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

Abstract

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 $\hbox{a-}{\bar{\rm v}\hbox{DO}_2}$.