Evidence that myoglobin does not support heart performance at maximal levels of oxygen demand

Abstract

ABSTRACT Myoglobin binds reversibly with oxygen and can facilitate oxygen diffusion across artificial membranes in vitro (Wittenberg, 1970). Myoglobin-enhanced oxygen consumption in heart is particularly important under conditions of hypoxia. This has been established directly with fish heart models (Bailey & Driedzic, 1986; Driedzic, Stewart & Scott, 1982) and indirectly by following discharge of high-energy phosphates in rat heart (Taylor, Matthews & Radda, 1986). Simple mathematical models are consistent with the importance of myoglobin during hypoxia and, in addition, predict that the protein should play a role in the support of oxygen consumption at maximal rates of respiration (Meyer, Sweeney & Kushmerick, 1984). In this study, the hypothesis that myoglobin-enhanced oxygen consumption is vital in meeting the demands of elevated levels of respiration by a teleost heart is tested indirectly. Myoglobin’s importance was assessed by monitoring isometric force development of ventricle strips from sculpin bathed in media with a constant level of either 21 % or 1 % O2. Additions to the bathing media included 2,4-dinitrophenol (DNP) to uncouple mitochondria and induce maximal oxygen consumption, and hydroxylamine which effectively converts myoglobin into the iron III form incapable of binding oxygen (Driedzic, 1983; Wittenberg, Wittenberg & Caldwell, 1975). The major finding is that myoglobin does not play a critical role in the maintenance of performance under normoxia at maximal rates of oxygen consumption.