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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain
IS THE TRAINING-INDUCED INCREASE OF INTRINSIC VENTRICULAR REFRACTORINESS MEDIATED BY POSTGANGLIONIC PARASYMPATHETIC NEURONS ACTIVITY? AN EXPERIMENTAL STUDY.
Abstract number: P29
Zarzoso1 M, Such-Miquel2 L, Parra1 G, Trapero3 I, Lopez2 L, Alberola1 J, Chorro4 FJ, Such1 L, Alberola1 AM
1Department of Physiology1
2Physiotherapy2
3Nursing3
4Medicine4, University of Valencia, 46010 Valencia (Spain). [email protected]
Aim:
Our aim was to determine the role of postganglionic parasympathetic neurons in the increase of ventricular refractoriness produced by physical training in isolated rabbit heart.
Methods:
The study was carried out in 16 New Zealand rabbits which were assigned to a control (n=5), a sham operated (n=6) and a trained (n=5) groups. The trained group followed through 6 weeks of chronic physical exercise on treadmill, while the other groups were housed in the animal quarters. After these 6 weeks, rabbits were anaesthetized, sacrificed and their hearts excised and isolated in a Langendorff system. Pacing and recording electrodes were positioned on left ventricle. Extrastimulus test using four different pacing cycle lengths (10% less than the basal cycle length, 250, 200 and 150ms) was performed before and after the infusion of atropine (1mM). Ventricular effective (VERP) and functional (VFRP) refractory periods were determined to assess ventricular refractoriness. An ANOVA test (repeated measures) was applied to analyze the effects of parasympathetic blocking on refractoriness.
Results:
In the sham operated group, both VERP and VFRP did not change with time. VFRP was longer (p<0.05) in trained animals than in controls (i.e. 15110 versus 124.52.12ms at 250ms of pacing cycle length). There were no differences in VERP and VFRP after atropine administration within both groups.
Conclusion:
Ventricular refractoriness increase produced by physical training in isolated heart does not seem to be dependent on parasympathetic postganglionic neurons activity.
Supported by MEC (DEP2007-73234-C03-01) and Generalitat Valenciana (BFPI/2008/003).
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :P29