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European Journal of Heart Failure 2005 7(2):189-193; doi:10.1016/j.ejheart.2004.07.012
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© 2005 European Society of Cardiology

Exercise training in chronic heart failure: effects on pro-inflammatory markers

Josef Niebauera,b,*, Andrew L. Clarkc, Katherine M. Webb-Peploea and Andrew J.S. Coatsa,d

a Cardiac Medicine, Royal Brompton Hospital and NHLI London, UK
b Herzzentrum der Universität Leipzig Leipzig, Germany
c Cardiac Medicine, University of Hull UK
d University of Sydney Australia

* Corresponding author. Herzzentrum der Universität Leipzig, Innere Medizin/Kardiologie, Strümpellstr. 39, 04289 Leipzig. Tel.: +49 341 865 0; fax: +49 341 865 1461. E-mail address: j.niebauer{at}medizin.uni-leipzig.de


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
 References
 
Background: Acute bouts of exercise have been shown to induce inflammatory cytokine activation and peripheral hypoxia in patients with chronic heart failure (CHF). In this study, we set out to investigate the impact of chronic exercise training on pro-inflammatory cytokines and markers of endothelial damage.

Methods and results: We measured tumor necrosis factor {alpha} (TNF{alpha}), its soluble TNF-receptors 1 and 2, interleukin 6 (IL-6), soluble e-selectin, soluble intracellular adhesion molecule-1 (sICAM) and sCD14 in 18 patients with CHF and 9 age-matched controls in a randomized cross-over study of 8 weeks of exercise training (5 days/week, submaximal bicycle ergometer training, 30 min/day; calisthenics 9 min/day) versus 8 weeks of rest. At baseline, patients had a lower peak VO2 (p=0.009) and a trend for higher levels of e-selectin (p=0.08) and sCD14 (p=0.06), in addition to significantly elevated levels of sICAM (p=0.02), TNF{alpha} (p=0.02) and TNF-R2 (p=0.002); TNF-R1 and IL-6 were not elevated. Although exercise training was effective and led to an increase in peak VO2 in CHF (p<0.003), there was no activation of any of the above variables observed, neither in patients nor controls.

Conclusions: Chronic heart failure is associated with increased levels of TNF{alpha} and markers of endothelial damage. Whereas acute bouts of exercise have been reported to lead to an increase in pro-inflammatory cytokines and markers of endothelial damage, these effects are not seen when exercise is performed chronically.

Key Words: Heart failure • Endothelial damage • Tumor necrosis factor {alpha} • Exercise

Received March 22, 2004; Revised June 3, 2004; Accepted July 21, 2004


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
 References
 
Chronic heart failure is a condition characterized by exercise intolerance. Although the primary abnormality is impairment of the pumping function of the heart, widespread changes to all body systems occur, and amongst other changes, there is activation of inflammatory mediators [1], such as tumor necrosis factor (TNF) {alpha} [2–4] and IL-6 [5] and their receptors [6–9]. Although exercise training can improve exercise capacity in heart failure [10] and some of the neurohormonal abnormalities associated with a poor outcome[11–13], acute bouts of exercise lead to increases in markers of endothelial damage, pro-inflammatory cytokines and may induce peripheral hypoxia.

The aim of the present study was to investigate the relation between an exercise training regime for heart failure patients and markers of pro-inflammatory cytokine activation and endothelial damage. Markers were assessed in 18 patients with chronic heart failure and 9 age-matched controls in a randomized cross-over study of exercise training versus rest.

E-selectin is expressed on inflamed endothelial cells in response to treatment with inflammatory cytokines [14] and is involved in the process of binding white cells to the endothelium. sICAM mediates the binding of inflammatory cells to vascular endothelium [15]. Inflammatory states, including atheroma [16] and heart failure, [17] cause a rise in circulating sICAM. CD14 is the principle receptor for the complex of endotoxin and its binding protein [18,19], which results in the up-regulation of cell surface molecules, including adhesion molecules.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
 References
 
Patients were recruited if they had had heart failure for at least 3 months, and had been clinically stable with no admissions and no changes in medication for 3 months. Heart failure was defined as symptoms of exercise limitation by breathlessness or fatigue in the presence of objective evidence of left ventricular systolic dysfunction on echocardiography (left ventricular end diastolic dimension (LVEDD) greater than 6.5 cm, and a shortening fraction less than 25%). No patient was limited by angina or had sustained ventricular arrhythmia on Holter monitoring. All patients had a serum creatinine of < 125 mmol/l and were biochemically euthyroid. None of the patients or control subjects had obstructive lung disease as assessed by spirometry.

