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(Chest. 2000;118:53-60.)
© 2000 American College of Chest Physicians

Role of Respiratory Function in Exercise Limitation in Chronic Heart Failure*

Ashok Chauhan, MD; Guruswamy Sridhar, MD; Ron Clemens; Bharath Krishnan, MBBS, PhD; Darcy D. Marciniuk, MD, FCCP and Charles G. Gallagher, MD, FCCP

* From the Division of Respiratory Medicine (Drs. Chauhan, Sridhar, and Marciniuk, and Mr. Clemens), Department of Medicine, University of Saskatchewan, Saskatoon, and the Faculty of Physical Activity Studies (Dr. Krishnan), University of Regina, Regina, Saskatchewan, Canada; and the Department of Respiratory Medicine (Dr. Gallagher), St. Vincent’s Hospital, Dublin, Ireland.

Correspondence to: Darcy D. Marciniuk, MD, FCCP, Division of Respiratory Medicine, 5th Floor Ellis Hall, Royal University Hospital, Saskatoon, Saskatchewan, Canada S7N OW8; e-mail: darcy.marciniuk{at}skyway.usask.ca


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Objective: To test the hypothesis that respiratory function contributes to limit maximal exercise performance in patients with chronic heart failure by using the technique of dead space loading during exercise.

Design: Blinded subjects underwent two maximal incremental exercise tests in random order on an upright bicycle ergometer: one with and one without added dead space.

Setting: Tertiary-care university teaching hospital.

Subjects: Seven patients with stable chronic heart failure (mean ± SEM left ventricular ejection fraction, 27 ± 3%).

Results: Subjects were able to significantly increase their peak minute ventilation during exercise with added dead space when compared with control exercise (57.4 ± 5.9 vs 50.0 ± 5.6 L/min; p < 0.05). Peak oxygen uptake, workload, heart rate, and exercise duration were not significantly different between the added dead space and control tests. Breathing pattern was significantly deeper and slower at matched levels of ventilation during exercise with added dead space.

Conclusion: Because patients with chronic heart failure had significant ventilatory reserve at the end of exercise and were able to further increase their maximal minute ventilation, we conclude that respiratory function does not contribute to limitation of exercise in patients with chronic heart failure.

Key Words: breathing pattern • chronic heart failure • exercise • ventilatory limitation


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
This study tested the hypothesis that respiratory factors contribute to limitation of maximal exercise tolerance in patients with chronic heart failure. It has traditionally been assumed that impaired exercise tolerance in chronic heart failure is primarily related to abnormal cardiac function. Although cardiac function is important, studies have suggested that other factors may also contribute to exercise limitation in chronic heart failure.1 2 For example, the increase in exercise cardiac output, related to short-term vasodilator therapy, does not increase exercise capacity.3 A number of studies have clearly documented limb muscle dysfunction in chronic heart failure.1 4 5 6 Several studies have also shown that limb muscle dysfunction in chronic heart failure is at least partly independent of limb blood flow.1 6

Other studies have also suggested that respiratory function may contribute to exercise limitation in chronic heart failure.7 8 9 10 11 12 13 14 Patients with chronic heart failure have to generate greater inspiratory muscle pressures during exercise compared with normal humans.7 This is because of their increased minute ventilation (E)14 and, in some patients, reduced lung compliance and increased airway resistance.15 We and others have shown that inspiratory muscle strength is frequently reduced in patients with chronic heart failure or valvular heart disease.8 9 10 Therefore, the stress on inspiratory muscles (ie, the pressure generated as a fraction of pressure-generating capacity) is increased in chronic heart failure patients during exercise.8 Studies using near-infrared spectroscopy provide evidence of respiratory muscle dysfunction during exercise in chronic heart failure.11 More important, Mancini et al12 13 reported improved maximal exercise capacity in chronic heart failure patients after respiratory muscle training and also after unloading the work of breathing. However, recently, Dimopoulou et al16 concluded that respiratory function is not the major determinant of exercise capacity in stable chronic heart failure patients.

