Physiological mechanisms dissociating pulmonary CO2 and O2 exchange dynamics during exercise in humans.

During moderate exercise (below the lactate threshold, (thetaL)), muscle CO(2) production ( Q(CO2)) kinetics are monoexponential, with a time constant (tau) similar to that of O(2) consumption. Following a delay incorporating the muscle-lung vascular transit time, Q(CO2) is expressed at the lungs (V(CO2)) with an appreciably longer tau, reflecting the influence of intervening high-capacitance CO(2) stores. Above (thetaL), kinetics become complex, resulting from the conflation of the differing rates of HCO(3)(-) breakdown and degrees of compensatory hyperventilation with that of the underlying aerobic component. During incremental exercise, the increased rate of relative to pulmonary O(2) uptake (V(CO2)) can be used to quantify (thetaL) validly if aerobic and hyperventilatory sources can be ruled out, i.e. (thetaL) is then attributable to the decrease in muscle and blood [HCO(3)(-)]. In many cases, however, very rapid incrementation of work rate and/or prior depletion of CO(2) stores (by volitional or anticipatory hyperventilation) can yield a 'false positive' non-invasive estimation of (thetaL) ('pseudo-threshold') resulting from a slowing of the rate of wash-in of transient CO(2) stores.