In this review some of the issues and controversies involved in the neural control of the myocardial inotropic response to stress have been discussed. For example, it is surprising that either direct or reflex activation of the sympathetic nerves induces a relatively small increase (20-40%) in the left ventricular inotropic state when compared with the three-five-fold increase associated with maximal dynamic exercise. Studies contrasting the levels of circulating catecholamines with the left ventricular inotropic responses induced by hemorrhage, exercise and exogenously administered catecholamines, suggest that the catecholamine concentration at the synaptic cleft is the primary determinant of the left ventricular inotropic response. Although parasympathetic neural activation alone appears to have little direct influence on the left ventricular inotropic state and central nervous system integration of the autonomic nervous system usually insures there is a reciprocal relationship between sympathetic and parasympathetic neural activity, the potential for parasympathetic inhibition of the response to sympathetic or sympathomimetic augmentation of the intropic response exists. The importance of sympathetic-parasympathetic nervous system interaction in physiologic and pathologic conditions has yet to be defined. It is this type of knowledge of the interactions of reflex pathways which will be critical to the full understanding of autonomic reflex control of myocardial performance under physiologic and pathologic conditions.