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 (V̇O₂) 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 (a-v̄DO₂) to the V̇O₂) 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 V̇O₂ 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 V̇O₂ speeding at 10 and 30 s, respectively. After this, the contribution of a-v̄DO₂ to the V̇O₂ became increasingly more predominant: being responsible to an estimated 64% of the V̇O₂ speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and a-v̄DO₂ clearly interact to determine the V̇O₂ response, the speeding of V̇O₂ kinetics by prior high-intensity KE exercise is predominantly attributable to increases in a-v̄DO₂.