Contribution of vascular hyperpolarization to augmented skeletal muscle hyperemia during hypoxic exercise in humans (1079.20)

Abstract

Exercise hyperemia during hypoxia is augmented relative to normoxia. At moderate exercise intensities, nitric oxide (NO) and vasodilating prostaglandins (PGs) explain ~50% of this response, yet the remaining signaling mechanisms remain unclear. We hypothesized that vascular hyperpolarization via activation of inwardly rectifying potassium (KIR) channels and Na+/K+‐ATPase accounts for the remaining ~50% of the augmented hyperemia. In 10 young adults, we measured forearm blood flow (FBF; Doppler ultrasound) during 5 min of rhythmic handgrip exercise at 20% maximal voluntary contraction in normoxia (NormEx) and isocapnic hypoxia (HypEx; O2 saturation 80%) before and after local combined inhibition of NO synthase (L‐NMMA), cyclooxygenase (ketorolac), KIR channels (barium chloride) and Na+/K+‐ATPase (ouabain). All trials were performed during local α‐ and β‐adrenoceptor blockade to isolate local vasodilation. In control conditions, FBF during HypEx was augmented vs. NormEx by 62±8 ml/min (P<0.05). In the blocked condition, this compensatory increase in FBF was only 29±6 ml/min (47±10% decrease), but O2 extraction was increased to maintain forearm VO2. These findings are similar to our previous observations with combined inhibition of NO and PGs alone, suggesting that vascular hyperpolarization via these pathways does not contribute to the augmented hyperemic response during hypoxic exercise.Grant Funding Source: Supported by NIH award HL‐095573 (FAD)