In healthy individuals exercising heavily the ‘dogma’ has implicated a significant role of fatiguing respiratory muscle work in the sympathetically mediated vasoconstriction of exercising limb muscle vasculature (1). In the absence of actual respiratory muscle blood flow measurements, it was suggested that the reduction in limb blood flow with fatiguing respiratory muscle work was directed towards the respiratory muscles (2). Use of near-infrared spectroscopy over the left 7th intercostal space and the light-absorbing tracer indocyanine green dye injected intravenously, made it possible for the first time to quantify respiratory muscle blood flow at different levels of isocapnic hyperpnoea in humans (3). Subsequent studies were designed to test the ‘dogma’ of blood flow redistribution between the respiratory and locomotor muscles during exercise in healthy trained individulas and those with lung disease. In healthy trained individuals this was achieved by exacerbating exercise-induced diaphragmatic muscle fatigue via reductions in systemic oxygen delivery (hypoxia), whilst simultaneously assessing intercostal and quadriceps muscle blood flow during heavy, near-maximal exercise (4). Despite the greater degree of diaphragmatic fatigue in hypoxia compared to normoxia, blood flow to the intercostal and quadriceps muscles was not significantly different between the two conditions. Nonetheless, diaphragmatic muscle blood flow was not possible to be assessed in these experiments to verify potential blood flow redistribution between the diaphragm and the limb muscles. In patients with chronic obstructive pulmonary disease (COPD) studies were designed to reduce the work of breathing during exercise via supplementation of oxygen (causing an increase in systemic oxygen delivery through an increase in arterial oxygen content), or heliox (also increasing systemic oxygen delivery via an increase in cardiac output). In these experiments both respiratory and locomotor muscle blood flow and oxygen delivery were simultaneously assessed during exercise (5). None of the respiratory muscle unloading strategies (oxygen or heliox administration) was associated with a decrease in respiratory (intercostal and abdominal) muscle blood flow compared with exercise in room air, whilst both ergogenic strategies significantly increased quadriceps, and respiratory (both intercostal and abdominal) muscle oxygen delivery (5). Similarly to the experiments in trained athletes, diaphragmatic muscle blood flow was not assessed. Different approaches to unload the respiratory muscles via proportional assist ventilation strategies have been associated with improved leg muscle oxygenation in COPD (6) and chronic heart failure (CHF) patients (7). However, actual respiratory and/or leg muscle blood flow measurements were not available in these studies. In this presentation the case will be made that the available evidence is still inconclusive to support the hypothesis of blood flow redistribution between the respiratory and locomotor muscles as the basis for improved exercise capacity under conditions of respiratory muscle unloading in patients with COPD or CHF. Emphasis will be given to studies that reduce the work of breathing via pharmacological and non-pharmacological interventions in patients with COPD and CHF and the effect of these interventions on patients exercise tolerance and peripheral muscle oxygen availability.