In response to ramp exercise, changes in ventilation, gas exchange and arterial blood gases, which are closely interrelated, reflect the two roles of ventilation: 1) providing O(2) and eliminating metabolic CO(2) (from rest to maximal exercise); and 2) contributing to acid-base balance by eliminating non metabolic CO(2) from the alkaline reserve (from the first ventilatory threshold [VT(1)] to maximal exercise). Hyperpnea before VT(1) increases gas exchanges as needed for aerobic metabolism without large changes in ventilatory equivalent of O(2) and CO(2) (VE/V(O2) or VE/V(CO2)), in P(O2) and P(CO2) in alveoli or arterial blood (except for a small widening of alveolo-arterial P(O2) gradient), and in bicarbonate concentration. In contrast, above VT(1), CO(2) is washed-out from the alkaline reserve due to the combined effect of the fall in PA(CO2) (because of hyperventilation) and in pH, and this helps maintaining acid-base balance. Pa(CO2) and bicarbonate concentration decrease while PA(O2) and VE/V(O2) increase, and V(CO2), which follows VE, becomes higher than V(O2). In healthy young subjects, but very seldom in patients, the end of exercise can occur after a second ventilatory threshold (VT(2)), which is the zone where the increase in V(CO2) fails to follow that in VE in spite of hyperventilation and acidosis because of the progressive depletion of the alkaline reserve.