Patients with heart failure with reduced ejection fraction (HFrEF) are characterised by increased sympathetic nerve traffic directed to skeletal muscle and exercise intolerance; both associate with increased mortality. Our studies with direct microneurographic recordings of muscle sympathetic nerve activity (MSNA) revealed a qualitative difference in MSNA response during mild exercise in HFrEF patients compared with age-matched healthy controls: an increase in MSNA in patients vs. a drop in healthy controls. The elevation in MSNA at rest and during exercise in HFrEF relates inversely to peak oxygen uptake, supporting a neurogenic limit to exercise. The augmented exercise-induced sympathetic response is due partially to greater muscle metaboreflex activation and is exaggerated in those with low exercise capacity. When patients undergo 6 months of exercise training, MSNA burst frequency is lowered, peak oxygen uptake is improved and the autonomic benefit is particularly effective in those who can train at higher intensity. This sympathoinhibitory effect of training partially reflects a blunted muscle metaboreflex but little is known about the contributions of other reflexes. This invited talk will examine what is known about the abnormal reflex rise in sympathetic activity during exercise in HFrEF patients and the relative contributions of excitatory and inhibitory reflexes which may be modifiable by exercise training.