Department of Human Physiology and Sports Medicine, Vrije Universiteit Brussel, Brussels, Belgium.
Neurosci Lett. 2011 Apr 25;494(2):150-4. doi: 10.1016/j.neulet.2011.03.001. Epub 2011 Mar 6.
Serum brain-derived neurotrophic factor (BDNF) is known to increase with exercise. This increase is believed to originate from the brain and it is suggested that monoamines are involved in BDNF regulation. Heat exposure could influence the supposed BDNF output from the brain. Therefore, we hypothesized that administration of a selective serotonin reuptake inhibitor could influence the exercise-induced increase in BDNF, and that peripheral BDNF will be higher when exercise is performed in the heat.
Eleven well-trained males performed 4 experimental trials on a cycle ergometer with citalopram or placebo treatment (20 mg in 12 h) in an environmental temperature of 18°C or 30°C. Blood samples (BDNF and cortisol) were taken at 4 time points: at rest, after 60 min at 55% W(max), after a time trial of 30 min at 75% W(max) and following 15 min of recovery. Heart rate and core temperature were measured.
Performance on the time trial was 20% worse in 30°C compared to 18°C (p<0.01), without influence of citalopram. Serum BDNF was found to be lower under citalopram treatment, while basal cortisol levels were increased (p<0.05). Exercise triggered an increase in both BDNF and cortisol (p<0.001). BDNF followed the same pattern as core temperature during exercise, with higher levels of both variables in 30°C. Cortisol was also increased in 30°C compared to temperate conditions (p<0.01).
Exercise caused a rise in serum BDNF and cortisol. This increase was enhanced with exercise in the heat. Since permeability of the blood-brain barrier increases with exercise in the heat, the hypothesis was raised that this causes a higher cerebral output of BDNF. Serotonergic stimulation did not increase peripheral BDNF, which was even lower with citalopram administration. Future research should focus on mechanisms behind BDNF increase with exercise.
已知血清脑源性神经营养因子(BDNF)会随着运动而增加。这种增加被认为源自大脑,并且有人认为单胺类物质参与了 BDNF 的调节。热暴露可能会影响大脑中所谓的 BDNF 输出。因此,我们假设选择性 5-羟色胺再摄取抑制剂的给药会影响运动引起的 BDNF 增加,并且当在热环境中进行运动时,外周 BDNF 会更高。
11 名训练有素的男性在环境温度为 18°C 或 30°C 的情况下,在自行车测力计上进行了 4 项实验试验,分别接受西酞普兰或安慰剂(12 小时内 20mg)治疗。在 4 个时间点采集血液样本(BDNF 和皮质醇):休息时、55% W(max) 运动 60 分钟后、75% W(max) 运动 30 分钟的时间试验后和 15 分钟恢复后。测量心率和核心体温。
在 30°C 下进行的时间试验比在 18°C 下差 20%(p<0.01),而西酞普兰没有影响。在西酞普兰治疗下,血清 BDNF 水平较低,而基础皮质醇水平升高(p<0.05)。运动引起 BDNF 和皮质醇均增加(p<0.001)。BDNF 在运动过程中与核心体温呈现相同的模式,两个变量在 30°C 时的水平更高。与温和条件相比,30°C 下皮质醇也增加(p<0.01)。
运动导致血清 BDNF 和皮质醇升高。在热环境中运动时,这种增加得到了增强。由于热环境下运动时血脑屏障的通透性增加,因此提出了这种情况导致大脑中 BDNF 输出增加的假设。血清素能刺激并未增加外周 BDNF,西酞普兰给药甚至更低。未来的研究应集中在运动引起 BDNF 增加的机制上。