Peripheral and central chemoreflexes are the dominant autonomic mechanisms regulating ventilatory patterns in response to changes in partial pressures of oxygen and carbon dioxide in arterial blood and exert powerful effects on neural circulatory control. Both reflex pathways are capable of eliciting increases in sympathetic nerve traffic and consequent increases in blood pressure. Chronic heart failure is accompanied by a sustained elevation in sympathetic nerve traffic, which is thought to be an important component in the pathophysiology and progression of the disease. The role of chemoreflex mechanisms in the control of sympathetic function during heart failure is an important topic for which there are many questions and few answers. This review summarizes available evidence documenting peripheral and central chemoreflex function in heart failure, possible mechanisms for their alteration, and their possible contribution to ventilatory, and circulatory abnormalities that occur in heart failure.