Central circulatory and peripheral O2 extraction changes as interactive facilitators of pulmonary O2 uptake during a repeated high-intensity exercise protocol in humans

It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake (VO2) response at the onset of subsequent identical exercise. To clarify the roles of central O-2 delivery and/or peripheral O2 extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O-2 content difference (a-(v) over bar DO2) to the VO2 transient during repeated bouts of high-intensity knee extension (KE) exercise. Nine healthy subjects volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate 70-75% of peak power) separated by 6 min of rest. Throughout the protocol, continuous-wave Doppler ultrasound was used to measure beat-by-beat CO (i.e., via simultaneous measurement of stroke volume and the diameter of the arterial aorta). The phase II VO2 response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the VO2 speeding at 10 and 30 s, respectively. After this, the contribution of (a-(v) over bar DO2) became increasingly more predominant: being responsible to an estimated 64% of the VO2 speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and a-(v) over bar DO2 clearly interact to determine the VO2 response, the speeding of VO2 kinetics by prior high-intensity KE exercise is predominantly attributable to increases in a-(v) over bar DO2.