| Summary: | Minute ventilation (VE, and its pattern) is the result of an interaction between the drive to breathe (from the respiratory controller) and the mechanical properties of the respiratory system. While there is abundant information about the chemoreceptor based control of exercise V E, the present studies were designed to examine the roles of other neuro-mechanical stimuli from the airways, lungs, chest wall, respiratory muscles and/or the limbs in healthy humans performing constant work-rate heavy exercise (CWHE) or maximal incremental exercise (MIE) on a cycle-ergometer. With increasing V E during CWHE, there was a progressive increase in inspiratory (I) and a relatively greater increase in expiratory (E) muscle pressures (Pmus ). Furthermore, the Total Pmus (I + E) - VE and inspiratory tension time index - VE relationships were significantly linear, while post-inspiratory inspiratory activity decreased progressively throughout CWHE. However, when the load on all the respiratory muscles was significantly reduced With flow-proportional mouth pressure assist) throughout CWHE, there was no effect on VE (or breathing pattern) or other metabolic variables and on exercise performance. These results differ from the hyperventliatory response that results when airflow resistance is reduced with heliox (HeO2) substituted for air as the breathing mixture. The results suggest that receptors from large and central airways play a major role in the mediation of the transient, but not the sustained V E response to HeO2 breathing during exercise. However, airway receptors do not appear to be involved in the mediation of VE and breathing pattern responses during MIE, or affect the ventilatory and breathing pattern adaptations to added external deadspace during exercise. While some subjects developed spontaneous locomotor-respiratory coupling (LRC, manifesting as entrainment of breathing to pedalling frequency, coupling of I and/or E to limb movements) when pedalling freely (without imposed or fixed pedalling roles), LRC had no effect on VE for breathing pattern) control or metabolic variables throughout MIE. It is concluded that ventilatory control during exercise in humans, is the result of the integration of a variety of numerous and apparently "redundant" stimuli and is ultimately directed towards optimal gas exchange and maintenance of acid-base homoeostasis, while minimizing both respiratory muscle work and the oxygen cost of breathing.
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