Neural control of the circulation during exercise: insights from the 1970-1971 Oxford studies

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. Two mechanisms have been postulated to regulate this response. In one mechanism the changes in autonomic nerve activity to the heart and blood vessels are caused by signals arising in a central area of the brain and in the other mechanism the changes are caused by signals arising in the contracting skeletal muscle. In 1970-71 two studies were performed in Oxford which furthered our understanding of these two mechanisms. In one of these studies it was shown in cats that a reflex arising in the contracting skeletal muscle reflexly increased blood pressure and heart rate and that the thinly myelinated (Group III or A ) and the unmyelinated (Group IV or C) afferent nerve fibers were responsible. In the second of these studies 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. Tendon vibration of a skeletal muscle induces an involuntary reflex contraction. Utilizing this effect the central command needed to produce the same tension development was reduced or increased. When the same force was achieved with less central command the cardiovascular response was reduced and with more central command was increased. This demonstrated that descending motor commands from higher brain centers have an effect on the cardiovascular response to exercise.