Breakdown of short-term fractal-like behaviour of HR indicates an increased
risk for adverse cardiovascular events and mortality, but the pathophysiol
ogical background for altered fractal HR dynamics is not known. Our aim was
to study the effects of pharmacological modulation of autonomic function o
n fractal correlation properties of heart rate (HR) variability in healthy
subjects. Short-term fractal scaling exponent (alpha (1)) along with spectr
al components of HR variability were analysed during the following pharmaco
logical interventions in healthy subjects: (i) noradrenaline (NE) infusion
(n=22), (ii) NE infusion after phentolamine (PHE) (n=8), (iii) combined NE
+ adrenaline (EPI) infusion (n=12), (iv) vagal blockade with high dose of a
tropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Th
en alpha (1) decreased progressively during the incremental doses of NE (fr
om 0.85 +/- 0.250 to 0.55 +/- 0.23, P <0.0001). NE also decreased the avera
ge HR (P <0.001) and increased the high frequency spectral power (P <0.001)
. Vagal blockade with atropine increased the alpha (1) value (from 0.82 +/-
0.22 to 1.24 +/- 0.41, P <0.05). Combined NE + EPI infusion and vagal acti
vation with a low dose atropine did not result in any changes in alpha (1),
and alpha -adrenergic blockade by PHE did not completely reverse the effec
ts of NE on alpha (1). Increased levels of circulating NE result in reducti
on of short-term correlation properties of HR dynamics. The results suggest
that coactivation of cardiac vagal outflow at the time of high levels of a
circulating sympathetic transmitter explains the breakdown of fractal-like
behaviour of human HR dynamics.