Department of Anaesthesia and The Copenhagen Muscle Research Centre, Rigshospitalet 2041, University of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark.
Prog Neurobiol. 2011 Nov;95(3):406-26. doi: 10.1016/j.pneurobio.2011.09.008. Epub 2011 Sep 24.
This review focuses on the possibility that autonomic activity influences cerebral blood flow (CBF) and metabolism during exercise in humans. Apart from cerebral autoregulation, the arterial carbon dioxide tension, and neuronal activation, it may be that the autonomic nervous system influences CBF as evidenced by pharmacological manipulation of adrenergic and cholinergic receptors. Cholinergic blockade by glycopyrrolate blocks the exercise-induced increase in the transcranial Doppler determined mean flow velocity (MCA Vmean). Conversely, alpha-adrenergic activation increases that expression of cerebral perfusion and reduces the near-infrared determined cerebral oxygenation at rest, but not during exercise associated with an increased cerebral metabolic rate for oxygen (CMRO(2)), suggesting competition between CMRO(2) and sympathetic control of CBF. CMRO(2) does not change during even intense handgrip, but increases during cycling exercise. The increase in CMRO(2) is unaffected by beta-adrenergic blockade even though CBF is reduced suggesting that cerebral oxygenation becomes critical and a limited cerebral mitochondrial oxygen tension may induce fatigue. Also, sympathetic activity may drive cerebral non-oxidative carbohydrate uptake during exercise. Adrenaline appears to accelerate cerebral glycolysis through a beta2-adrenergic receptor mechanism since noradrenaline is without such an effect. In addition, the exercise-induced cerebral non-oxidative carbohydrate uptake is blocked by combined beta 1/2-adrenergic blockade, but not by beta1-adrenergic blockade. Furthermore, endurance training appears to lower the cerebral non-oxidative carbohydrate uptake and preserve cerebral oxygenation during submaximal exercise. This is possibly related to an attenuated catecholamine response. Finally, exercise promotes brain health as evidenced by increased release of brain-derived neurotrophic factor (BDNF) from the brain.
这篇综述重点探讨了自主活动在人体运动期间影响脑血流 (CBF) 和代谢的可能性。除了脑自动调节、动脉二氧化碳张力和神经元激活之外，自主神经系统可能通过对肾上腺素能和胆碱能受体的药理学操作来影响 CBF。用格隆溴铵阻断胆碱能可阻断经颅多普勒测定的平均血流速度 (MCA Vmean) 的运动诱导增加。相反，α-肾上腺素能激活增加了脑灌注的表达，并减少了近红外光测定的脑氧合作用在休息时，但不是在与增加的脑氧代谢率 (CMRO(2)) 相关的运动期间，这表明 CMRO(2) 和交感神经对 CBF 的控制之间存在竞争。即使在剧烈的手握运动中，CMRO(2) 也不会发生变化，但在自行车运动中会增加。即使在高强度的手握运动中，CMRO(2) 也不会改变，但在自行车运动中会增加。β-肾上腺素能阻断剂甚至不会影响 CMRO(2) 的增加，尽管 CBF 减少，这表明脑氧合作用变得至关重要，并且有限的脑线粒体氧张力可能会导致疲劳。此外，在运动期间，交感活动可能会驱动大脑非氧化碳水化合物摄取。肾上腺素似乎通过β2-肾上腺素能受体机制加速大脑糖酵解，因为去甲肾上腺素没有这种作用。此外，运动诱导的大脑非氧化碳水化合物摄取被联合β 1/2-肾上腺素能阻断剂阻断，但不受β1-肾上腺素能阻断剂阻断。此外，耐力训练似乎降低了大脑非氧化碳水化合物摄取，并在亚最大运动期间保持脑氧合。这可能与儿茶酚胺反应的减弱有关。最后，运动促进了大脑的健康，这表现为大脑源性神经营养因子 (BDNF) 从大脑中的释放增加。
