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 \(({\dot{V}\hbox{O}_2})\) response at the onset of subsequent identical exercise. To clarify the roles of central O2 delivery and/or peripheral O2 extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O2 content difference \((\hbox{a-}{\bar{\rm v}\hbox{DO}_2})\) to the \({\dot{V}\hbox{O}_2}\) 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 \({\dot{V}\hbox{O}_2}\) 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 \({\dot{V}\hbox{O}_2}\) speeding at 10 and 30 s, respectively. After this, the contribution of \(\hbox{a-}{\bar{\rm v}\hbox{DO}_2}\) became increasingly more predominant: being responsible to an estimated 64% of the \({\dot{V}\hbox{O}_2}\) speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and \(\hbox{a-}{\bar{\rm v}\hbox{DO}_2}\) clearly interact to determine the \({\dot{V}\hbox{O}_2}\) response, the speeding of \({\dot{V}\hbox{O}_2}\) kinetics by prior high-intensity KE exercise is predominantly attributable to increases in \(\hbox{a-}{\bar{\rm v}\hbox{DO}_2}\).