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Other than during sleep and contrived laboratory testing protocols, humans rarely exist in prolonged metabolic steady states; rather, they transition among different metabolic rates (V[spacing dot above]O2). The dynamic transition of V[spacing dot above]O2 (V[spacing dot above]O2 kinetics), initiated, for example, at exercise onset, provides a unique window into understanding metabolic control. This brief review presents the state-of-the art regarding control of V[spacing dot above]O2 kinetics within the context of a simple model that helps explain the work rate dependence of V[spacing dot above]O2 kinetics as well as the effects of environmental perturbations and disease. Insights emerging from application of novel approaches and technologies are integrated into established concepts to assess in what circumstances O2 supply might exert a commanding role over V[spacing dot above]O2 kinetics, and where it probably does not. The common presumption that capillary blood flow dynamics can be extrapolated accurately from upstream arterial measurements is challenged. From this challenge, new complexities emerge with respect to the relationships between O2 supply and flux across the capillary-myocyte interface and the marked dependence of these processes on muscle fiber type. Indeed, because of interfiber type differences in O2 supply relative to V[spacing dot above]O2, the presence of much lower O2 levels in the microcirculation supplying fast-twitch muscle fibers, and the demonstrated metabolic sensitivity of muscle to O2, it is possible that fiber type recruitment profiles (and changes thereof) might help explain the slowing of V[spacing dot above]O2 kinetics at higher work rates and in chronic diseases such as heart failure and diabetes.

(C)2008The American College of Sports Medicine