During exercise, the cardiovascular response is rapidly and appropriately matched to the intensity of the physical activity. The autonomic nervous system plays an important role in achieving this closely matched circulatory response by an increase in the sympathetic nerve activity to the heart, blood vessels, and adrenal medulla and a decrease in the parasympathetic nerve activity to the heart. Early insights into the mechanisms that controlled these cardiovascular changes during exercise were reported in the 19th century. At that time, two mechanisms were hypothesized to be responsible for these changes. In one mechanism, a signal arising in a central area of the brain causes a parallel activation of skeletal muscle contraction and of autonomic nervous system changes (now termed, Central Command). In the other mechanism, a signal arising in the contracting skeletal muscle causes a reflex activation of the autonomic nervous system changes (now termed, Exercise Pressor Reflex). Some important investigators involved in early studies include Johan Johansson, August Krogh, Johannes Lindhard, and Horace Smirk. Also, Frances Buchanan and Louis Fridericia should be recognized for their contributions. Since those early insights, experiments in both animals and humans have confirmed these early hypotheses (Exp.Physiol. 97:10-69, 2012). In more recent years, the important involvement of a third mechanism, the Arterial Baroreflex, has been elucidated. Thus, all three of these mechanisms (Central Command, the Exercise Pressor Reflex, and the Arterial Baroreflex) contribute to the closely matched and coordinated response of the circulatory system to the intensity of the exercise being performed.