In view of these considerations and the conflicting results, we tested the hypothesis that respiratory function contributes to limitation of maximal incremental exercise performance in patients with stable chronic heart failure. We used the technique of dead space (VD) loading, which increases E at a given metabolic rate,17 to stress the respiratory system during exercise. The principles and methods of VD loading are described in greater detail in our previous studies.17 18 19 We reasoned that if respiratory function significantly contributes to exercise limitation in this population, further increasing E during exercise by VD loading will result in a decrease in peak oxygen uptake (O2) and no increase in E at the end of exercise.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Design
The study was designed to determine whether added VD increases peak E or decreases exercise capacity during incremental exercise in patients with stable chronic heart failure. Patients performed two maximal incremental exercise tests on a cycle ergometer (Godart; Utrecht, The Netherlands) in random order; one was performed with added VD, and one without added VD. Apart from the added VD, the two tests were identical.

Patients
Patients were considered eligible for the study if they had stable heart failure caused by a cardiomyopathy. Heart failure was defined as symptomatic left ventricular dysfunction with a left ventricular ejection fraction (LVEF) < 0.45. Left ventricular systolic dysfunction was documented by either two-dimensional echocardiography or radionuclide ventriculography. Stability was defined as absence of change in symptoms, clinical status, or medications in the preceding 2 months. Patients were excluded if they had any pulmonary, rheumatologic, neuromuscular, peripheral vascular, or any disease apart from heart failure that might impair exercise tolerance. Patients were also excluded if they had angina pectoris or a documented myocardial infarction in the preceding 6 months, or a viral illness within the previous 6 weeks.

Equipment
Exercise was performed on an electrically braked cycle ergometer. ECG leads were attached to monitor heart rate (HR) and ECG. Arterial oxygen saturation (SaO2) was monitored continuously by pulse oximetry (N200; Nellcor; Hayward, CA). Subjects breathed through a mouthpiece attached to a breathing valve. Inspiratory flow was obtained from an inspiratory pneumotachograph/transducer/demodulator system as described previously.20 The inspiratory flow signal was integrated to provide inspiratory volume. The expiratory line was connected to a mixing chamber with baffles. Oxygen and carbon dioxide concentrations at the mouth and mixing chamber were measured by a mass spectrometer (Airspec MGA 2000; Kent, UK). Sampling by the analyzer was alternated between the mouthpiece and the mixing chamber to yield breath-by-breath and mean expiratory concentrations, respectively.

Patients breathed through an added VD (measured by water displacement) placed between the mouthpiece and the breathing valve during the added VD test. The volume (~300 mL) was chosen, based on our previous studies, to be approximately 20% of peak exercise tidal volume (VT) during a preliminary practice test without added VD. Identical tubing was added to both the inspiratory and the expiratory lines of the breathing circuit during the control tests only so as to maintain identical breathing circuit resistance on the control and added VD days.21 The tubing arrangement was concealed in a rectangular box, and no patient was aware of the particular arrangement (added VD or control) during any exercise test. The resistance of the inspiratory and expiratory breathing circuit was < 1 cm H2O/L/s at flow rates up to 4 L/s.

All equipment was calibrated before each exercise test, and the calibration was rechecked immediately after the test.

Protocol
Each patient performed maximal incremental exercise on 2 days, one with added VD and one without added VD (control). The order of tests was randomized among subjects. The two tests for a given subject were performed at the same time of day separated by >= 48 h. Subjects were instructed not to have any caffeinated drink or to eat for at least 2 h before testing, and to avoid exercise on the day of testing.

After sitting on the cycle for at least 4 min, the patient started exercising at 10 W, and the work rate was increased by 10 W/min. Patients chose their own pedaling rate between 50 and 70 revolutions/min, with the help of tachometer feedback. All subjects were instructed in an identical manner by the same investigator for all exercise studies. They were told to exercise for as long as they could until they were unable to continue. No other form of encouragement was given to any subject. Each patient estimated the intensity of dyspnea and of leg effort at maximal exercise using the modified Borg scale.22 They were also asked after exercising which of these (or other) symptoms caused them to stop exercising. Spirometry was performed in all subjects before and immediately after each exercise test using recommended techniques.23 The highest values of three well-coordinated maximal efforts are reported both before and after exercise.

Data Analysis
E, VT, respiratory frequency (f), O2, carbon dioxide output (CO2), and HR were calculated using standard methods. E and VT were expressed at body temperature, pressure, saturated; O2 and CO2 were expressed at standard temperature, pressure, dry. Data from the control and added VD tests at end exercise were compared by paired t tests. Measured variables at matched work rates during exercise were compared by analysis of variance with repeated measures. Analysis of Borg scale results was performed using Wilcoxon’s signed rank test. A p < 0.05 was taken to be statistically significant. Data are presented as mean ± SEM.

