Abstract

BackgroundIt has been proposed that adenosine triphosphate (ATP) released from red blood cells (RBCs) may contribute to the tight coupling between blood flow and oxygen demand in contracting skeletal muscle. To determine whether ATP may contribute to the vasodilatory response to exercise in the forearm, we measured arterialised and venous plasma ATP concentration and venous oxygen content in 10 healthy young males at rest, and at 30 and 180 seconds during dynamic handgrip exercise at 45% of maximum voluntary contraction (MVC).ResultsVenous plasma ATP concentration was elevated above rest after 30 seconds of exercise (P < 0.05), and remained at this higher level 180 seconds into exercise (P < 0.05 versus rest). The increase in ATP was mirrored by a decrease in venous oxygen content. While there was no significant relationship between ATP concentration and venous oxygen content at 30 seconds of exercise, they were moderately and inversely correlated at 180 seconds of exercise (r = -0.651, P = 0.021). Arterial ATP concentration remained unchanged throughout exercise, resulting in an increase in the venous-arterial ATP difference.ConclusionsCollectively these results indicate that ATP in the plasma originated from the muscle microcirculation, and are consistent with the notion that deoxygenation of the blood perfusing the muscle acts as a stimulus for ATP release. That ATP concentration was elevated just 30 seconds after the onset of exercise also suggests that ATP may be a contributing factor to the blood flow response in the transition from rest to steady state exercise.

Highlights

  • It has been proposed that adenosine triphosphate (ATP) released from red blood cells (RBCs) may contribute to the tight coupling between blood flow and oxygen demand in contracting skeletal muscle

  • The RBC releases adenosine triphosphate (ATP) in proportion to the number of unoccupied binding sites on the haemoglobin molecule in response to both low oxygen and mechanical deformation, which are characteristic of the microvasculature in vivo

  • Arterialised ATP concentration was 0.79 ± 0.30 at rest, and remained unchanged with exercise (P > 0.05). These responses resulted in a tendency for a larger venous-arterialised ATP difference during exercise compared with rest, this did not reach significance (P = 0.076)

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Summary

Introduction

It has been proposed that adenosine triphosphate (ATP) released from red blood cells (RBCs) may contribute to the tight coupling between blood flow and oxygen demand in contracting skeletal muscle. One mechanism that has strong logical appeal proposes a role for the red blood cell (RBC) in the regulation of vascular tone [1]. According to this hypothesis, the RBC releases adenosine triphosphate (ATP) in proportion to the number of unoccupied binding sites on the haemoglobin molecule in response to both low oxygen and mechanical deformation, which are characteristic of the microvasculature in vivo. BMC Physiology 2009, 9:24 http://www.biomedcentral.com/1472-6793/9/24 and effects a conducted vasodilation via an endotheliumdependent mechanism [2] It has been shown using an isolated cell model that RBCs release ATP upon exposure to hypoxia [3] and mechanical deformation [4,5]. Despite some evidence to the contrary [8], findings in intact mammals during exercise tend to support a role for RBC-released ATP in the regulation of vascular tone [9,10,11]

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