14th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 2000

Jan. 29 - Feb. 5, 2000
Marilleva, Trento, Italy

RT-71

Physiological and non physiological vagotonia in athletes and sportsmen: an old problem revisited

Paolo Zeppilli, Francesco Scarcella, Serena Bria, Antonio Gianfelici, Massimiliano Bianco, Vincenzo Palmieri.
Centro Studi di Medicina dello Sport, Istituto di Medicina Interna e Geriatria, Universita Cattolica, Roma, Italy

Physiological vagotonia

Physiological bradycardia in healthy athletes is the result of a relative increase in vagal tone due to a decrease in cardiac sympathetic discharge. This condition, called “physiological vagotonia”, is characterized by excellent exercise capacity, particularly aerobic power, absence of symptoms and a quite benign prognosis. Bradycardia more or less rapidly disappear with complete detraining. Nevertheless, endurance trained athletes seem to have a higher predisposition to neurally-mediated syncope during the head-up tilt test than asymptomatic untrained people and strength athletes^13,14, probably because of training-induced changes in neurovegetative regulation¹⁵, reduced orthostatic tolerance of the physiologically dilated heart¹⁶ or both. The predisposition of athletes to collapse, especially after the end of a strenuous exercise (“exhaustion collapse”), was known since the late 1940s¹⁷. This type of syncope (post-exercise syncope)¹⁸ is facilitated by abrupt interruption of effort and can be safely reproduced in laboratory¹⁹. Post-exercise syncope presents so many similarities with syncope during head-up tilt test^20-22. As the latter, the former is probably linked to an activation of ventricular mechano-receptors due to a critical decrease in left ventricular volume for the reduction of venous return. The physiopathologic cascade, besides orthostatic position, is facilitated by the persistence, in the early recovery, of massive vasodilation in exercised muscles of lower limbs and by the abrupt failure of muscular pump, responsible for a dramatic reduction of venous return. This hypothesis is confirmed by incapability in reproducing syncope after an exercise of analogous intensity but followed by active recovery (Zeppilli et al, unpublished data). However, since post-exercise syncope on field is very rare in asymptomatic highly-trained athletes, those having many episodes of syncope must suffer of an impairment or of a defect of vasal contro-regulatory mechanisms (probably a distorted a-adrenergic reactivity) that should withstand the blood pressure drop with a vasoconstriction.

A contribution to understand the mechanisms of neurally-mediated syncopes has offered once again by heart rate variability²³. During head-up tilt test the “normal” response of heart rate variability is characterized by a raise of low-frequency (sympathetic) component and a reduction of high frequency (vagal) component, as well as by a quick return to basal condition. In subjects with predisposition to neurally-mediated syncope, the raise of the low frequency component and the reduction of the high frequency component in the orthostatic phase are more pronounced and the return to basal conditions is slower.