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The role of vascular function on exercise capacity in health and disease
Author(s) -
Poole David C.,
Behnke Brad J.,
Musch Timothy I.
Publication year - 2020
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp278931
Subject(s) - oxygen transport , skeletal muscle , context (archaeology) , cardiology , medicine , exercise intolerance , microcirculation , vascular smooth muscle , vo2 max , blood flow , chemistry , endocrinology , blood pressure , oxygen , heart rate , heart failure , biology , paleontology , organic chemistry , smooth muscle
Three sentinel parameters of aerobic performance are the maximal oxygen uptake ( V ̇O 2 max ), critical power (CP) and speed of theV ̇ O 2kinetics 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. FastV ̇ O 2kinetics 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 elevatesV ̇ O 2 . Chronic disease and ageing create an O 2 delivery (i.e. blood flow × arterial [O 2 ],Q ̇ O 2 ) dependency that slowsV ̇ O 2kinetics, decreasing CP andV ̇O 2 max , 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 muscleQ ̇ O 2and thus defend microvascular O 2 partial pressures and capillary blood–myocyte O 2 diffusion across a ∼100‐fold range of muscleV ̇ O 2values. Recent discoveries, especially in the muscle microcirculation andQ ̇ O 2 ‐to‐ V ̇ O 2heterogeneity, are integrated with the O 2 transport pathway to appreciate how local and systemic vascular control helps defendV ̇ O 2kinetics and determine CP andV ̇O 2 maxin 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.