During exercise, blood is redistributed to meet the metabolic demands of the working skeletal muscle and to regulate core temperature and systemic haemodynamics, primarily mean arterial pressure. The redistribution of blood is the result of an integrated response involving the complex interplay between systemic sympathetic vasoconstrictor outflow and vasoactive signals released locally from the muscle, endothelium and red blood cells. Despite sympathetic vasoconstrictor activity being directed to many vascular beds, including the contracting skeletal muscle, blood vessels within skeletal muscle are able to oppose this sympathetic vasoconstriction, a response termed functional sympatholysis. While this mechanism is not fully understood, indications are that functional sympatholysis is effectuated downstream of α‐adrenoceptors, in the active skeletal muscle. Since the emergence of the concept of functional sympatholysis in 1962 (Remensnyder et al. ), researchers across the world have been puzzled by which mechanism/substance is responsible for the localised attenuation of adrenergic vasoconstriction, with ATP recently suggested as a potential candidate. Interestingly, ATP expresses some of the same characteristics as muscle activity when it comes to attenuating adrenergic vasoconstriction, but the underlying mechanisms have been difficult to elucidate.The study by Hearon et al. in The Journal of Physiology is the most recent in a series of
The Journal of Physiology – Wiley
Published: Jan 15, 2018
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