Muscular exercise imposes the most potent sustained stress to cellular energetics. At work rates below the anaerobic threshold (i.e. no sustained lactic acidosis), the ventilatory and cardiovascular responses regulate arterial PCO2, [H+] and PO2 at or close to their resting levels in the steady state. However, dynamic forcing and systems-analytic techniques reveal two phases of the non-steady-state response dynamics. In the first phase, increased gas flow to the lungs results solely from increased pulmonary blood flow, with alveolar gas tensions being maintained at their resting levels by a coupled increase in ventilation (VE): evidence for cardiopulmonary coupling being provided by experimentally-altered in man and dog. Arterial chemoreception does not impose humoral feedback control in this phase. Rather, rapid feedforward mechanisms operate, with both intrathoracic (largely cardiac) and exercising-limb mechanoreception proposed as afferent sources. In the second phase, cardiogenic gas flow to the lungs is augmented by altered mixed venous blood gas contents; ventilation responding exponentially with a time constant (tau) which is an inverse function of carotid body gain. The close dynamic coupling of VE with CO2 output (tau VE tau TVCO2) in this phase results in arterial PCO2 and [H+] being maintained close to their resting levels. However, the kinetic dissociation between VE and O2 uptake, with tau VE much greater than tau VO2, leads to an appreciable transient fall of arterial PO2. The respiratory compensation for the sustained lactic acidosis at higher work rates is predominantly mediated by the carotid bodies in man: the aortic bodies subserving no discernible role. Control of the respiratory and circulatory responses to exercise is therefore mediated by both neural and humoral mechanisms: and an important control link appears to couple the responses, via feedforward ventilatory control of cardiac origin.