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Robin Hood for the lungs? A respiratory metaboreflex that 'steals' blood flow from locomotor muscles

Douglas R. Seals

In this issue of The Journal of Physiology, Dempsey and colleagues (Sheel et al. 2001) contribute another key chapter in their ongoing series of elegant investigations on novel interactions involving the respiratory muscles, autonomic nervous system and cardiovascular regulation in humans. Earlier, they demonstrated that manipulation of the work of breathing during maximal exercise resulted in marked changes in locomotor muscle blood flow, cardiac output and both whole-body and active limb oxygen uptake (Harms et al. 1997, 1998). They also established the remarkable metabolic costs of supporting respiratory muscle function during maximal exercise, requiring up to 16 % of the cardiac output (Harms et al. 1998). Importantly, the reduced locomotor muscle blood flow and vascular conductance in the elevated work of breathing condition was associated with augmented noradrenaline (norepinephrine) spillover from the active limbs, suggesting enhanced sympathetic vasoconstriction (Harms et al. 1997). These physiological effects of the work of breathing have important functional consequences, as demonstrated by an ~15 % improvement in endurance performance with respiratory muscle unloading (Harms et al. 2000).