Below the lactate threshold ((thetaL)), ventilation (V(E))responds in close proportion to CO(2) output to regulate arterial partial pressure of CO(2) (PaCO2). While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic 'coupling' between and V(E) and V(CO2). Above (thetaL), PaCO2 is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, probably of carotid body origin. When V(E) requirements are high (as in highly fit endurance athletes), V(E) can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power, which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance.