Convective oxygen transport and fatigue

Abstract

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 O2delivery; however, reductions in O2supply 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 O2transport. Changes in convective O2delivery in the healthy human can result from modifications in arterial O2content, 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 O2delivery on the development of central and peripheral fatigue.