Convective oxygen transport and fatigue

1 John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison Medical School, Madison, Wisconsin; and 2 Department 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 O 2 delivery; however, reductions in O 2 supply exacerbate and increases attenuate the rate of accumulation. In this regard, peripheral fatigue development is mediated via the O 2 -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 O 2 -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 O 2 transport. Changes in convective O 2 delivery in the healthy human can result from modifications in arterial O 2 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 O 2 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 )