Sleep Apnea Increases Sympathetic Activity Independent Of Decreased Neurovascular Transduction

Abstract

Introduction: Patients with obstructive sleep apnea (OSA) have elevated sympathetic outflow independent of obesity or hypertension. However, greater outflow may not result in reduced limb blood flow, suggesting lower sympathetic neurovascular transduction that may cause elevated outflow for appropriate hemodynamic control. Aims: We tested the hypothesis that greater resting sympathetic activity in OSA would relate to lesser sympathetic neurovascular transduction. Methods: We assessed resting sympathetic outflow and sympathetic neurovascular transduction in newly diagnosed OSA without comorbidities (N=10) and in age-matched (N=10) and young (N=10) healthy controls. Sympathetic activity was directly measured (microneurography) at rest and in response to sustained isometric handgrip exercise. Neurovascular transduction was derived from the relationship of sympathetic activity and blood pressure to leg blood flow during exercise. Results: Sympathetic activity in OSA was almost 2x the age-matched and 3x the younger controls. Neurovascular transduction was not different between OSA and age-matched controls, but was lower in both compared to younger controls. Among all subjects, resting activity was related to transduction (r 2 0.12, p=0.04), however this relation was much stronger without those with OSA (r 2 0.55, p Conclusions: Greater sympathetic activity in OSA does not appear to derive solely from lesser neurovascular transduction. Hence, other potential mechanisms associated with OSA per se likely result in greater sympathetic outflow. However, elevated outflow without lesser transduction may underlie the prevalent development of hypertension in this population.