Scale exponents of blood pressure and heart rate during autonomic blockade as assessed by detrended fluctuation analysis

Non-technical summary It is still unknown how the autonomic nervous system influences the fractal dynamics of cardiovascular signals. We show that in supine volunteers vagal and sympathetic outflows contribute differently to the fractal structures of heart rate and blood pressure. The vagal outflow contributes with a 'white-noise' component to the heart rate dynamics, indirectly influencing also the fractal dynamics of blood pressure. The sympathetic outflow contributes with a Brownian motion component to the heart rate dynamics, increasing long-term fractal coefficients, without affecting long-term coefficients of blood pressure. Results are explained by the different distribution and dynamics of acetylcholine receptors and of alpha- and beta-adrenergic receptors. Our findings may allow better delineating alterations of cardiovascular fractal dynamics in physiological and pathophysiological settings.How the autonomic nervous system influences the fractal dynamics of heart rate (HR) and blood pressure (BP) remains unclear. The purpose of our study was to separately assess cardiac vagal and sympathetic (cardiac vs. vascular) influences on fractal properties of HR and BP as described by scale exponents of detrended fluctuation analysis (DFA). R-R intervals, systolic and diastolic BP were measured in nine supine volunteers before and after administration of autonomic blocking agents (atropine, propranolol, atropine + propranolol, clonidine). Spectra of DFA scale exponents, alpha(t), were calculated for scales between 5 and 100 s. HR and BP scale structures differed at baseline, being alpha(t) of HR < 1, with a minimum between 10 and 20 s followed by a higher plateau between 40 to 80 s, while alpha(t) of BP decreased with t from values > 1. Comparison of atropine and propranolol with baseline and combined cardiac parasympathetic and sympathetic blockade (atropine + propranolol) indicated opposite influences of vagal and cardiac sympathetic outflows on HR exponents. The vagal outflow adds white-noise components, amplifying differences with BP exponents; the cardiac sympathetic outflow adds Brownian motion components at short scales and contributes to the plateau between 40 and 80 s. Overall sympathetic inhibition by clonidine decreased short- and long-term exponents of HR, and short-term exponents of BP, so that their alpha(t) spectra had different means but similar profiles. Therefore, cardiac vagal, cardiac sympathetic and vascular sympathetic outflows contribute differently to HR and BP fractal structures. Results are explained by different distribution and dynamics of acetylcholine receptors and of alpha- and beta-adrenergic receptors between heart and vasculature.