We examined the effects of inspiratory muscle training (IMT) upon volitional hyperpnoea-mediated increases in blood lactate ([lac−]B) during cycling at maximal lactate steady state (MLSS) power, and blood lactate and oxygen uptake kinetics at the onset of exercise. Twenty males formed either an IMT (n = 10) or control group (n = 10). Prior to and following a 6-week intervention, two 30 min trials were performed at MLSS (207 ± 28 W), determined using repeated 30 min constant power trials. The first was a reference trial, whereas during the second trial, from 20 to 28 min, participants mimicked the breathing pattern commensurate with 90% of the maximal incremental exercise test minute ventilation (\documentclass[12pt]{minimal}
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\begin{document}$$ \dot{V}_{\text{E}} $$\end{document}). Prior to the intervention, the MLSS [lac−]B was 3.7 ± 1.8 and 3.9 ± 1.6 mmol L−1 in the IMT and control groups, respectively. During volitional hyperpnoea, \documentclass[12pt]{minimal}
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\begin{document}$$ \dot{V}_{\text{E}} $$\end{document} increased from 79.9 ± 9.5 and 76.3 ± 15.4 L min−1 at 20 min to 137.8 ± 15.2 and 135.0 ± 19.7 L min−1 in IMT and control groups, respectively; [lac−]B concurrently increased by 1.0 ± 0.6 (+27%) and 0.9 ± 0.7 mmol L−1 (+25%), respectively (P < 0.05). Following the intervention, maximal inspiratory mouth pressure increased 19% in the IMT group only (P < 0.01). Following IMT only, the increase in [lac−]B during volitional hyperpnoea was abolished (P < 0.05). In addition, the blood lactate (−28%) and phase II oxygen uptake (−31%) kinetics time constants at the onset of exercise and the MLSS [lac−]B (−15%) were reduced (P < 0.05). We attribute these changes to an IMT-mediated increase in the oxidative and/or lactate transport capacity of the inspiratory muscles.