Review
Respiratory Muscle Dysfunction and Training in Chronic Heart Failure

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A characteristic feature of chronic heart failure (CHF) is reduced exercise tolerance. Several factors contributing to this have been identified, including alterations in central haemodynamics, skeletal muscle oxygen utilisation and respiratory muscle dysfunction. This review focuses on abnormalities identified in respiratory muscle structure and function in CHF and recent evidence for the benefit of selective inspiratory muscle training in CHF. Included in this review are findings from original investigations, with a specific focus on recent published data.

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.

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