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Sympathovagal modulation in
athletes assessed by power spectrum analysis of heart rate variability
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Paolo Zeppilli, Carlo Picani,
Roberto Corsetti, Antonio Angelucci, Antonio Gianfelici, Carlo Pagliaricci, Roberto
Vannicelli, Vincenzo Palmieri, Cesare Santini, Luca Mainardi*, Sergio Cerutti*.
Cattedra e Centro Studi di Medicina dello Sport, Istituto di Medicina Interna e
Geriatria, Universita Cattolica del Sacro Cuore, Rome, *Dipartimento di Bioingegneria,
Politecnico, Milan, Italy
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Introduction
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The observation that regular training significantly
reduces the spontaneous frequency of sinoatrial discharge was first referred in the 1930s,
quite later than the Henschen's finding of cardiac enlargement in Swedish endurance skiers1. In the 1950s, studies dedicated to understand the
genesis of sinus bradycardia in the "athlete's heart" focused attention on the
prominent role of the cardiac autonomic nervous system.
In the last thirty years, the neural cardiovascular regulation was thought to take
place exclusively in the encephalic structures where conveyed all peripheral information
coursing in the afferent vagal and Hering's fibers. The evidence, at spinal level, of
cardiovascular sympathetic afferent and efferent fibers introduced the concept of a
neurovegetative reflex regulation, integrated through complex interactions involving
various supraspinal centres. Vagal and sympathetic efferent activity is the result of
inhibitory and excitatory feed-back mechanisms submitted to central integration,
continuously modulating the cardiovascular response to spontaneous blood pressure and
heart rate oscillations2. The aortic and carotid
baroreceptor unloading, stimulating via vagal afferents the midbrain cardioinhibitory
centre, elicites a parasympathetically mediated heart rate reduction with peri-pheral
vasodilation by sympathetic withdrawal (negative feed-back loop). The opposite response
occurs whenever a blood pressure drop induces norepinephrine release at the cardiovascular
sympathetic nervous endings (positive feed-back loop). The final "output" of
such a complex system can be simplified in a sympathovagal balance capable, with large
flexibility, to mitigate or to amplify the effects of different physiological or
pathological stimula on cardiovascular variables.
In the athletic population, especially engaged in endurance training, resting
bradycardia was thought to be the result of vagal dominance, perhaps in consequence of
increased sensibility of atrial cholinergic receptors3.
Raised concentrations of acetylcholine, observed in the myocardium of trained rats,
supported the assumption of a vagal drive enhancement4.
Other researchers attributed athlete's bradycardia exclusively to a decrease in cardiac
sympathetic discharge and/or to lower levels of plasma cathecolamines at rest and during
submaximal exercise5,6. Moreover, athlete's bradycardia
was attributed also to non-neural components, although the true mechanisms responsible and
their real contribute are yet debated7. Simultaneous
beta-adrenergic and parasympathetic blockade (with propranolol and atropine infusion) was
utilized to establish the intrinsic rhythmicity of the "pharmacologically
denervated" heart in healthy sedentary subjects suggesting that at rest vagal
modulation prevails on sympathetic activity, with a 2:1 ratio8.
With the same method, a 10-25 beats/minute decrease in intrinsic heart rate was observed
both in trained animals and sportsmen9,10.
A major contribute to understanding the role of autonomic nervous system in
determining cardiovascular adaptive responses to physical training was provided by
mathematical analysis of beat-to-beat heart rate signal spontaneous fluctuations. This new
ECG technique, termed heart rate variability (HRV), examines the intervals between
consecutive beats rather than the heart rate per se11.
Nowadays, it represents the most simple and unexpensive tool to investigate the relative
impact of the two cardiac autonomic components not only in different clinical and
experimental conditions but also in the evaluation of "athlete's heart".
In this paper, we summarize our experience about short-term HRV spectral analysis in
top level athletes practising different sports in order to demonstrate the usefulness of
such method in the monitoring of acute and chronic fatigue, also in relation to the
environment in which sports activity occurs. Moreover, we will report the possibility to
apply HRV analysis to the clinical evaluation of disabled athlete.
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Key Words
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Arrhythmias in athletes
heart rate varibility, sympatho-vagal balance modulation, power spectrum analysis,
endurance training, physiologic vagotonia induced by training, pathologic conditions, OA
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