German Sport University Cologne, Department for Molecular and Cellular Sports Medicine, Am Sportpark Müngersdorf 6, 50933 Cologne, Germany.
Dr. Freese Institute for Exercise & Nutritional Immunology, Josef-Lammerting-Allee 7-13, 50933 Cologne, Germany.
Exerc Immunol Rev. 2019;25:8-19.
Feelings of fatigue not only occur in chronic and acute disease states, but also during prolonged strenuous exercise as a symptom of exhaustion. The underlying mechanisms of fatigue in diseases seem to rely on neuroinflammatory pathways. These pathways are interesting to understand exerciseinduced fatigue regarding immune system to brain signaling and effects of cerebral cytokines. Activation of the immune system incurs a high-energy cost, also in the brain. In consequence immune cells have high energetic priority over other tissues, such as neurons. A neuronal inactivation and corresponding changes in neurotransmission can also be induced by end products of ATP metabolism and elicit feelings of fatigue in diseases and after intensive and prolonged exercise bouts. Since there are no existing models of exercise-induced fatigue that specifically address interactions between neuroimmunologic mechanisms and neuroenergetics, this article is combining scientific evidence across a broad range of disciplines in order to propose an inflammation- and energy-based model for exercise-induced fatigue.
疲劳感不仅出现在慢性和急性疾病状态中，在长时间剧烈运动时作为疲惫的症状也会出现。疾病中疲劳的潜在机制似乎依赖于神经炎症途径。这些途径对于理解运动引起的疲劳很有意思，涉及免疫系统到大脑信号以及大脑细胞因子的影响。免疫系统的激活会产生很高的能量成本，即使在大脑中也是如此。因此，免疫细胞比其他组织（如神经元）具有更高的能量优先级。ATP 代谢的终产物也可以诱导神经元失活和相应的神经递质传递变化，并在疾病和剧烈及长时间运动后引起疲劳感。由于目前没有专门针对神经免疫机制和神经能量学相互作用的运动引起的疲劳模型，本文结合了广泛学科的科学证据，提出了一个基于炎症和能量的运动引起的疲劳模型。
