The influence of oxygen deprivation on mammalian heart muscle has been measured in terms of the mechanical capabilities open to the muscle as described by the interrelationship between force, velocity of shortening, and length using isolated cat papillary muscle preparations. Velocity-length relationships have been directly measured from isometric to near zero force. The three-dimensional surface relating force, velocity, and length was reversibly depressed by hypoxia but asymmetrically, which contrasts with the symmetrical shift with altered buffer calcium. On reoxygenation a transient further decrease in maximum unloaded shortening velocity occurred with prolongation of contraction. Experimental evidence is presented that Vmax is truly decreased by hypoxia and that this may not be caused solely by a decrease in the number of actin-myosin crossbridges activated.