title: Does cerebral hypoxia facilitate central fatigue?
abstract: What is the topic of this review? This review addresses whether a mismatch between cerebral O2demand 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 O2availability for exercise performance is to manipulate cerebral O2availability independently of muscular O2availability. 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 O2availability 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 O2availability to the brain itself promotes central fatigue. This short review presents some of the recent findings supporting a direct effect of inadequate cerebral O2availability on central fatigue and addresses the persisting limitations.
authors.affiliation: Department of Environmental Physiology, School of Technology and Health, Royal Institute of Technology, Solna, Sweden.
authors.forename: Christoph
authors.initials: C
authors.lastname: Siebenmann
authors.affiliation: H. Lundbeck A/S, Valby, Denmark.|Department of Neuroscience and Pharmacology, University of Copenhagen, Denmark.
authors.forename: Peter
authors.initials: P
authors.lastname: Rasmussen