Efeito do bloqueio dopaminérgico central sobre a ativação neuronal hipotalâmica durante o exercício físico

Abstract

Dopamine is a monoamine that influences thermoregulation, motivation, reward and motor control. To evaluate the role of the central dopaminergic system on neuronal activation of hypothalamic nuclei involved in physical performance and thermoregulation, 2µL of saline (0.15 M, SAL, n = 15) or SCH-23390 (10 nmol, D1 receptor blocker, SCH, n = 15) were injected into the right cerebral lateral ventricle of Wistar rats before submaximal exercise (mean velocity of 15 m.min-1 and 5º of treadmill inclination) until fatigue. Some animals were also microinjected with saline and submitted to the same duration of exercise as the SCH group (SALtSCH, n = 8). In addition, the animals underwent SALtSCH (n=10) and SCH (n=10) treatments during a resting period of 13 minutes, which corresponded to the mean exercise time of SCH. Exercise time (ET), internal body temperature (Tbody) and tail skin temperature (Ttail) were recorded, and workload (W), body heating rate (BHR), heat storage (HS), HS / W ratio, heat dissipation index, thermal index, heat loss threshold and heat loss sensitivity were calculated. Ninety minutes after the protocols, the animals were anesthetized and submitted to euthanasia through transcardiac perfusion. The brains were analyzed by immunohistochemical assay to determine the expression of c-Fos in the following hypothalamic areas: median preoptic nucleus (MnPO), medial preoptic nucleus (MPO), paraventricular nucleus of the hypothalamus (PVN) and supra-optical nucleus (SON). During the resting period, there was no difference in BHR, HS, Tbody, Ttail and thermal index between SALtSCH and SCH. The D1 blockade reduced physical performance by 78% (p < 0.05) and no difference in BHR, HS, HS/W ratio and thermal index in the dynamic phase of exercise were observed between the experimental situations. The heat dissipation index, the heat loss threshold and heat loss sensitivity during exercise were also not different between groups. Tbody at the end of the physical exercise was similar between treatments, unlike Ttail that was smaller in SALtSCH (1.5 ºC; p < 0.05) and SCH (1.4 ºC; p < 0.05). During post-exercise recovery, Tbody of the animals remained elevated in comparison to baseline values and was not different between groups. However, Ttail in SAL and SCH returned to baseline at 15º minutes after fatigue. After the resting period, D1 blockade suppressed neuronalactivation only in SON (60%; p < 0.05) in comparison to the SALtSCH. Physical exercise increased neuronal activation in MnPO (144%; p < 0.05), MPO (102%; p < 0.05), PVN (562%; p < 0.05) and SON (131%; p < 0.05). Treatment with SCH23390 increased neuronal activation in MnPO (81%; p <0.05), PVN (116%; p <0.05) and SON (68%; p <0.05) after exercise, when compared to SALtSCH. In contrast, there was no difference in neuronal activation between the treatments SCH-23390 and SAL (p > 0.05). The data from this study show that D1 dopaminergic receptors are important modulators of physical performance during running exercise. However, the ergolytic effect was not related to thermoregulatory adjustments required during exercise. Since neuronal activation was similar between SCH and SAL animals, which ran until fatigue, it is possible that D1 receptor blockade modifies the perception of effort as suggested by the fact that despite being able to continue exercise, SCH animals had fatigue anticipated.