Physiological background of the loss of fractal heart rate dynamics

Altered fractal heart rate (HR) dynamics occur during various disease states, but the physiological background of abnormal fractal HR behavior is not well known. We tested the hypothesis that the fractal organization of human HR dynamics is determined by the balance between sympathetic and vagal outflow.

A short-term fractal scaling exponent (alpha1) of HR dynamics, analyzed by the detrended fluctuation analysis (DFA) method, and the high-frequency (HF) and low-frequency (LF) spectral components of R-R intervals (0.15 to 0.4 Hz; n=13), along with muscle sympathetic nervous activity (MSNA) from the peroneus nerve (n=11), were assessed at rest and during cold face and cold hand immersion in healthy subjects. During cold face immersion, HF power increased (from 6.9+/-1.3 to 7.6+/-1.2 ln ms2, P<0.01), as did MSNA (from 32+/-17 to 44+/-14 bursts/100 heartbeats, P<0.001), and LF/HF ratio decreased (P<0.01). Cold hand immersion resulted in a similar increase in MSNA (from 34+/-17 to 52+/-19 bursts/100 heartbeats, P<0.001) but a decrease in HF spectral power (from 7.0+/-1.3 to 6.5+/-1.1 ln ms2, P<0.05) and an increase in the LF/HF ratio (P<0.05). The fractal scaling index alpha1 decreased in all subjects (from 0.85+/-0.27 to 0.67+/-0.30, P<0.0001) during cold face immersion but increased during cold hand immersion (from 0.77+/-0.22 to 0.97+/-0.20, P<0.01).

The fractal organization of human HR dynamics is determined by a delicate interplay between sympathetic and vagal outflow, with the breakdown of fractal HR behavior toward more random dynamics occurring during coactivation of sympathetic and vagal outflow.