The nine healthy volunteers had no symptoms suggestive of heart disease and no history of hypertension, effort-induced chest pain or shortness of breath. There was no evidence of significant heart disease on echocardiography and no ischaemic electrocardiographic change on maximal exercise testing.

The study was approved by the Ethics Committee of the Royal Brompton Hospital, London, UK. All patients gave written informed consent before starting the trial.


   3. Exercise program
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
 References
 
Patients and healthy subjects were randomized to start with either 8 weeks of exercise training or 8 weeks rest. Exercise training consisted of at least 5 days a week of a combination of calisthenics and bicycle ergometry, performed at home. Participants were asked to do the first nine exercises in the Canadian airforce XBX program. The XBX Plan is a physical fitness program in which the work load increases as physical fitness improves. The time limit for each exercise remains the same (9 min in total), but the number of times the exercise is performed within this time limit is increased at each level. The exercises are made more difficult from each level to the next higher one.

In addition, subjects were loaned a bicycle ergometer (Tunturi original ergometer W1 electronics) and asked to exercise on it for 20 min a day. They were asked to warm up by pedaling at a work load of 25W at 50 rev/min for 3 min and then to increased the resistance until their pulse rate was between 70% and 80% of the maximum pulse rate achieved on their initial maximal treadmill test. They then pedaled at 50 rev/min for 20 min before decreasing the resistance to 25W to cool down for 2–3 min.

During the 8-week rest period, the exercise bicycles were withdrawn (where the subjects had been randomized to training first) and subjects were asked to avoid any strenuous activity that might lead to shortness of breath or exhaustion.

The subjects were investigated at the Royal Brompton Hospital over 2 days at the start and end of each phase of the trial. After the first phase, they crossed over immediately to the second phase of the trial. Investigations were carried out at the same time of day at each visit.


   4. Cardiopulmonary exercise testing
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
 References
 
Subjects exercised using an incremental treadmill protocol. We used the Bruce protocol modified by the addition of a 3-min "stage 0" at the onset of exercise (1 mph at 5% gradient). During the test, expired air was collected and analyzed with a respiratory mass spectrometer (Amis, 2000, Innovision, Odense Denmark). Oxygen consumption (VO2), carbon dioxide (VCO2) and minute ventilation (VE) were measured online. Peak oxygen consumption was calculated off line.


   5. Blood tests
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
6. Statistical analyses
 7. Results
 8. Discussion
 References
 
After 40 min lying supine, blood was taken from the ante-cubital vein and sent for routine analysis of urea and electrolytes. Blood samples drawn for analysis were put on ice, immediately centrifuged at 4 °C and 1300 rpm. Plasma was then transferred into Eppendorf tubes and stored at –80 °C until further analysis. The above variables were all measured by enzyme-linked immunosorbent assay (ELISA) using commercially available kits (TNF-{alpha}: Medgenix, Belgium; sTNF-R1, -R2, IL-6, e-selectin, sICAM-1, sCD14: all R&D Systems, Minneapolis, MN, USA).


   6. Statistical analyses
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
7. Results
 8. Discussion
 References
 
Data are presented as mean±standard deviation and were analyzed according to the recommendation of Altman for cross-over trials [20] using StatView 4.5 (SAS Institute, Cary, NC, USA). Numerical values are presented as mean ±SD. Differences were considered significant when the two-sided probability of the null hypothesis was ≤0.05. Baseline characteristics and comparisons between two groups (patients versus healthy volunteers) were made using unpaired t-test. The results after rest and after exercise training were compared using paired t-test.


   7. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
8. Discussion
 References
 
7.1. Baseline data for patients and controls are shown in Table 1
Patients and control subjects were all male with the exception of one female in each group (Table 1). Patients' age span was 28–64 years and control-subjects age range was 36–65. Three of the patients were receiving a thiazide diuretic and 11 received an average of 117±93 mg furosemide or its equivalent daily. All were receiving an angiotensin converting enzyme inhibitor (an angiotensin receptor blocker in one subject), one was taking a beta adrenoceptor antagonist. Eight patients were on oral nitrates (47.5±5.5 mg/day).


