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Does cerebral hypoxia facilitate central fatigue?
KTH, School of Technology and Health (STH), Basic Science and Biomedicine, Environmental Physiology.
2016 (English)In: Experimental Physiology, ISSN 0958-0670, E-ISSN 1469-445XArticle in journal (Refereed) PublishedText
Abstract [en]

New Findings: What is the topic of this review? This review addresses whether a mismatch between cerebral O2 demand and delivery accelerates the development of central fatigue during endurance-type exercise. What advances does it highlight? The difficulty with studying the importance of cerebral O2 availability for exercise performance is to manipulate cerebral O2 availability independently of muscular O2 availability. The different approaches to overcome this limitation indicate that cerebral oxygenation is not a major limiting factor in normoxia, but may limit performance in submaximal exercise tasks in hypoxia. Central fatigue originates within the central nervous system and is characterized by a decrease in voluntary muscle activation. Reduced systemic O2 availability can facilitate central fatigue by enhancing the afferent input of the chemosensitive nerves that play a pivotal role in development of central fatigue. There is accumulating evidence that, in some situations, inadequate O2 availability to the brain itself promotes central fatigue. This short review presents some of the recent findings supporting a direct effect of inadequate cerebral O2 availability on central fatigue and addresses the persisting limitations.

Place, publisher, year, edition, pages
IEEE Press, 2016.
National Category
Cardiac and Cardiovascular Systems
URN: urn:nbn:se:kth:diva-188241DOI: 10.1113/EP085640ScopusID: 2-s2.0-84963851615OAI: diva2:935902

QC 20160613

Available from: 2016-06-13 Created: 2016-06-09 Last updated: 2016-06-13Bibliographically approved

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