ReviewRespiratory Muscle Dysfunction and Training in Chronic Heart Failure
Introduction
Chronic heart failure (CHF) is a major cause of morbidity and mortality, especially amongst the elderly. Depending on the definition, about 3-6% of the general adult population have CHF. Of patients ≥60 years of age attending family physicians, 13% have CHF [1]. A characteristic feature of CHF is exercise intolerance, with marked fatigue and dyspnoea at low exercise intensities. This has been attributed to alterations in central haemodynamics and skeletal muscle oxygen utilisation, including reduced regional blood flow to exercising skeletal muscle [2], [3], mitochondrial abnormalities [4], reduced oxidative enzyme activity [5], increased proportion of type IIb fibres [6] and skeletal muscle atrophy [7]. Some of these skeletal muscle abnormalities can be reversed by exercise training [8].
Several studies have revealed that the structure and function of respiratory muscles are also altered in CHF. Patients commonly exhibit reduced respiratory muscle strength and endurance. Thus, respiratory muscle abnormalities may exacerbate exertional dyspnoea and contribute to early fatigue in patients with CHF. From a therapeutic point of view, the beneficial effects of selective respiratory muscle training, in improving respiratory muscle strength and overall aerobic capacity in CHF, were first demonstrated by Mancini et al. [9], with further data being published over the last decade.
This brief review summarises the published research on the alterations in respiratory muscle function in patients with CHF, and discusses recent evidence for selective respiratory muscle training in these patients.
Section snippets
Respiratory Muscle Strength and Endurance
Respiratory muscle strength is commonly assessed by measuring the static pressures generated at the mouth during maximal inspiratory or expiratory efforts. Although limited by its dependence on patient effort, the measurements of maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP) obtained from this technique have been shown to be reliable [10].
Several studies have observed that MIP and MEP are reduced in patients with CHF [11], [12], [13]. In addition, MIP and MEP
Alterations in Fibre Type and Oxidative Capacity
Human and animal studies have repeatedly found histological and biochemical alterations of the diaphragm muscle in CHF. De Sousa et al. [18] observed that there was an increase in the proportion of type I and type IIa muscle fibres in rats with heart failure induced by aortic banding compared with sham-operated control rats. There was a concurrent decrease in type IIb fibres. Howell et al. [19] also noticed fibre atrophy in the diaphragm of minipigs with CHF. Similar alterations have been found
Intracellular Calcium Regulation
The reduction in respiratory muscle strength and endurance noted in patients with CHF may also be a result of alterations in intracellular calcium regulation. In a rabbit model of heart failure, MacFarlane et al. [23] observed that there was a leftward shift in the relationship between phrenic stimulation frequency and intracellular calcium ([Ca2+]i) in the diaphragm muscle, such that peak [Ca2+]i occurred at lower frequencies in rabbits with CHF compared to controls. In addition, the
Role of TNF-α in Respiratory Muscle Dysfunction
Despite longstanding awareness of respiratory muscle dysfunction in patients with CHF, little is known concerning the underlying mechanism responsible. Recent research has highlighted that the over-expression of cytokines, particularly tumour necrosis factor-α (TNF-α), may contribute to respiratory as well as limb skeletal muscle myopathy in CHF.
Cardiac over-expression of TNF-α is a feature of CHF [27]. Numerous cell types within the myocardium have the capacity to synthesise and release TNF-α,
Evidence for Selective Respiratory Muscle Training in Chronic Heart Failure
There is evidence that indicates that the respiratory muscle weakness observed in CHF patients is reversible. Since respiratory muscle weakness inversely correlates with aerobic capacity amongst these patients, these interventions have the potential to improve aerobic and hence functional capacity. For example, treatment with the angiotensin converting enzyme (ACE) inhibitor, perindopril, has been shown to improve respiratory muscle strength amongst CHF patients, possibly by preserving
Conclusion and Future Directions
Patients with chronic heart failure exhibit significantly reduced respiratory muscle strength and endurance. These impairments are associated with numerous alterations in respiratory muscle structure and function, including a shift in muscle fibre phenotype, reduced oxidative capacity, and altered intracellular calcium regulation. There is now substantial evidence that selective respiratory muscle training in patients with CHF increases respiratory muscle strength and overall aerobic capacity.
Acknowledgments
No external financial support was received for this work.
References (48)
- et al.
Skeletal muscle function and its relation to exercise tolerance in chronic heart failure
Journal of the American College of Cardiology
(1997) - et al.
Evidence of reduced respiratory muscle endurance in patients with heart failure
Journal of the American College of Cardiology
(1994) - et al.
Dual influence of disease and increased load on diaphragm muscle in heart failure
Journal of Molecular and Cellular Cardiology
(2001) - et al.
Tumour necrosis factor is expressed in cardiac tissues of patients with heart failure
International Journal of Cardiology
(1996) - et al.
Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: a report from the studies of left ventricular dysfunction (SOLVD)
Journal of the American College of Cardiology
(1996) - et al.
Cytotoxic activity of tumor necrosis factor is mediated by early damage of mitochondrial functions. Evidence for the involvement of mitochondrial radical generation
Journal of Biological Chemistry
(1992) - et al.
Inspiratory muscle training improves blood flow to resting and exercising limbs in patients with chronic heart failure
Journal of the American College of Cardiology
(2008) - et al.
Chronic heart failure in Australian general practice. The Cardiac Awareness Survey and Evaluation (CASE) Study
The Medical Journal of Australia
(2001) - et al.
Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle
Circulation
(1984) - et al.
Regional blood flow in chronic heart failure: the reason for the lack of correlation between patients’ exercise tolerance and cardiac output?
British Heart Journal
(1992)