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  		Table 1 Baseline characteristics of patients and controls

 
Patients documented adherence to the exercise program in their diaries. There were 16 correctly filled out diaries from the patients and 7 correctly filled out diaries from healthy volunteers. Patients exercised on 38±7 days and the healthy volunteers on 38±4 days. Patients completed 1235±218 revolutions/day on their bicycles, the healthy volunteers 1283±73 (p=n.s.). All but one of these patients performed calisthenics all the days that they biked. This particular patient only performed the XBX exercises on 16 of 40 days.

Patients had a lower peak VO2 at baseline (p=0.009) and a trend for higher levels of e-selectin (p=0.08) and sCD14 (p=0.06), in addition to significantly elevated levels of sICAM (p=0.02), TNF{alpha} (p=0.02) and TNF-R2 (p<0.002); TNF-R1 and IL-6 were not elevated (p=0.12). There was a weak relation between sICAM and sCD14 (r=0.47; P=0.01). There was no association between NYHA class of symptoms, age or left ventricular function and any of the measured variables.

There was an increase in peak VO2 in the patient group from 25.3±1.8 to 28.0±2.1 ml kg–1 min–1 (p=0.008) but there was no significant increase in either peak VO2 or exercise time in the controls.

There was no effect of training on TNF-{alpha}, TNF-R 1 and 2, IL-6, e-selectin, sICAM, sCD14 in either patients or controls (Fig. 1).


Figure 1
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  		Fig. 1 Blood samples were obtained after rest and after training and the results of TNF{alpha}, TNF-R1, TNF-R2, IL-6, sCD14, soluble e-selectin and sICAM are shown.

 

   8. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
References
 
Despite all the known beneficial effects of exercise training, it is only slowly becoming part of the routine management of chronic heart failure. Although definitive data on the effects of training on prognosis are not yet available, many of the variables associated with a poor prognosis, such as exercise performance [10], sympathetic [21] and neurohormonal activation [11,22], peripheral hypoxia [23] and endothelial function [24] improve with exercise training. Also, the cardinal symptom of heart failure, i.e., shortness of breath on exertion and the resulting impaired exercise capacity measured as peak VO2 improves by around 20%. Furthermore, a recent meta-analysis supports the notion that training may even improve prognosis [25].

Nevertheless, there are also reports that exercise itself may cause the release of endothelial factors such as VCAM [26] and p-selectin [27] and increasing free radical formation [28]. Training regimes have, however, generally shown an improvement in endothelial function in normal subjects [29] and patients with heart failure [24,30].

In order to assess the molecular changes induced by exercise training in heart failure patients, we initiated the present study. Our results show that whilst there were higher levels of circulating TNF and its soluble receptors, IL-6, sICAM, CD14 and e-selectin, a training regime sufficient to induce a systemic training effect in heart failure patients did not cause an increase in cytokines and endothelial factors that might be associated with an adverse outcome. Other studies, however, not only reported the lack of an exercise-induced cytokine activation, but found a decrease in at least some cytokines or their soluble receptors [11,12,31–34]. Since these studies did not uniformly report improved levels of TNF-{alpha}, interleukin 6 and other cytokines, it remains unclear what causes such a heterogeneous response to exercise training. Taking all trials together, it may be speculated that a training period of only 8 weeks, as chosen in our study, may not be long enough to induce changes in cytokines, since most studies were carried out for 12–26 weeks. Also, our patients only showed mildly impaired oxygen consumption and exercise intolerance, so that exercise training only led to a small, albeit significant improvement in maximal oxygen consumption. It may be speculated that despite pronounced pathological findings in the echocardiogram, the stimulus for cytokine activation at baseline was not strong enough to induce a state of cytokine activation that would be more amenable to an exercise-based intervention.

In conclusion, it can be stated that unsupervised, home-based exercise training can be carried out safely in patients with chronic heart failure and that it leads to improved exercise capacity. An activation of pro-inflammatory cytokines does not occur, if exercise is not carried out in acute bouts but chronically. In patients with only mildly impaired oxygen consumption 8 weeks of exercise training does not improve pro-inflammatory cytokines.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Exercise program
 4. Cardiopulmonary exercise...
 5. Blood tests
 6. Statistical analyses
 7. Results
 8. Discussion
 References
 

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