European Heart Journal Advance Access originally published online on October 7, 2007
European Heart Journal 2007 28(22):2697-2698; doi:10.1093/eurheartj/ehm431
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Exercise training and baroreflex sensitivity in patients with neurally mediated syncope
1 Departments of Cardiovascular Rehabilitation and Cardiology, University Hospital Gasthuisberg, Leuven, Belgium
2 Department of Cardiology, University Hospital Gasthuisberg, Leuven, Belgium
3 Department of Rehabilitation Sciences, University of Leuven (KU Leuven), Leuven, Belgium
* Corresponding author. Tel: +32 16 342181; fax: +32 16 342184. E-mail address: tony.reybrouck{at}uz.kuleuven.ac.be
This editorial refers to ‘The effects of exercise training on arterial baroreflex sensitivity in neurally mediated syncope patients’ by G. Gardenghi et al., on page 2749
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
Neurally mediated syncope (NMS) is the result of a critical cerebral hypoperfusion. The pathophysiology of this abnormality is multifactorial. Optimal cerebral perfusion depends on an adequate functioning of the control mechanisms maintaining cerebral oxygen delivery. This includes baroreflex-induced adjustments of the systemic vascular resistance, intravascular volume regulation, and also cerebral autoregulation.1 The tool to diagnose NMS has been the tilt table test. The complexity of the pathophysiology of NMS is illustrated by the different types of syncope as a response to a tilt table test: cardioinhibitory with or without asystole, vasodepressor, and mixed type.1 Furthermore, the type of syncope can vary in the same patient from one tilt test to another.2 The treatment of NMS has been shown to be difficult, with conflicting results. Treatment options vary from vagolytic drugs, ß-blocking agents, fludrocortisone (to increase plasma volume), serotonin re-uptake inhibitors, 
-constrictors, salt and water supplements, and sleeping with the bed in a head-up tilt position. Physical manoeuvres have also been proposed, such as crossing legs, isometric tensing of arm muscles,3,4 and prolonged standing training (tilt training).5,6 Moreover, endurance training has also been recommended in some studies.7 For patients with the cardioinhibitory type of syncope, pacemaker therapy has been used, with conflicting results,8 because pacemaker therapy may prevent asystole but not hypotension.
Gardenghi et al., 9 compare the effects of exercise training, pharmacotherapy, and tilt training on the sympathetic arterial baroreflex activity and on the short-term recurrence of syncope. Following a period of 4 months physical training, there was a better response of the muscle sympathetic activity after infusions of phenylephrine or nitroprusside in the exercise-trained group compared with the other groups (tilt training, pharmacotherapy, and control group). Moreover, during a follow-up period of 4 months, syncope recurrence was observed in two patients treated with exercise training and in four patients treated with pharmacotherapy. No syncope recurrence was observed for the tilt training group. Two patients in the control group also developed syncope recurrence during the follow-up.
The authors speculate that the improved vagal and sympathetic arterial baroreflex gain in the group treated with exercise training could be beneficial for the prevention of NMS.
Among the many mechanisms which may explain NMS, excessive autonomic activity with sympatethic overactivity may be operational before the onset of frank syncope. Indeed, in many circumstances, syncope is preceded by an episode of an excessive increase in heart rate. One of the well known effects of physical training is the decrease of orthostatic stimulation and ß-receptor stimulation, with a lowering of the heart rate. Therefore, it seems logical to expect some benefits from a physical training programme in patients with NMS. Another possible mechanism of physical training could be the volume expanding effect.7 On the other hand, very intensive physical training leads to a decrease in orthostatic tolerance.10 Furthermore, the authors also demonstrate that the autonomic tone showed considerable fluctuation in the same patients. This may explain why patients with NMS may develop recurrent syncope after long periods of remission.
We feel that patients with NMS could benefit from a triple therapy: (i) moderate exercise training; (ii) adding exercise to a programme of tilt training; and (iii) physical manoeuvres such as leg crossing or isometric arm tensions.
For this reason, in NMS, physical training should not be recommended as monotherapy. It can be complementary to other interventions.
Acknowledgments
Conflict of interest: none declared.
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
doi:10.1093/eurheartj/ehm208 
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EHJ 2007 28: 2749-2755.[Abstract] [FREE Full Text]
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