Contribution of Arteriolar Distension to Rapid Onset Vasodilation Following a Single Contraction

Abstract

Oxygen consumption of the skeletal muscle increases at the onset of exercise. This increase in oxygen consumption requires an increase in oxygen delivery to match the demand in order to sustain exercise. Increased in oxygen delivery is predominantly achieved through increased vascular conductance to the exercising muscle. The rapid onset vasodilation response at the onset of exercise is traditionally thought to be achieved solely through mechanisms that act to reduce arteriolar smooth muscle tone. Contracting smooth muscle exerts an inward force, with blood pressure exerting an outward acting force, so when the vascular smooth muscle relaxes, it exerts less force, resulting in vasodilation. The elastic structure of arterioles also exerts an inward acting elastic recoil force. However, due to its elastic properties, resistance vessel walls are distensible with an increase in arteriolar transmural pressure. Distension could further contribute to an increase in conductance for blood flow when transmural pressure is increased (distension-mediated vasodilation). Whether distension-mediated vasodilation is increased when there is more active vasodilation (reduced inward acting force) is unknown. The purpose of the current study was to test the hypothesis that distension mediated vasodilation is increased with increased active vasodilation magnitude. We tested this hypothesis by increasing forearm blood flow (FBF) via a lower (LO, 20% maximal voluntary contraction, MVC) or higher (HI, 80%MVC) magnitude of immediate active vasodilation in humans (n=21) with a single handgrip contraction. This was done with the arm in an above-heart position, and also when the arm was moved from an above-heart to below-heart position during a single contraction where gravity increased transmural pressure in the arterioles. The increase in forearm vascular conductance (FVC) that was attributed to distensibility was calculated by subtracting the FVC response in the above-heart position from the FVC response in the below-heart position. When transmural pressure was increased in the below-heart position, FBF and FVC was increased in both LO and HI conditions. However, the increase in FVC attributed to distension (FVCD) was not different between LO and HI conditions. These results demonstrate that FVCD is not affected by active vasodilation magnitudes created in this study.