Back to the future: re-evaluation of the possible role for oxygen supplementation during exercise in chronic heart failure

Reduced exercise tolerance is the key symptom in chronic heart failure (CHF) leading to reductions in functional status and quality of life. The underlying mechanisms behind the muscle fatigue and dyspnoea which limit exercise capacity in heart failure are very complex, with multiple factors in the chain from the heart and lungs to the muscles contributing to the symptoms. In addition to altered cardiac function and haemodynamics as the central initiator of the heart failure syndrome, abnormalities have been identified in pulmonary function, ventilatory efficiency, peripheral vascular and in particular endothelial function, skeletal muscle structure and skeletal muscle metabolism. Over the last 20 years, the key role of the peripheral changes in skeletal muscle has been appreciated.1 Some of the changes which have been documented in the periphery and which may be important in causing reduced exercise tolerance include muscle wasting (especially in those with more advanced disease), a shift in muscle fibre type from type I fibres, which are relatively fatigue resistant, to type II fibres, and particularly type IIb fibres, which are less fatigue resistant and have reduced oxidative capacity. Ultrastructural myocyte changes have also been documented with reductions in the mitochondrial density and in oxidative enzymes. Reductions in oxygen delivery to working muscles have been identified in CHF with reduced capillary density seen in males with CHF. One of the key physiological parameters which is strongly linked to exercise capacity in almost all settings is peak oxygen consumption (peak VO2).2 This exercise-derived parameter quantifies the body's ability to take up oxygen, deliver it …