Effects of ageing on muscle O2 utilization and muscle oxygenation during the transition to moderate-intensity exercise

At the onset of exercise, an increase in muscle and pulmonary O-2 consumption is met by increases in muscle O-2 delivery and muscle O-2 extraction. Thus, the study of pulmonary O-2 uptake kinetics reflects the integrated response between the convective and diffusive O-2 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 O-2 consumption. Pulmonary O-2 uptake kinetics are slowed in older adults compared with young adults and previous studies suggest that the slower O-2 uptake kinetics may be the result of an age-associated decline in the ability of older adults to increase O-2 delivery to active muscles. However, an inherent limitation to understanding the control of and limitations to pulmonary O-2 uptake kinetics is that it is methodologically difficult to examine the adaptation of muscle perfusion and O-2 delivery and muscle O-2 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 O-2 uptake kinetics (reflecting the activation of muscle O-2 consumption) during the transition to moderate-intensity exercise. Age-related changes in O-2 delivery systems and muscle oxidative capacity are examined as potential limitations to pulmonary O-2 uptake kinetics. We then review recent studies from our laboratory that have investigated the control of pulmonary O-2 uptake kinetics at the level of the muscle microcirculation by examining the adaptation of muscle O-2 delivery and muscle O-2 utilization using near-infrared spectroscopy during the transition to exercise in healthy young and older adults.