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J Appl Physiol 104: 861-870, 2008. First published October 25, 2007; doi:10.1152/japplphysiol.01008.2007
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INVITED REVIEW

HIGHLIGHTED TOPIC
Fatigue Mechanisms Determining Exercise Performance

Convective oxygen transport and fatigue

Markus Amann1 and Jose A. L. Calbet2

1John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison Medical School, Madison, Wisconsin; and 2Department of Physical Education, University of Las Palmas de Gran Canaria, Spain

During exercise, fatigue is defined as a reversible reduction in force- or power-generating capacity and can be elicited by "central" and/or "peripheral" mechanisms. During skeletal muscle contractions, both aspects of fatigue may develop independent of alterations in convective O2 delivery; however, reductions in O2 supply exacerbate and increases attenuate the rate of accumulation. In this regard, peripheral fatigue development is mediated via the O2-dependent rate of accumulation of metabolic by-products (e.g., inorganic phosphate) and their interference with excitation-contraction coupling within the myocyte. In contrast, the development of O2-dependent central fatigue is elicited 1) by interference with the development of central command and/or 2) via inhibitory 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 they can be induced via heavy exercise even at sea level; these changes 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.

oxygenation; hypoxia; blood flow; exercise; hyperoxia


Address for reprint requests and other correspondence: M. Amann, The John Rankin Laboratory of Pulmonary Medicine, 4245 Medical Science Center, 1300 University Ave., Madison, WI 53706 (e-mail: amann{at}wisc.edu)




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