12/27/2023 0 Comments Masako endo![]() ![]() This suggests that, while both CO and a-v̄DO 2 clearly interact to determine the V̇O 2 response, the speeding of V̇O 2 kinetics by prior high-intensity KE exercise is predominantly attributable to increases in a-v̄DO 2.Ībstract = "It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake (DO2.", After this, the contribution of a-v̄DO 2 to the V̇O 2 became increasingly more predominant: being responsible to an estimated 64% of the V̇O 2 speeding at 90 s, which rose to 100% by 180 s. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the V̇O 2 speeding at 10 and 30 s, respectively. The phase II V̇O 2 response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. 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 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. Nine healthy subjects volunteered to participate in this study. To clarify the roles of central O 2 delivery and/or peripheral O 2 extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O 2 content difference (a-v̄DO 2) to the V̇O 2) transient during repeated bouts of high-intensity knee extension (KE) exercise. It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake (V̇O 2) response at the onset of subsequent identical exercise.
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