Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?
Version of Record online: 25 MAR 2010
© 2010 The Authors. Journal compilation © 2010 Scandinavian Physiological Society
Special Issue: HUMAN INTEGRATIVE PHYSIOLOGY-THE LEGACY OF THE COPENHAGEN SCHOOL: IN THE FOOTSTEPS OF LINDHARD AND KROGH
Volume 199, Issue 4, pages 393–406, August 2010
How to Cite
Calbet, J. A. L. and Joyner, M. J. (2010), Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?. Acta Physiologica, 199: 393–406. doi: 10.1111/j.1748-1716.2010.02125.x
- Issue online: 1 JUL 2010
- Version of Record online: 25 MAR 2010
- Received 5 June 2009, accepted 31 August 2009
- cardiac output;
- exercise hyperaemia;
In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [∼300 mL (100 g)−1 min−1], but the pumping capacity of the human heart is limited to 20–25 L min−1 in untrained subjects and ∼35 L min−1 in elite endurance athletes. This means that when more than 7–10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when ∼80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure.