Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/50933
Título: Skeletal muscle vasodilatation during maximal exercise in health and disease
Autores/as: Calbet, Jose A.L. 
Lundby, Carsten
Clasificación UNESCO: 241106 Fisiología del ejercicio
Palabras clave: Leg Blood-Flow
Chronic Heart-Failure
Rapid Onset Vasodilatation
Cardiac-Output
Oxygen-Uptake, et al.
Fecha de publicación: 2012
Editor/a: 0022-3751
Publicación seriada: Journal of Physiology 
Resumen: Maximal exercise vasodilatation results from the balance between vasoconstricting and vasodilating signals combined with the vascular reactivity to these signals. During maximal exercise with a small muscle mass the skeletal muscle vascular bed is fully vasodilated. During maximal whole body exercise, however, vasodilatation is restrained by the sympathetic system. This is necessary to avoid hypotension since the maximal vascular conductance of the musculature exceeds the maximal pumping capacity of the heart. Endurance training and high‐intensity intermittent knee extension training increase the capacity for maximal exercise vasodilatation by 20–30%, mainly due to an enhanced vasodilatory capacity, as maximal exercise perfusion pressure changes little with training. The increase in maximal exercise vascular conductance is to a large extent explained by skeletal muscle hypertrophy and vascular remodelling. The vasodilatory capacity during maximal exercise is reduced or blunted with ageing, as well as in chronic heart failure patients and chronically hypoxic humans; reduced vasodilatory responsiveness and increased sympathetic activity (and probably, altered sympatholysis) are potential mechanisms accounting for this effect. Pharmacological counteraction of the sympathetic restraint may result in lower perfusion pressure and reduced oxygen extraction by the exercising muscles. However, at the same time fast inhibition of the chemoreflex in maximally exercising humans may result in increased vasodilatation, further confirming a restraining role of the sympathetic nervous system on exercise‐induced vasodilatation. This is likely to be critical for the maintenance of blood pressure in exercising patients with a limited heart pump capacity.
URI: http://hdl.handle.net/10553/50933
ISSN: 0022-3751
DOI: 10.1113/jphysiol.2012.241190
Fuente: Journal of Physiology[ISSN 0022-3751],v. 590, p. 6285-6296
Colección:Reseña
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