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1 The John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States
2 Department of Physical Education, University of Las Palmas de Gran Canaria, Spain
* To whom correspondence should be addressed. E-mail: amann{at}wisc.edu.
Fatigue is defined as a reversible reduction in force/power generating capacity and can be elicited by central and/or peripheral mechanisms. During skeletal muscle contractions both aspects of fatigue develop independent of alterations in convective O2 delivery, however, reductions in O2, peripheral fatigue development is mediated via the O2 dependent rate of accumulation of metabolic byproducts (e.g. inorganic phosphate) and their well known interference with excitation-contraction coupling within the myocyte. In contrast, the development of O2-depending central fatigue is elicited a) directly by interference with the development of central command and/or b) indirectly via inhibitory afferent feedback on central motor drive secondary to the peripheral effects of low convective O2 transport. Changes in convective O2 delivery in the healthy human can result from modifications in arterial O2 content, blood flow, or a combination of both and can be induced via heavy exercise at sea level and are exacerbated during acute and chronic exposure to altitude. This review focuses on the effects of changes in convective O2 delivery on the development of central and peripheral fatigue.
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