Chronic heart failure (CHF) is often characterized by exercise intolerance with marked fatigue and dyspnoea. Many changes in the periphery affecting muscle and blood vessels contribute to this exercise intolerance and may be improved by exercise training.
The contra-indication to exercise for patients with significant left ventricular impairment was challenged in the 1980’s. The first controlled study of training in chronic heart failure (CHF) was a cross-over trial in stable class II-III patients [1]. These were carefully selected patients who could exercise without serious ventricular arrhythmias. After baseline evaluation and familiarization with laboratory procedures, all patients performed 8 weeks of exercise training and 8 weeks of exercise avoidance in a randomized cross-over study. The training regime leads to approximately a 20-25% increase in exercise tolerance and peak oxygen consumption. There was also a significant reduction in questionnaire-rated symptoms attributable to heart failure and a coincident increase in both the extent and ease of performing daily activities. There was an improvement in sympatho-vagal balance and an increase in sub-maximal and peak cardiac output and a reduction in the ventilatory response to exercise.
Other cross-over studies since have explored the physiological effects of training in patients with stable mild to moderate chronic heart failure demonstrating improvements in muscle metabolism and autonomic control. Similarly in several parallel group controlled trials improvements have been shown in indices of left ventricular diastolic function, and in “Feelings of Being Disabled” and “Self-Assessment of General Well-Being” along with increased exercise capacity. A summary of all trials performed to 1998 [2] has demonstrated a consistent increase in exercise capacity across a broad range of heart failure patients of approximately 15-20%.
Finally and perhaps most significantly Belardinelli in 1999 [3] reported on 50 trained and 49 control CHF patients including a supervised 8 week training program of cycling at 60% peak capacity three times per week followed by a supervised 12 month maintenance program. Training was associated with a lower mortality (n=9 versus n=20, relative risk =0.37; 95% CI, 0.17 to 0.84; p=0.01). There were also fewer hospital readmissions for heart failure (5 versus 14; RR=0.29; 95% CI, 0.11 to 0.88; P=0.02). It is too early to say that this is the proof we need to recommend training as a disease modifying intervention, but clearly it encourages further study. Important questions such as the optimal frequency and intensity of training and the most appropriate selection of patients remain to be seen.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.
Conclusion:
Acknowledgements
Professor Coats was supported by the Viscount Royston Trust, the British Heart Foundation, the Clinical Research Committee of the Royal Brompton Hospital and the Asmarley Trust