Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901, Belo Horizonte, Brazil.
Pharmacol Rep. 2010 Jan-Feb;62(1):54-61. doi: 10.1016/s1734-1140(10)70242-5.
To assess the effects of a blockade of central D1- and D2-dopaminergic receptors on metabolic rate, heat balance and running performance, 10 nmol (2 microl) of a solution of the D(1) antagonist SCH-23390 hydrochloride (SCH, n = 6), D2 antagonist eticlopride hydrochloride (Eti, n = 6), or 2 microl of 0.15 M NaCl (SAL, n = 6) was injected intracerebroventricularly into Wistar rats before the animals began graded running until fatigue (starting at 10 m/min, increasing by 1 m/min increment every 3 min until fatigue, 5% inclination). Oxygen consumption and body temperature were recorded at rest, during exercise and following 30 min of recovery. Control experiments with injection of two doses (10 and 20 nmol/rat) of either SCH or Eti solution were carried out in resting rats as well. Body heating rate, heat storage, workload and mechanical efficiency were calculated. Although SCH and Eti treatments did not induce thermal effects in resting animals, they markedly reduced running performance (-83%, SCH; -59% Eti, p < 0.05) and decreased maximal oxygen uptake (-79%, SCH; -45%, Eti, p < 0.05) in running rats. In addition, these treatments induced a higher body heating rate and persistent hyperthermia during the recovery period. Our data demonstrate that the alteration in dopamine transmission induced by the central blockade of dopamine- D1 and D2 receptors impairs running performance by decreasing the tolerance to heat storage. This blockade also impairs the dissipation of exercise-induced heat and metabolic rate recovery during the post-exercise period. Our results provide evidence that central activation of either dopamine- D1 or D2 receptors is essential for heat balance and exercise performance.
为了评估中枢 D1 和 D2 多巴胺受体阻断对代谢率、热平衡和跑步表现的影响，将 10 nmol（2 微升）SCH-23390 盐酸盐（SCH，n = 6）、D2 拮抗剂盐酸埃替克洛德（Eti，n = 6）或 2 微升 0.15 M NaCl（SAL，n = 6）的溶液注入 Wistar 大鼠的侧脑室，然后让动物开始分级跑步直至疲劳（起始速度为 10 m/min，每 3 分钟增加 1 m/min，坡度为 5%）。在休息、运动期间和 30 分钟恢复期间记录耗氧量和体温。还在休息大鼠中进行了用两种剂量（10 和 20 nmol/大鼠）SCH 或 Eti 溶液进行的对照实验。计算体热产生率、热储存、工作量和机械效率。尽管 SCH 和 Eti 处理在休息动物中没有引起热效应，但它们明显降低了跑步表现（-83%，SCH；-59%，Eti，p < 0.05）并降低了最大耗氧量（-79%，SCH；-45%，Eti，p < 0.05）在跑步大鼠中。此外，这些处理在恢复期引起更高的体热产生率和持续的体温过高。我们的数据表明，多巴胺传递的改变由中枢多巴胺 D1 和 D2 受体阻断引起，通过降低对热储存的耐受性来损害跑步表现。这种阻断还损害了运动引起的热量耗散和运动后期间代谢率的恢复。我们的结果提供了证据，表明中枢激活多巴胺 D1 或 D2 受体对于热平衡和运动表现是必要的。
