A Comparison between Active and Reactive Hyperemia Induced Brachial Artery Vasodilation

An increase in local brachial artery shear stress induces the relaxation of the smooth muscle which results in vasodilation of the artery. Shear stress can be elicited by both active and reactive hyperemic stimuli. The measurement of brachial artery vasodilation (BAV) in response to a hyperemic stimulus has been extensively used to assess changes in endothelial function. Whether or not similar changes occur in response to an active hyperemic stimulus is unknown. PURPOSE: To compare the BAV in response to an active versus reactive hyperemic stimulus following a known perturbation of endothelial function. METHODS: Eight healthy college students (5 men, 3 women), age 25.5±2.3 yrs, were assigned to four treatment conditions in a counter balanced design: 1) Low-fat meal with active hyperemic stimulus (LFM-A), 2) High-fat meal with active hyperemic stimulus (HFM-A), 3) Low-fat meal with reactive hyperemic stimulus (LFM-R), and 4) High-fat meal with reactive hyperemic stimulus (HFM-R). Meals were isocaloric (900 kcal) and ingested at 8:00 am of each treatment day. Brachial artery vasodilation was assessed via high resolution ultrasound. Active hyperemic stimulus was induced by 5 min of rhythmic (1 sec contraction: 1 sec relaxation) handgrip exercise at 10% maximal voluntary isometric contraction where as reactive hyperemic stimulus was induced by 5 min of forearm blood flow occlusion. Four hours after the ingestion of the meal, brachial artery diameters were measured at baseline and 60 sec following each 5-min condition. Brachial artery vasodilation was expressed as the percent change in diameter from baseline to post active/reactive hyperemia. Peak hyperemic velocities (cm-s1) were measured in all conditions. To test the difference in BAV and hyperemic velocity among conditions, a 2 × 2 repeated measures ANO VA (stimulus × intervention) was performed. RESULTS: A significant stimulus × intervention interaction (P=0.025) was found. Simple main effects revealed no difference (P=0.541) in BAV between LFM-A (5.75±1.64%) and HFM-A (6.39±1.45%); however, a significant decrease in BAV (P=0.014) was found in the HFM-R (4.29±1.64%) compared to the LFM-R (7.18±1.13%). Hyperemic velocities were similar within hyperemic stimulus (LFM-A=47.30±5.86 versus HFM-A=50.69±6.47 cm-s−1, P=0.624;LFM-R=88.77±7.91 versus HFM-R=79.58±5.20 cm-s4, P=0.986); however, velocities were lower (P=0.003) in active compared to reactive hyperemia. CONCLUSIONS: The measurement of BAV in response to an active hyperemic stimulus did not detect a change in endothelial function following a single perturbation meal whereas reactive hyperemia did.