高原缺氧显著降低运动能力，但原因仍不清楚。肝脏色氨酸代谢产物--犬尿氨酸（kynurenine，KYN），反馈中枢并调节运动疲劳。当氧供/需矛盾加剧时，肝脏色氨酸加双氧酶(TDO)及其酶促产物KYN增多，KYN跨血脑屏障后存在于突触间隙，直接或间接与运动皮层突触后膜NMDA受体结合后抑制运动神经元兴奋性。在脑组织，运动皮层是调节运动的高级中枢，同时NMDA受体表达丰富。因此，本项目以肝脏KYN代谢通路为中心，以运动皮层NMDA受体为观察对象，研究急进高原KYN产生的机理，KYN中枢积累后对运动能力的影响及分子机制；探讨久居高原后，肝脏KYN代谢途径和中枢KYN-NMDA信号的变化，阐明高原缺氧降低运动能力的机制，为有针对性的寻求更有效的提高高原运动能力的措施奠定基础。

Exposure to high altitude reduces lowlanders’ physical performance, the cause is still unclear. Kynurenine (KYN), which is the liver tryptophan metabolite, feedback center and regulate the exercise fatigue. When contradictory about oxygen supply and demand are intensified, liver tryptophan dioxygenase (TDO) and its enzymatic product KYN increase. KYN exists in synaptic cleft after crossing the blood-brain barrier, and directly or indirectly combine the NMDA receptor located in postsynaptic membrane of motor cortex to inhibit motoneuron excitability. Motor cortex is the senior center of the movement regulation, where NMDA receptor is expressed in abundance. Therefore, focusing on KYN metabolic pathways and NMDA receptor, we research KYN mechanism when rushing into high altitude, and the effect and molecular mechanism of KYN accumulation on exercise capacity. Moreover, we explore the KYN metabolic pathways and central KYN-NMDA signal changes of people who live in high altitude for a long time, and clarify the molecular mechanism of exercise acclimatization in hypobaric hypoxia. These studies will provide theoretical foundation and profound insight for seeking more effective measures to raise the physical performance at high altitude.