Importância da transmissão oxidonitrérgica central na modulação dos ajustes termorregulatórios e sobre a ativação de áreas hipotalâmicas induzida pelo exercício físico submáximo em esteira

• Ano de defesa: 2011
• Autor(a) principal: Paulo Marcelo de Andrade Lima
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Fisiologia e farmacologia; Farmacologia; Fisiologia
• Link de acesso: http://hdl.handle.net/1843/BUOS-8PKKZ8

Previous studies in our laboratory showed that central oxidonitrergic transmission is important to thermoregulatory adjustments during treadmill-running and, consequently, to improve physical performance. However, the brain areas involved in these mechanisms are not known yet. On the other hand, according to the type, intensity, and duration of physical exercise activates several brain areas, among them, the hypothalamic paraventricular (PVN) and supraoptic (SON) nucleus. Besides expressing nitric oxide synthase (NOS), these nuclei are involved in autonomic regulation of body temperature, cardiorespiratory activity and hormonal functions that need to be adjusted during the exercise. The aim of this study was to verify if the PVN and SON were involved in the thermoregulatory adjustments and physical performance mediated by central nitric oxide (NO). Therefore, rats submitted to acute submaximal treadmill-exercise (18 m.min-1, 5% inclination) until fatigue received an intracerebroventricular (i.c.v.) injection of 1.43 mol N-nitro-L-arginina metil éster (L-NAME NOS competitive inhibitor) or 0.15 M NaCl (SAL as a control). Tail temperature (Tt) and internal body temperature (Ti) were continuously recorded. Ninety minutes after fatigue, animals were anesthetized and transcardiacally perfused. Brains were removed and processed for immunohistochemical quantification of c-Fos expression in the PVN and SON. Increases in the order of 656% in the PVN and 136% in the SON c-Fos expression were observed in animals after physical exercise when compared to REST-GROUP (p < 0.05). However, treatment with L-NAME attenuated the exercise-induced neuronal activation in the PVN by 53% (p < 0.05) but not in the SON (p = 0.42). As expected, i.c.v. L-NAME reduced physical performance by 42% (p < 0.01), and this was accompanied by a lower tail vasodilation capacity and higher heat storage rate (HSR) (10.74 ± 5.2 cal/min L-NAME vs. 15:25 ± 2.21 cal/min SAL, p < 0.01). In both exercised groups, c-Fos expression in the PVN was directly associated with physical performance (r = 0.917, p < 0.01) and inversely related to HSR (r = -0.739, p < 0.05). In the SAL-GROUP, it was correlated with greater changes in tail temperature (r = 0.978, p < 0.05). These results indicate that inhibition of central NO attenuates exercise-induced c-Fos expression in the PVN and thus, it leads to impaired autonomic regulation of heat dissipation, anticipating the fatigue