Received November 28, 2006
Revised December 11, 2006
Accepted after revision December 13, 2006

¹ University of Leeds

^* To whom correspondence should be addressed. E-mail: b.whipp{at}leeds.ac.uk.

	Abstract

During moderate exercise (below the lactate threshold, _L), muscle CO₂ production (QCO₂) kinetics are mono-exponential, with a time constant () similar to that of O2 consumption. Following a delay incorporating the muscle-lung vascular transit time, QCO₂ is expressed at the lungs (VCO₂) with an appreciably-longer , reflecting the influence of intervening high-capacitance CO2 stores. Above _L, VCO₂ 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 VCO₂ relative to pulmonary O₂ uptake (VO₂) can be used to quantify _L validly if aerobic and hyperventilatory sources can be ruled out; i.e. then attributable to muscle and blood [HCO₃^-] decrease. In many cases, however, very rapid work-rate incrementation and/or prior CO₂-stores depletion (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 transient CO₂ stores wash-in.

Key Words: Carotid body, pH regulation, Ventilation

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