Rapid-onset vasodilator responses to exercise in humans: Effect of increased baseline blood flow

Abstract

New findings: What is the central question of this study? What is the effect of an elevated baseline blood flow, induced by high-dose intra-arterial infusion of either adenosine or ATP, on the rapid-onset vasodilatory response to a single forearm muscle contraction? What is the main finding and its importance? The peak response to a single contraction is unaffected by augmented baseline blood flow, and thus, is likely to be attributable to a feedforward vasodilatory mechanism.

Abstract: The hyperaemic responses to single muscle contractions are proportional to exercise intensity, which, in turn, is proportional to tissue metabolic demand. Hence, we tested the hypothesis that the rapid-onset vasodilatory response after a single muscle contraction would be unaffected when baseline blood flow was increased via high-dose intra-arterial infusion of either adenosine (ADO) or ATP. Twenty-four healthy young participants (28 ± 1 years) performed a single forearm contraction (20% maximal voluntary contraction) 75 min after commencement of a continuous infusion of ADO (n = 6), ATP (n = 8) or saline (control; n = 10). Brachial artery diameter and blood velocity were measured using Doppler ultrasound. Resting forearm vascular conductance (FVC; in millilitres per minute per 100 mmHg per decilitre of forearm volume) was significantly higher during ADO (33 ± 17) and ATP infusion (33 ± 17) compared with the control infusion (8 ± 3; P < 0.05). The peak FVCs post-contraction during ADO and ATP infusions were significantly greater than during the control infusion (P < 0.05), but not different from one another. The peak change in FVC from baseline was similar in all three conditions (control, 14 ± 1; ADO, 24 ± 2; and ATP, 23 ± 6; P = 0.15). Total FVC (area under the curve) did not differ significantly between ADO and ATP (333 ± 69 and 440 ± 125); however, total FVC during ATP infusion was significantly greater compared with the control value (150 ± 19; P < 0.05). We conclude that the peak response to a single contraction is unaffected by augmented baseline blood flow and is therefore likely to be attributable to a feedforward vasodilatory mechanism.

Keywords: adenosine; exercise hyperaemia; vascular conductance.

Figure 1.

Overview of the experimental timeline. After 74 minutes of continuous intra-arterial infusion of either saline, adenosine (ADO), or adenosine triphosphate (ATP), participants performed a single forearm muscle contraction at 20% of their maximal voluntary contraction (MVC). Continuous measurements were taking for a minute following the contraction. Artery diameter measurements are indicated by the upside-down closed triangles.

Figure 2.

Change in FVC before and after rapid single muscle contraction did not differ between groups. Delta was calculated as peak FVC post contraction - baseline FVC, for each respective condition. Each participants is represented by an individual circle. Bar values are the mean of each group. p=0.147.

Figure 3.

Total Adjusted FVC (AUC) over 30 cardiac cycles following a single forearm contraction at 20% maximal voluntary contraction was greater with ATP compared to control, but not ADO. Each participants is represented by an individual circle. Bar values are the mean of each group*p<0.05 ATP vs. control.

Figure 4.

Vasodilator [change (Δ) in forearm vascular conductance (FVC)] responses over 30 cardiac cycles following a single forearm contraction at 20% maximal voluntary contraction (MVC). Values are mean ± SD. Some error bars are not visible because they are smaller than the representative symbol. *p<0.05 vs. control. †p<0.05 vs. ADO.