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¹ Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK

Abstract

During moderate exercise (below the lactate threshold, _L), muscle CO₂ production () kinetics are monoexponential, with a time constant () similar to that of O₂ consumption. Following a delay incorporating the muscle–lung vascular transit time, is expressed at the lungs () with an appreciably longer , reflecting the influence of intervening high-capacitance CO₂ stores. Above _L, kinetics become complex, resulting from the conflation of the differing rates of HCO₃^– breakdown and degrees of compensatory hyperventilation with that of the underlying aerobic component. During incremental exercise, the increased rate of relative to pulmonary O₂ uptake () can be used to quantify _L validly if aerobic and hyperventilatory sources can be ruled out, i.e. _L is then attributable to the decrease in muscle and blood [HCO₃^–]. In many cases, however, very rapid incrementation of work rate and/or prior depletion of CO₂ stores (by volitional or anticipatory hyperventilation) can yield a ‘false positive’ non-invasive estimation of _L (‘pseudo-threshold’) resulting from a slowing of the rate of wash-in of transient CO₂ stores.

(Received 28 November 2006; accepted after revision 13 December 2006; first published online 21 December 2006)
Corresponding author B. J. Whipp: Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK. Email: b.whipp{at}leeds.ac.uk

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