Analysis of our study sample size showed that it could detect a 10% fall in peak O2 with a power of 93%, and a 10% fall in exercise duration with a power of 97%.24


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Seven patients (four men and three women) were studied. Their average age was 55 years, with a range of 37 to 70 years. The mean LVEF of our study population was 0.28, with a range of 0.20 to 0.40. Heart failure was secondary to idiopathic dilated cardiomyopathy in four patients, ischemic cardiomyopathy in two patients, and hypertensive cardiomyopathy in one patient. All patients used an angiotensin-converting enzyme inhibitor, five used digoxin, four used diuretics, two used aspirin, one used warfarin, and one used a nitrate skin patch. All patients had heart failure for >= 2 years. All subjects completed both exercise tests without any complications, and no exercise test was terminated by the physician. Subject characteristics and maximal exercise data are presented in Table 1 .


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  		Table 1. Subject Characteristics and Maximal Exercise Data*

 
There was no evidence of significant bronchodilation or bronchoconstriction after exercise on either day (pre-exercise FEV1, control 2.61 ± 0.22 vs VD 2.59 ± 0.19 L; postexercise FEV1, control 2.66 ± 0.24 vs 2.68 ± 0.20 L).

O2 and HR at end exercise on the control day were 67 ± 5% and 84 ± 4% of predicted, respectively. Figure 1 compares E, VT, O2, and HR at end exercise in the control study to those at end exercise with added VD. Table 2 compares end-exercise variables in the control and VD tests. E and VT at end exercise were significantly higher with added VD. The VT/vital capacity (VC) ratio was 51.4 ± 4.6% at end exercise in the control study, which is similar to that reported in previous studies.20 25 The VT/VC ratio was significantly higher with added VD. There was no significant differences in O2, CO2, HR, exercise duration, or work rate at end exercise between the two tests. E/O2 and E/CO2 were elevated during control exercise26 and were significantly higher with added VD than during control exercise. There was no significant difference in f, end-tidal CO2 (PETCO2), or SaO2 at end exercise between the two tests.



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  		Figure 1. Comparison of E (I), VT, O2, and HR at peak exercise with and without (control) added VD. Each point indicates the results of one subject. Diagonal lines are lines of identity. E and VT increased significantly with added VD.

 

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  		Table 2. Mean Values Obtained at End Exercise*

 
The intensity of dyspnea (Borg score) and leg effort at the end of control exercise were 4.7 ± 0.5 and 5.3 ± 0.6, respectively. The corresponding values with added VD were 5.3 ± 0.6 and 4.9 ± 0.9, which were not significantly different from the control values. Four patients reported dyspnea and two patients reported leg effort as their reason for stopping during control exercise; in none of these patients did the reason for stopping change with added VD. One patient stated that she stopped because of both dyspnea and leg effort during control exercise. She stopped because of dyspnea alone with added VD.

Figure 2 shows E throughout exercise for each subject in both control and added VD studies. As expected, E was higher throughout exercise with added VD for all subjects. Figure 3 shows group mean results of E, VT, f, and PETCO2 throughout exercise. E and VT were significantly higher throughout exercise with added VD, but there was no significant difference in f or PETCO2 throughout exercise.



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  		Figure 2. Comparison of E throughout exercise for each subject with and without added VD.

 


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  		Figure 3. Group mean comparisons of E, VT, f, and PETCO2 at matched work rates during exercise in the control and added VD tests. Dashed lines join data from last common work rate to mean data at end exercise. ANOVA = analysis of variance.

 
Figure 4 shows group mean results for O2, CO2, SaO2, and HR throughout exercise. There was no significant difference in O2, CO2, or SaO2 at any time. HR was slightly greater at some, but not all, work rates with added VD.



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  		Figure 4. Group mean comparisons of O2, CO2, SaO2, and HR at matched work rates during exercise in the control and added VD tests. Dashed lines join data from last common work rate to mean data at end exercise. See Figure 3 legend for abbreviation.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
We have demonstrated that chronic heart failure patients have significant ventilatory reserve at end exercise and are able to further increase their maximal E, indicating that respiratory function does not contribute to limitation of exercise in chronic heart failure patients.

