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

During moderate exercise ( below the lactate threshold, theta(L)), muscle CO2 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, QCO(2) is expressed at the lungs (V-CO2) with an appreciably longer t, reflecting the influence of intervening high-capacitance CO2 stores. Above theta(L), V-CO2 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. V-CO2 relative to pulmonary O-2 uptake (V-O2) can be used to quantify theta(L) validly if aerobic and hyperventilatory sources can be ruled out, i.e. theta(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 theta(L) (pseudo-threshold') resulting from a slowing of the rate of wash-in of transient CO2 stores.