At the onset of exercise, an increase in muscle and pulmonary O2 consumption is met by increases in muscle O2 delivery and muscle O2 extraction. Thus, the study of pulmonary O2 uptake kinetics reflects the integrated response between the convective and diffusive O2 delivery systems and the muscle metabolic machinery (i.e., mitochondrial enzyme activation and provision of acetyl groups to the tricarboxcylic acid cycle) to increase muscle O2 consumption. Pulmonary O2 uptake kinetics are slowed in older adults compared with young adults and previous studies suggest that the slower O2 uptake kinetics may be the result of an age-associated decline in the ability of older adults to increase O2 delivery to active muscles. However, an inherent limitation to understanding the control of and limitations to pulmonary O2 uptake kinetics is that it is methodologically difficult to examine the adaptation of muscle perfusion and O2 delivery and muscle O2 utilization in the muscle microcirculation of active muscles in the dynamically exercising human. In this review, we provide an overview of the effect of ageing on pulmonary O2 uptake kinetics (reflecting the activation of muscle O2 consumption) during the transition to moderate-intensity exercise. Age-related changes in O2 delivery systems and muscle oxidative capacity are examined as potential limitations to pulmonary O2 uptake kinetics. We then review recent studies from our laboratory that have investigated the control of pulmonary O2 uptake kinetics at the level of the muscle microcirculation by examining the adaptation of muscle O2 delivery and muscle O2 utilization using near-infrared spectroscopy during the transition to exercise in healthy young and older adults.