LAUSR

Exercise intolerance is one of the cardinal symptoms experienced by patients with heart failure (HF); however, the precise pathophysiology has not been fully elucidated.1 Traditionally, it was thought that cardiac dysfunction was the major determinant of exercise capacity, particularly as peak oxygen consumption is strongly correlated with cardiac output. However, the demonstration of persistent exercise limitation in HF patients following heart transplantation or left ventricular assist device implantation points the contribution of other, non-cardiac, mechanisms.2 As such, we now know that maladaptive responses in the peripheral and pulmonary vasculature, respiratory system, skeletal muscles and autonomic nervous system triggered in the setting of HF are key factors.3 Exercise training can target both the peripheral and cardiac disturbances in HF and hence is an attractive treatment option.4 Preclinical and clinical data have shown exercise to: (i) improve vascular function, by improving endothelial function, decreasing peripheral vasoconstriction, neoangiogenesis, and improving myocardial blood flow; (ii) favourably alter sympathovagal balance together with a reduction in angiotensin II and aldosterone levels; (iii) reverse adverse changes in skeletal muscle morphology, histochemistry and metabolic function as well as restore muscle ergoreflexes; and (iv) improve cardiac function (normalizing myocyte calcium handling, increasing myocyte contractility and left ventricular ejection fraction, reducing end-diastolic volumes).5 These studies promoted a series of randomised controlled trials evaluating the role of exercise training in HF. In this issue of the Journal, Taylor and colleagues performed a meta-analysis upon individual data from 3912 patients with HF and reduced ejection fraction from 18 randomised controlled trials.6 Compared to control (standard care), exercise cardiac rehabilitation (involving both exercise training and HF-related disease management counselling) had no effect on all-cause mortality or hospitalisation and had no effect on HF-specific mortality or HF