During control exercise, our chronic heart failure patients demonstrated impaired exercise performance as evident by their low peak O2. The ventilatory response to exercise (ie, E/CO2) was increased, and there was no desaturation during exercise. Peak exercise VT was reduced, but the ratio of peak exercise VT to VC was normal. These results are consistent with previous studies of chronic heart failure patients.1 2 25 26 27 28

Consistent with previous studies of normal humans and patients with respiratory disease,17 18 19 29 added VD resulted in an increased E with no change in O2 or CO2 at a given work rate during submaximal exercise. If respiratory function contributes to exercise limitation, one would expect a fall in peak O2 because of the respiratory loading with added VD. This did not occur in this study. There was no fall in peak O2 because the chronic heart failure patients were able to increase their E at end exercise compared with the control situation. In other words, the ventilatory demands of exercise in chronic heart failure patients can be significantly increased without any impairment in maximal exercise performance. Therefore, the respiratory system is not operating at its maximal capacity during incremental exercise, and respiratory function does not contribute to limitation of maximal exercise performance in patients with moderate chronic heart failure. Similarly, VD loading during incremental exercise in normal humans causes no impairment in exercise capacity, but it does cause a significant increase in E at maximal exercise.17 18 In contrast, VD loading causes a reduction in peak O2 with little or no increase in E at maximal exercise in patients with COPD or those with interstitial lung disease.19 28 29 30

Exercise Limitation in Chronic Heart Failure
Mancini et al12 examined the effects of respiratory muscle training on exercise capacity in patients with chronic heart failure. Respiratory muscle function improved after training. They also found an improvement in peak O2 and E during incremental exercise after respiratory muscle training. Therefore, the data of Mancini et al12 suggest that respiratory muscle function may contribute to exercise limitation in patients with chronic heart failure. How can we account for the discrepancy between the results of Mancini et al12 and the conclusions of this study? As emphasized by Mancini et al12 and by Wilson,1 there was no true control group in the former study; the control group was subjects who dropped out of the training program. It is possible that the improvements observed in their study were partly related to the careful attention they received. Also, the improvement in peak O2 in the study of Mancini et al12 was accompanied by no change in peak HR. This is suggestive of a generalized exercise training effect. This might have resulted from the leg exercises that were part of the "breathing calisthenics" during respiratory muscle training.

More recently, inspiring a helium/oxygen gas during exercise was found to increase exercise duration and reduce dyspnea in chronic heart failure patients with a mean LVEF of 0.19. However, importantly, peak O2 and peak E were unaffected by this intervention. Although the authors concluded that respiratory function significantly contributes to affect exercise performance in chronic heart failure patients, the lack of a significant change in objective variables, such as O2 or E, suggests that other mechanisms may have been responsible for the observed improvement in exercise duration and dyspnea. This is supported by the findings of Dimopoulou et al,16 who examined the relationship between respiratory factors and exercise performance in patients with stable chronic heart failure. Although studied indirectly, they reported that lung function indexes accounted for only ~30% of the variance in maximum exercise capacity in chronic heart failure patients.

Study Limitations
We examined the role of respiratory function contributing to limitation of maximal exercise tolerance in patients with stable chronic heart failure. The determinants of peak performance and endurance at submaximal exercise frequently differ,28 30 31 32 and it is therefore possible that respiratory function may contribute to the impairment of endurance exercise performance in chronic heart failure. Similarly, this study was not designed to examine whether respiratory function was normal, or what degree of respiratory reserve was present in these subjects. In addition, the conclusions of this study may not necessarily apply to patients with unstable or more severe chronic heart failure, in whom respiratory function might indeed contribute to exercise limitation. Additional studies are needed to examine the importance of respiratory function in exercise tolerance in these other populations.


   Acknowledgements
 
The authors thank Mrs. I. Fairlie for her assistance in preparation of this manuscript.


   Footnotes
 
Abbreviations: f = respiratory frequency; HR = heart rate; LVEF = left ventricular ejection fraction; PETCO2 = end-tidal CO2; SaO2 = arterial oxygen saturation; VC = vital capacity; CO2 = carbon dioxide output; VD = dead space; E = minute ventilation; O2 = oxygen uptake; VT = tidal volume

Supported by the Saskatchewan Lung Association, and the Heart and Stroke Foundation of Canada. Dr. Marciniuk is a Saskatchewan Lung Association Research Professor.

Received for publication September 13, 1999. Accepted for publication December 13, 1999.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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