Abstract
Three sentinel parameters of aerobic performance are the maximal oxygen uptake ( V̇O2max ), critical power (CP) and speed of the V̇O2 kinetics following exercise onset. Of these, the latter is, perhaps, the cardinal test of integrated function along the O(2) transport pathway from lungs to skeletal muscle mitochondria. Fast V̇O2 kinetics demands that the cardiovascular system distributes exercise-induced blood flow elevations among and within those vascular beds subserving the contracting muscle(s). Ideally, this process must occur at least as rapidly as mitochondrial metabolism elevates V̇O2 . Chronic disease and ageing create an O(2) delivery (i.e. blood flow × arterial [O(2) ], Q̇O2 ) dependency that slows V̇O2 kinetics, decreasing CP and V̇O2max , increasing the O(2) deficit and sowing the seeds of exercise intolerance. Exercise training, in contrast, does the opposite. Within the context of these three parameters (see Graphical Abstract), this brief review examines the training-induced plasticity of key elements in the O(2) transport pathway. It asks how structural and functional vascular adaptations accelerate and redistribute muscle Q̇O2 and thus defend microvascular O(2) partial pressures and capillary blood-myocyte O(2) diffusion across a ∼100-fold range of muscle V̇O2 values. Recent discoveries, especially in the muscle microcirculation and Q̇O2 -to- V̇O2 heterogeneity, are integrated with the O(2) transport pathway to appreciate how local and systemic vascular control helps defend V̇O2 kinetics and determine CP and V̇O2max in health and how vascular dysfunction in disease predicates exercise intolerance. Finally, the latest evidence that nitrate supplementation improves vascular and therefore aerobic function in health and disease is presented.