Alberto Malliani, Stefano
Guzzetti.
Centro Ricerche Cardiovascolari, CNR, L.I.T.A. di Vialba, Medicina Interna II,
Ospedale "L. Sacco", Universita degli Studi, Milan, Italy
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In physiological conditions, heart rate variability
(HRV) is the result of sinus node pacemaker rhythmicity and, mainly, of sympathetic and
vagal activities.
These two neural outflows are tonically and phasically modulated by the interaction,
in closed loop conditions, of at least three major factors: the central integration,
peripheral inhibitory reflex mechanisms (with negative feedback characteristics), and
peripheral excitatory reflex mechanisms (with positive feedback characteristics)1. One of the fundamental keys to understand the broad
dynamics of heart rate neural regulation is the concept of sympatho-vagal balance, which
corresponds to the observation that, in most physiological conditions, the activation of
either outflow is accompanied by the inhibition of the other2,3.
It is well known that reciprocal responses in cardiac vagal and sympathetic neurons are
reflexly elicited from the sinoaortic baroreceptors. Stimulation of these receptors
(mediating negative feedback reflexes) excites cardiac vagal neurons and inhibits cardiac
sympathetic neurons. This reciprocal relationship was also evident in experimental
conditions in which the reflex effects of sympathetic or vagal afferent stimulation were
tested on the discharge of single sympathetic or vagal efferent fibers isolated from the
same cardiac nerve impinging on the heart: in these experimental conditions the
stimulation of, e.g., afferent sympathetic fibers excited the sympathetic efferent and
inhibited the vagal efferent discharge (and viceversa for the stimulation of afferent
vagal fibers)2. Thus, in contradistinction to
sinoaortic reflexes, the afferent cardiac sympathetic pathway (mediating positive feedback
reflexes) reflexly inhibited cardiac vagal fibers and excited cardiac sympathetic fibers.
Although this reciprocity cannot be, at the moment, quantified and is likely to be
non-linear and composite of numerous sub-systems, it surely reflects a well-determined
biological strategy, more aimed at subserving complex synergistic patterns (including
excitation or inhibition of cardiac performance) rather than single reflexes.
One of the main achievements during the last years has been to progressively
demonstrate the hypothesis that this reciprocal interaction can be broadly explored in the
frequency domain of heart rate variability (HRV)1. In
fact, a conclusive evidence supports these general principles:
The respiratory rhythm of HRV, defined as high-frequency (HF) spectral component, is a
marker of vagal modulation1,4.
The rhythm corresponding to vasomotor waves and present in both heart rate and
arterial pressure variabilities, defined as low-frequency (LF) component is a marker of
sympathetic modulation1,5.
A reciprocal relation exists between these two rhythms which is similar to that
characterizing the sympatho-vagal balance1,5.
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Autonomic nervous system evaluation
heart rate variability, markers of vagal/sympathetic modulation, high-frequency spectral
component, low-frequency spectral component, sympatho-vagal balance, neural code, R
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