Longitudinal decline in peak V<sc>o</sc>2 with aging in a healthy population is associated with a reduction in peripheral oxygen utilization but not in cardiac output

Aging is associated with a significant decline in aerobic capacity assessed by maximal exercise oxygen consumption (Vo(2max)). The relative contributions of the specific Vo(2) components driving this decline, namely cardiac output (CO) and arteriovenous oxygen difference (A - V)O-2, remain unclear. We examined this issue by analyzing data from 99 community-dwelling participants (baseline age: 21-96 yr old; average follow-up: 12.6 yr old) from the Baltimore Longitudinal Study of Aging, free of clinical cardiovascular disease. Vo(2peak), a surrogate of Vo(2max), was used to assess aerobic capacity during upright cycle ergometry. Peak exercise left ventricular volumes, heart rate, and CO were estimated using repeated gated cardiac blood pool scans. The Fick equation was used to calculate (A - V)O-2(diff,peak) from COpeak and Vo(2peak). In unadjusted models, Vo(2peak), (A - V)O-2(diff,peak), and COpeak declined longitudinally over time at steady rates with advancing age. In multiple linear regression models adjusting for baseline values and peak workload, however, steeper declines in Vo(2peak) and (A - V)O-2(diff,peak) were observed with advanced entry age but not in COpeak. The association between the declines in Vo(2peak) and (A - V)O-2(diff,peak) was stronger among those >= 50 yr old compared with their younger counterparts, but the difference between the two age groups did not reach statistical significance. These findings suggest that age-associated impairment of peripheral oxygen utilization during maximal exercise poses a stronger limitation on peak Vo(2) than that of CO. Future studies examining interventions targeting the structure and function of peripheral muscles and their vasculature to mitigate age-associated declines in (A - V)O-2(diff) are warranted.