During exercise in young, healthy individuals cardinal features of the pulmonary oxygen uptake response (primary component time constant [Grassi et al., 1996], slow component [Poole et al., 1991]) reflect closely events within the exercising muscles. It is tenable therefore that the age-associated slowing of oxygen uptake kinetics (Bell et al., 1999) and also decreased maximal oxygen uptake, (McGuire et al., 2001) might result from impairments in the perfusive (oxygen delivery) and/or diffusive oxygen conductance within muscle. This presentation will examine evidence obtained through investigations in animals for ageing: 1. redistributing exercising oxygen delivery away from highly oxidative muscles and muscle fibers, 2. altering muscle capillary hemodynamics, and 3. reducing the oxygen pressure head within the microcirculation that serves to facilitate blood-muscle oxygen transfer. In many respects, these alterations found in healthy ageing bear a striking resemblance to those present in chronic diseases (diabetes, chronic heart failure) and may help explain the compromised exercise tolerance present in aged individuals. Putative mechanistic insights will be explored within the context of current knowledge and future investigative approaches.