pre-training. There were no statistical differences for the pressure parameters (P0.1 and PI/PIMAX) or TTMUS after training (Table 3).


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  		Table 3 Respiratory muscle performance parameters at rest and before and after exercise training in patients with CHF

 
During exercise, the pressure parameters (P0.1 at 30, 40, 50 W, Fig. 3; PI/PIMAX at 20, 30, 40, 50, 60 W, Fig. 4) and TTMUS (at 20, 30, 40, 50, 60 W, Fig. 5) were lower at comparable submaximal workloads post-training compared with pre-training, but at maximal exercise these differences were not statistically different.


Figure 3
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  		Fig. 3 Mouth occlusion pressure (P0.1) at comparable submaximal and maximal workloads before and after exercise training in patients with chronic heart failure The circles represent the workloads reached by all patients before ({circ}) and after (bullet) training. The triangles represent the means of the maximal workloads before ({triangleup}) and after ({blacktriangleup}) training. For this value, the S.D. on the horizontal axis represents the inter-subject variability of the maximal workload. *P<0.05; ns, not significant at comparable pre- and post-training workload; NS, not significant at maximal workload before and after training. The values are expressed as mean±S.D.

 


Figure 4
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  		Fig. 4 Ratio of mean inspiratory pressure to maximal inspiratory pressure (PI/PIMAX) at comparable submaximal and maximal workloads before and after exercise training in patients with chronic heart failure. The circles represent the workloads reached by all patients before ({circ}) and after (bullet) training. The triangles represent the means of the maximal workloads before ({triangleup}) and after ({blacktriangleup}) training. For this value, the S.D. on the horizontal axis represents the inter-subject variability of the maximal workload. *P<0.05; NS, not significant at maximal workload before and after training. The values are expressed as mean±S.D.

 


Figure 5
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  		Fig. 5 Tension–time index of the inspiratory muscles (TTMUS) at comparable submaximal and maximal workloads before and after exercise training in patients with chronic heart failure. The circles represent the workloads reached by all patients before ({circ}) and after (bullet) training. The triangles represent the means of the maximal workloads before ({triangleup}) and after ({blacktriangleup}) training. For this value, the S.D. on the horizontal axis represents the inter-subject variability of the maximal workload. *P<0.05; NS, not significant at maximal workload before and after training. The values are expressed as mean±S.D.

 
3.4. Dyspnoea
During exercise, dyspnoea scores were lower (at 50 and 60 W) at comparable submaximal workloads after training compared with before training, but at maximal exercise this difference was not statistically different (Fig. 6).


Figure 6
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  		Fig. 6 Dyspnoea score at comparable submaximal and maximal workloads before and after exercise training in patients with chronic heart failure. The circles represent the workloads reached by all patients before ({circ}) and after (bullet) training. The triangles represent the means of the maximal workloads before ({triangleup}) and after ({blacktriangleup}) training. For this value, the S.D. on the horizontal axis represents the inter-subject variability of the maximal workload. *P<0.05; ns, not significant at comparable pre- and post-training workload; NS, not significant at maximal workload before and after training. The values are expressed as mean±S.D.

 

   4. Conclusion
Top
 1. Introduction
 2. Methods
 3. Results
 4. Conclusion
References
 
This study demonstrates that aerobic exercise training improves maximal exercise capacity in patients with CHF, but with no change at maximal exercise in TTMUS, a non-invasive index assessing the performance of all the inspiratory muscles, or dyspnoea. In contrast, at comparable submaximal workloads during exercise, TTMUS and the dyspnoea score were significantly lower after exercise training, indicating greater inspiratory muscle performance and diminished dyspnoea sensation after 8 weeks of aerobic exercise training.

The mechanisms responsible for the increase in inspiratory muscle performance at comparable submaximal workloads after exercise training may be the same as those observed in limb skeletal muscles. Thus, exercise training may improve the under-perfusion of respiratory muscle [12] and may reverse the metabolic and histological abnormalities in respiratory muscles [32], with improved oxidative capacity of these muscles similar to that in the peripheral skeletal muscles [15,16]. Moreover, the diminished minute ventilation and increased inspiratory muscle performance appear to be closely related to the improvement in skeletal muscle oxidative capacity (peripheral and respiratory).

Although our study demonstrates improvements in exercise capacity, inspiratory muscle performance and dyspnoea after aerobic exercise training, it does not indicate causal mechanisms. Dyspnoea can be attenuated in the patients with CHF through aerobic exercise training, with concomitant improvements in exercise capacity, cardiac haemodynamic [33] and respiratory muscle function. However, controlled studies are needed to confirm our findings.

The benefits of aerobic exercise training observed suggest that specific attention to the muscles (peripheral and respiratory) of these patients may improve the management of this disease.


   References
Top
 1. Introduction
 2. Methods
 3. Results
 4. Conclusion
 References
 

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