Vascular hyperpolarization contributes to onset and steady‐state exercise hyperemia in humans

Abstract

We tested the hypothesis that vascular hyperpolarization contributes to both the onset and steady‐state hyperemic response to exercise. In Protocol 1 (n=11), forearm blood flow (FBF; Doppler ultrasound) was measured during rhythmic handgrip exercise at 10% maximal voluntary contraction for 5 minutes under control (intra‐arterial saline; T1) conditions, after combined inhibition of Na+/K+ATPase and KIR channels [via ouabain and barium chloride (BaCl2), respectively; T2] alone and in the presence of combined nitric oxide synthase (L‐NMMA) and cyclooxygenase inhibition (ketorolac; T3). Drugs were not infused during exercise due to potential influences on basal vascular tone. The total hyperemic responses were significantly (P<0.05) attenuated from control at 30 seconds (50 ± 4 and 65 ± 2%), 1 minute (34 ± 4 and 41 ± 3%), and 2 minutes (20 ± 4 and 23 ± 4%; T2 and T3 respectively) of exercise. FBF was not different in the last 2 minutes of exercise. In Protocol 2 (n=6), all study drugs were infused prior to and during exercise to assess the impact on steady‐state hyperemia. Steady‐state FBF was significantly reduced during T2 vs T1 (123 ± 18 vs 156 ± 21 ml/min; −21 ± 4%), and further reduced during T3 (108 ± 17 ml/min; −32 ± 3%). Our data indicate vascular hyperpolarization as a novel contributing vasodilatory pathway in the complex blood flow response to exercise at the onset and during steady‐state hyperemia.Supported by HL102720