4.6 Review

The role of vascular function on exercise capacity in health and disease

Journal

JOURNAL OF PHYSIOLOGY-LONDON
Volume 599, Issue 3, Pages 889-910

Publisher

WILEY
DOI: 10.1113/JP278931

Keywords

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Funding

  1. NHLBI [HL50306, HL108328, HL137156, HL142877, 4350011]

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Three essential parameters of aerobic performance are maximal oxygen uptake, critical power, and speed of oxygen uptake kinetics following exercise onset. Vascular adaptations play a crucial role in accelerating and redistributing oxygen supply to muscles, improving aerobic function.
Three sentinel parameters of aerobic performance are the maximal oxygen uptake ((V) over dot(2max)), critical power (CP) and speed of the (V) over dot(2max) 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. (V) over dot(2max) 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 (V) over dot(2max). Chronic disease and ageing create an O-2 delivery (i.e. blood flow x arterial [O-2], (Q)over dot(2max)) dependency that slows (V) over dot(2max) kinetics, decreasing CP and (V) over dot(2max), 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 (seeGraphical 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. (Q) over dot(O2) and thus defend microvascular O-2 partial pressures and capillary blood-myocyte O-2 diffusion across a similar to 100-fold range of muscle. (V) over dot(O2) values. Recent discoveries, especially in the muscle microcirculation and. (Q) over dot(O2)-to-(V) over dot(O2) heterogeneity, are integrated with the O-2 transport pathway to appreciate how local and systemic vascular control helps defend. (V) over dot(O2) kinetics and determine CP and. (V) over dot(O2max) 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.

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