Theories on the nature of the coupling between ventilation and gas exchange during exercise.

For over a century of creative research, many theories on the possible mechanisms controlling respiration during exercise have been developed and discussed. One of the most enduring questions is certainly related to the mechanisms that can prevent P(a)(CO(2)) rising when CO(2) production increases. As multiple systems and structures are capable of increasing ventilation (V (E)), not all the mechanisms controlling respiration can provide a proper answer to this question. Indeed, exercise is a complex physiological condition combining motor activity with a change in metabolic rate. The most intriguing aspect of exercise is that when the changes in metabolism are dissociated from the motor and locomotor activity, the strategy 'chosen' by the respiratory control system is to follow the metabolic rate (or more precisely factors temporally associated with the pulmonary gas exchange rate) regardless of the motor act. The strategy used by the respiratory system during exercise therefore appears to select from among various sources of information the most relevant to follow the rate at which CO(2) is ultimately exchanged by the lungs. Yet, the nature of the signal(s) which prevents CO(2)/H(+) disturbance during exercise is the fundamental question addressed by this simple observation and remains to be clarified. This review illustrates the attempts of many physiologists to collect experimental evidence for theories which could provide satisfactory mechanisms accounting for the matching between ventilation and the rate at which CO(2) leaves the tissues and is exchanged at the lungs. More recent models based on somatic information of circulatory origin are presented and discussed.