Comparing spontaneous neurovascular and neurohemodynamic sympathetic transduction in response to hypoxia

Assessment of sympathetic transduction into its effects on the cardiovascular system is of great interest in human research. Analysis of sympathetic transduction has been divided into neurovascular and neurohemodynamic, highlighting the sympathetic effect on either regional vascular or systemic pressure responses. This study investigates whether indices of neurovascular transduction are reflected in parallel neurohemodynamic transduction during normoxia and hypoxia, with and without accounting for the confounds of prevailing tachypnea and tachycardia. In this retrospective study in 11 healthy individuals, we measured beat-by-beat blood pressure, multiunit sympathetic nerve activity (MSNA), and popliteal blood flow velocity with normoxia and isocapnic hypoxia (∼80% [Formula: see text]). Neurovascular transduction was indexed by leg vascular conductance and neurohemodynamic transduction by systemic pressure, derived from signal averaging either conductance or pressure over 10 cardiac cycles after a sympathetic burst. Responses were assessed from raw data and data corrected for ventilation and heart rate. Compared with transduction values during normoxia, sympathetic neurovascular transduction was increased (P = 0.001) and neurohemodynamic transduction was greater (P < 0.01) but delayed (P = 0.03) during hypoxia. When accounting for changes in respiration and cardiac interval, the two indices provided conflicting results-sympathetic neurovascular transduction was unaltered by hypoxia; on the contrary, neurohemodynamic transduction remained increased (P < 0.01), but there was no longer a delayed effect. Regardless, despite corrections for confounding effects of tachypnea and tachycardia, neither neurovascular nor neurohemodynamic transduction indices explained the integrated cardiovascular responses to hypoxia.NEW & NOTEWORTHY Spontaneous neurovascular and neurohemodynamic sympathetic transduction can provide conflicting insight into sympathetic effects on regional and systemic hemodynamics. We examined these transduction indices in response to acute hypoxia in healthy individuals, accounting for confounds of tachypnea and tachycardia. Neither transduction measure fully explained the integrated cardiovascular response. Surprisingly, we found a strong linear relation between neurohemodynamic transduction and low-frequency blood pressure variability, suggesting caution should be used when inferring sympathetic control from hemodynamic indices.