Physiological consequences of the work of breathing and of inspiratory muscle training
A reduced blood lactate concentration ([lac-]B) is commonly observed during whole-body exercise following inspiratory muscle training (IMT). However, whether the inspiratory muscles are, in part, the source of these reductions remains unknown. Accordingly, this thesis investigated: (I) the contribution of the respiratory muscles to the systemic [lac-]B and (II) the effects of IMT upon inspiratory muscle lactate exchange and clearance. In addition, the thesis also evaluated the determinants of inspiratory muscle strength (maximal inspiratory mouth pressure; MIP). All subjects were healthy, active and free of pulmonary and respiratory muscle disease. Under resting conditions, 10 min intense volitional hyperpnoea at 85% of maximal exercise minute ventilation (VE max) increased [lac-]B by 0.96 mmol.L-1. This was attenuated by 25% following 6 wks IMT. 8 min volitional hyperpnoea at 90% VE max imposed upon exercise at the maximal lactate steady state (MLSS) increased [lac-]B by 0.99 mmol.L-1. Following 6 wk IMT, the steady state and hyperpnoea-mediated increase in [lac-]B were lower by 8 and 26%, respectively. Relative to pre-IMT, loading the trained inspiratory muscles using a low-intensity pressure threshold resistance (15 cmH2O) immediately following maximal exercise accelerated both lactate exchange and clearance capacities by ~70%.
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