Abstract
Our review addresses the contributions of four sources of neural sensory feedback, namely, locomotor and respiratory muscle afferents, lung stretch receptors, and carotid chemoreceptors, to the cardiorespiratory responses to rhythmic exercise and to exercise limitation in health and disease. Experiments in healthy humans and animals that used a blockade or partial blockade of each feedback mechanism during physiological exercise demonstrated the obligatory nature of each of these sensory inputs to cardiorespiratory function, locomotor effort and muscle fatigue, and exercise performance. More recent research has revealed enhanced contributions of these feedback influences to exercise cardiorespiratory function in chronic heart failure, chronic obstructive pulmonary disease, and hypertension. Future research needs to address: 1) how these obligatory neural feedback mechanisms might interact with a raised respiratory CO(2) exchange in regulating the hyperpnea of exercise; and 2) the pathogenesis of feedback hypersensitivity in chronic diseases and the means and therapeutic benefits of its normalization.