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Skeletal muscle vasodilatation during maximal exercise in health and disease


Calbet, Jose A L; Lundby, Carsten (2012). Skeletal muscle vasodilatation during maximal exercise in health and disease. Journal of Physiology, 590(24):6285-6296.

Abstract

Leg blood flow increases almost linearly with exercise intensity and reaches peak values at maximal exercise. This is achieved by the combination of a small increase in perfusion pressure combined with massive vasodilatation. The greatest levels of muscle perfusion have been reported in the quadriceps muscle during knee extension exercise (250-450 ml (100 g tissue)(-1) min(-1))). A singularity of this exercise model is that the amount of muscle activated (about 2.5-3 kg) is small and, therefore, the pumping capacity of the heart is not taxed maximally. 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 increases 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 critical for the maintenance of blood pressure in exercising patients with a limited heart pump capacity. In summary, maximal muscle vasodilatation in exercising humans depends on the active muscle mass, is likely restrained by sympathetic nervous system during whole body exercise, increases with training, whilst it is reduced with ageing and in diseases accompanied by increased sympathetic overactivity or reduced pumping capacity of the heart.

Abstract

Leg blood flow increases almost linearly with exercise intensity and reaches peak values at maximal exercise. This is achieved by the combination of a small increase in perfusion pressure combined with massive vasodilatation. The greatest levels of muscle perfusion have been reported in the quadriceps muscle during knee extension exercise (250-450 ml (100 g tissue)(-1) min(-1))). A singularity of this exercise model is that the amount of muscle activated (about 2.5-3 kg) is small and, therefore, the pumping capacity of the heart is not taxed maximally. 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 increases 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 critical for the maintenance of blood pressure in exercising patients with a limited heart pump capacity. In summary, maximal muscle vasodilatation in exercising humans depends on the active muscle mass, is likely restrained by sympathetic nervous system during whole body exercise, increases with training, whilst it is reduced with ageing and in diseases accompanied by increased sympathetic overactivity or reduced pumping capacity of the heart.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:14 Dec 2012 16:14
Last Modified:10 Aug 2017 08:32
Publisher:Wiley-Blackwell
ISSN:0022-3751
Additional Information:The definitive version is available at www.blackwell-synergy.com’ and www.jphysiol.org
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1113/jphysiol.2012.241190
PubMed ID:23027820

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