The control of the exercise hyperpnoea
A relatively recent proposal suggests that a plastic element to the ventilatory control system might be held accountable for the experimentally observed matching of VE to VCO2. That is, Martin and Mitchell (1993) reported that goats consistently over-breathed during treadmill exercise, following conditioning to treadmill exercise while breathing through an external dead space. This has been taken as evidence that the steady-state ventilatory response can be modulated. Therefore, the existence of a similar mechanism in the human exercise hyperpnoea was investigated; replicating as closely as possible the study of Martin and Mitchell (1993). Furthermore, the requirement for such a mechanism was investigated by studying the control of the exercise hyperpnoea in the absence of such a 'learned-response'. The results show no evidence of plasticity during phase II or phase III of the exercise ventilatory response under normal conditions. Furthermore, subjects devoid of any exercise experience were able to generate an appropriate, in terms of PaCO2 regulation, ventilatory response during sub-lactate threshold cycle ergometer exercise. Therefore, under the conditions of the study, no requirement for an 'exercise-memory' in the genesis of a 'normal' exercise hyperpnoea could be found. In conclusion, there appears to be no primary role for respiratory plasticity in the control of the exercise hyperpnoea.