Adaptations in control of blood flow with training: splanchnic and renal blood flowsMcALLISTER, RICHARD M. Section Editor(s): Ray, Chester A. ChairMedicine & Science in Sports & Exercise: March 1998 - Volume 30 - Issue 3 - pp 375-381 Basic Sciences: Symposium: Adaptations and the control of blood flow with training Abstract Author Information Acute exercise is associated with large increases in cardiac and active skeletal muscle blood flows and reduced blood flows to inactive muscle, skin, kidneys, and organs served by the splanchnic circulation. Splanchnic and renal blood flows are reduced in proportion to relative exercise intensity. Increased sympathetic nervous system outflow to splanchnic and renal vasculature appears to be the primary mediator of reduced blood flows in these circulations, but the vasoconstrictors angiotensin II and vasopressin also make important contributions. Human and animal studies have shown that splanchnic and renal blood flows are reduced less from resting levels during acute exercise after a period of endurance exercise training. Investigations of mechanisms involved in these adaptations suggest that reductions in sympathetic nervous system outflow, and plasma angiotensin II and vasopressin concentrations, are involved in lesser splanchnic and renal vasoconstriction exhibited by trained individuals. In addition, a reduced response to the sympathetic neurotransmitter norepinephrine in renal vasculature may contribute to greater blood flow to the kidney during acute exercise after training. Greater splanchnic and renal blood flows during acute exercise following training are potentially beneficial in that disturbance from homeostasis would be less in the trained state. Additionally, increased splanchnic blood flow in the trained state may confer benefits for glucose metabolism during prolonged exercise. Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 Submitted for publication June 1997. Accepted for publication October 1997. © Williams & Wilkins 1998. All Rights Reserved.