title: Muscle O2 uptake kinetics in humans: implications for metabolic control.
abstract: Muscle O2 uptake (VO2) kinetics in response to an augmented energetic requirement (on-transition) has never been directly determined in humans. We have developed a constant-infusion thermodilution technique that allowed rapid measurements of leg blood flow (Qleg) and, in conjunction with frequent serial measurement of arteriovenous O2 content difference across the leg [(Ca - Cv)O2leg], permitted the determination of the VO2 of the leg (VO2leg) at 3- to 4-s time intervals. VO2leg kinetics during the on-transition was taken as a close approximation of muscle VO2 (VO2mus) kinetics. Alveolar VO2 (VO2A), Qleg, leg O2 delivery [(Q.CaO2leg)], (Ca - Cv)O2leg, and VO2leg kinetics were determined in six trained subjects [age 22.8 +/- 4.4 (SD) yr; maximal O2 uptake 59.1 +/- 5.3 ml.kg-1.min-1] during the transition from unloaded pedaling to a workload (loaded pedaling; LP) (183 +/- 20 W) well below the previously determined ventilatory threshold. For all variables, two distinct phases were recognized. During the first 10-15 s of loaded pedaling (phase I), VO2A, Qleg, and (Q.CaO2)leg increased rapidly, whereas VO2leg increased only slightly and (Ca - Cv)O2leg actually decreased. After phase I, all variables showed a monoexponential increase (phase II), with similar time courses [slightly faster for (Ca - CV)O2leg]. In a consideration of both phases, the half times of the responses among variables were not significantly different: 25.5 +/- 2.6 s for VO2A, 26.6 +/- 7.6 s for Qleg, 26.9 +/- 8.3 s for (Q.CaO2leg, 23.5 +/- 1.3 s for (Ca - Cv)O2leg, and 27.9 +/- 5.7 s for VO2leg. We conclude that during the on-transition the kinetics of VO2A and VO2leg, as measured by these methods, are similar. The analysis of the early phase (first 10-15 s) of the on-transition indicates that bulk delivery of O2 to the working muscles is not limiting VO2leg kinetics. However, the present results cannot discriminate between maldistribution of blood flow/VO2 vs. inertia the intracellular oxidative machinery as the limiting factor.
authors.affiliation: Department of Medicine, University of California, San Diego, La Jolla 92093-0623, USA.
authors.forename: B
authors.initials: B
authors.lastname: Grassi
authors.forename: D C
authors.initials: DC
authors.lastname: Poole
authors.forename: R S
authors.initials: RS
authors.lastname: Richardson
authors.forename: D R
authors.initials: DR
authors.lastname: Knight
authors.forename: B K
authors.initials: BK
authors.lastname: Erickson
authors.forename: P D
authors.initials: PD
authors.lastname: Wagner
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D006801:Humans; D007700:Kinetics; D008297:Male; D009132:Muscles / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D013997:Time Factors
chemical_list: D010100:Oxygen