Low‐intensity treadmill exercise‐related changes in the rat stellate ganglion neurons |
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Authors: | Renato Albuquerque de Oliveira Cavalcanti Demilto Yamaguchi da Pureza Mariana Pereira de Melo Romeu Rodrigues de Souza Cássia T Bergamaschi Sandra Lia do Amaral Helen Tang Andrzej Loesch Antonio Augusto Coppi Maciel Ribeiro |
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Institution: | 1. Laboratory of Stochastic Stereology and Chemical Anatomy (LSSCA), Department of Surgery, College of Veterinary Medicine, University of S?o Paulo (USP), S?o Paulo, Brazil;2. Department of Statistics, Institute of Mathematics and Statistics, University of S?o Paulo, Brazil;3. Physical Education Postgraduate Course, S?o Judas Tadeu University, S?o Paulo, Brazil;4. Department of Bioscience, Federal University of S?o Paulo, Santos, Brazil;5. Department of Physical Education, Faculty of Science, UNESP–S?o Paulo State University, Bauru, Brazil;6. Research Department of Inflammation, University College London Medical School, Royal Free Campus, London, United Kingdom |
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Abstract: | Stellate ganglion (SG) represents the main sympathetic input to the heart. This study aimed at investigating physical exercise–related changes in the quantitative aspects of SG neurons in treadmill‐exercised Wistar rats. By applying state‐of‐the‐art design‐based stereology, the SG volume, total number of SG neurons, mean perikaryal volume of SG neurons, and the total volume of neurons in the whole SG have been examined. Arterial pressure and heart rate were also measured at the end of the exercise period. The present study showed that a low‐intensity exercise training program caused a 12% decrease in the heart rate of trained rats. In contrast, there were no effects on systolic pressure, diastolic pressure, or mean arterial pressure. As to quantitative changes related to physical exercise, the main findings were a 21% increase in the fractional volume occupied by neurons in the SG, and an 83% increase in the mean perikaryal volume of SG neurons in treadmill‐trained rats, which shows a remarkable neuron hypertrophy. It seems reasonable to infer that neuron hypertrophy may have been the result of a functional overload imposed on the SG neurons by initial posttraining sympathetic activation. From the novel stereological data we provide, further investigations are needed to shed light on the mechanistic aspect of neuron hypertrophy: what role does neuron hypertrophy play? Could neuron hypertrophy be assigned to the functional overload induced by physical exercise? © 2008 Wiley‐Liss, Inc. |
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Keywords: | stereology extrinsic cardiac innervation physical exercise stellate ganglion rats |
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