中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (10): 4523-4528.doi: 10.4103/NRR.NRR-D-25-00864

• 综述:退行性病与再生 • 上一篇    下一篇

运动时增加氧气需求可刺激神经保护:一个可行的假设

  

  • 出版日期:2026-10-15 发布日期:2026-06-11

Increased oxygen demand during exercise as a stimulus for neuroprotection: A working hypothesis

Johannes Burtscher1, 2, *, Robert Motl3, Erich Hohenauer4, 5, Luis Santos6, Atbin Djamshidian7, Hannelore Ehrenreich8, Florian Krismer7, Klaus Berek7, Martin Burtscher1, Katharina Hüfner2, Martin Kopp1   

  1. 1Department of Sport Science, University of Innsbruck, Innsbruck, Austria; 
    2Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA; 
    3Rehabilitation and Exercise Science Laboratory, Department of Business Economics, Health and Social Care, University of Applied Sciences and Arts of Southern Switzerland, Landquart, Switzerland; 
    4Department of Neurosciences and Movement Science, University of Fribourg, Fribourg, Switzerland; 
    5Department Ciencias de la Educación, Universidad de Oviedo, Oviedo, Spain; 
    6Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria; 
    7Experimental Medicine, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany; 
    8Department of Psychiatry, Psychotherapy, Psychosomatics and Medical Psychology, University Hospital for Psychiatry II, Medical University of Innsbruck, Innsbruck, Austria
  • Online:2026-10-15 Published:2026-06-11
  • Contact: Johannes Burtscher, PhD, Johannes.Burtscher@i-med.ac.at.

摘要: https://orcid.org/0000-0002-2889-0151 (Johannes Burtscher)

Abstract: Aerobic (endurance) exercise training protects from age-related neurological and psychiatric diseases. The bidirectional signaling between tissues directly involved in aerobic exercise, such as skeletal muscle and the brain, is well established; however, the precise mechanisms by which exercise benefits the brain remain elusive. We summarize the role of hypoxia (reduced oxygen availability) signaling as a potential mediator of exercise outcomes on the brain. The increased oxygen demand in organs such as skeletal muscle and heart during aerobic exercise induces hypoxia responses, including the activation of hypoxia-inducible factor pathways. These responses promote adaptations leading to improved oxygen transport, mitochondrial functions, and oxidative stress management in the brain and thereby counteract central pathological developments associated with neuropsychiatric and neurodegenerative diseases. Passive hypoxia exposures can similarly improve brain functions; we provide an extensive overview of the existent literature on that topic. We conclude that the combination of aerobic exercise and ambient hypoxia can result in synergistic and/or additive positive outcomes in the brain. However, the dose of either stimulus and individual resilience/vulnerabilities determines if the induced stress responses are successful and safe. If the stress management capacities are insufficient, the different stimuli may have antagonistic effects or inhibit beneficial adaptations. The selection of combinations for optimal adaptation is an important challenge for future research.

Key words: cardiorespiratory fitness, exercise, hypoxia inducible factor, mental health, mitochondria, neurodegeneration, neurological disorders, neuroprotection, oxygen, physical activity