During exercise the magnitude of the cardiovascular response is closely matched to the intensity of the exercise. In achieving this appropriate matching, an important role is played by the autonomic nervous system. Over 100 years ago Johansson (Scand. Arch. Physiol., 5:20-66, 1895) postulated that there were two possible mechanisms which regulated this response. In one mechanism the changes in autonomic nerve activity to the heart and circulation are caused by signals arising in a central area of the brain and in the other mechanism the changes in autonomic nerve activity are caused by signals arising in the contracting skeletal muscle. Studies by Krogh and Lindhard (Journal of Physiology, 47:112-136, 1913) supported the central mechanism concept which they first termed “Cortical Irradiation”. Later studies by Alam and Smirk (Journal of Physiology, 89:372-383, 1937) supported the response originating in muscle which they termed the “Blood Pressure Raising Reflex”. In 1971 two studies were performed in Oxford which furthered our understanding of these two mechanisms. In one of these studies performed by McCloskey and Mitchell, (Journal of Physiology, 224: 173-186, 1972) it was shown in cats that a reflex arising in the contracting skeletal muscle reflexly increased blood pressure and heart rate. This finding confirmed a study by Coote, Hilton and Perez-Gonzalez (Journal of Physiology, 215: 789-804, 1971) and further defined, by using anodal and anesthetic blocking techniques, that thinly myelinated (Group III or Aδ) and the unmyelinated (Group IV or C) afferent nerve fibers were responsible for the reflex changes in blood pressure and heart rate. This mechanism is now commonly called the “Exercise Pressor Reflex”. In the second of these studies performed by Goodwin, McCloskey and Mitchell (Journal of Physiology, 226: 173-190, 1972) it was shown in humans that a central mechanism could also increase the blood pressure and heart rate during static contraction at a fixed force. In this study high frequency vibration of a tendon was used to activate the primary afferents of the muscle spindles (Ia). If these afferents are activated in a contracting muscle, they reflexly increase the motor activity of the muscle, so less central command is required to maintain the same force. However, if the (Ia) afferents are activated in the antagonist muscle, they cause a reflex inhibition of the contracting muscle, so that a greater central command is required. When the same force was achieved with less central command, the elevation in blood pressure and heart rate was decreased, and when the same force was achieved with more central command, the elevation in blood pressure and heart rate was increased. From these findings it was concluded that descending motor commands from higher brain centers had an effect on the cardiovascular control centers during exercise and this was termed “Central Command”. During the last 40 years a much greater understanding of the neural control of the circulation during exercise has been achieved. In addition to a more detailed knowledge of the mechanisms involved in central command and the exercise pressor reflex, it has been shown that the arterial baroreceptors also play a role in determining the autonomic nervous system activity to the heart and circulation during exercise. All three of these neural mechanisms play a role in regulating the precise response of the cardiovascular system to the intensity of exercise.