Low frequency (LF, apprxeq 0.1 Hz) spontaneous oscillations of heart period in humans have been attributed to and correlated with the sympathetic efferent control of the heart. However, this interpretation is controversial, because sympathetic blockade does not suppress these oscillations, while parasympathetic blockade strongly affects them. The sympathetic origin of LF of arterial pressure, on the contrary, has been convincingly demonstrated. Four 10 min cycle-by-cycle time series of R-R interval (RR), and systolic (SAP) and diastolic (DAP) arterial pressure were produced by automatic analysis of data obtained with non-invasive methods in 10 healthy humans during supine rest and while standing, both before and after beta-1-selective blockade (atenolol). Time series were analysed by autoregressive transfer function analysis. beta-blockade failed to induce systematic changes on the power of the LF peak of RR, in any condition. The coherence between RR and SAP in the same region remained high (0.77 +- 0.03) and a constantly negative phase ( apprxeq 50-60 degree , corresponding to a delay of 1-2 heart beats of RR on SAP) was always seen. beta-blockade decreased the power of the LF peak of SAP, increased the transfer function gain between SAP and RR at LF, and the HF power of RR. We conclude that LF oscillations of RR are not directly generated by the sympathetic drive to the heart but reflect mainly the parasympathetic activity. The results suggest that the LF oscillations of the vagal outflow, and of RR, are generated by the baroreceptor reflex, driven by sympathetically-induced blood pressure LF waves.
Does low-frequency variability of heart period reflect a specific parasympathetic mechanism?
Grasso R.;Schena F.;Gulli G.;Cevese A.
1997-01-01
Abstract
Low frequency (LF, apprxeq 0.1 Hz) spontaneous oscillations of heart period in humans have been attributed to and correlated with the sympathetic efferent control of the heart. However, this interpretation is controversial, because sympathetic blockade does not suppress these oscillations, while parasympathetic blockade strongly affects them. The sympathetic origin of LF of arterial pressure, on the contrary, has been convincingly demonstrated. Four 10 min cycle-by-cycle time series of R-R interval (RR), and systolic (SAP) and diastolic (DAP) arterial pressure were produced by automatic analysis of data obtained with non-invasive methods in 10 healthy humans during supine rest and while standing, both before and after beta-1-selective blockade (atenolol). Time series were analysed by autoregressive transfer function analysis. beta-blockade failed to induce systematic changes on the power of the LF peak of RR, in any condition. The coherence between RR and SAP in the same region remained high (0.77 +- 0.03) and a constantly negative phase ( apprxeq 50-60 degree , corresponding to a delay of 1-2 heart beats of RR on SAP) was always seen. beta-blockade decreased the power of the LF peak of SAP, increased the transfer function gain between SAP and RR at LF, and the HF power of RR. We conclude that LF oscillations of RR are not directly generated by the sympathetic drive to the heart but reflect mainly the parasympathetic activity. The results suggest that the LF oscillations of the vagal outflow, and of RR, are generated by the baroreceptor reflex, driven by sympathetically-induced blood pressure LF waves.
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