Med pustetrening blir melkesyrekonsentrasjonen lavere under trening. 2 studier her, første fra 2008 og den andre fra 2012.
Den første nevner at melkesyre synker med opptil 59% (25+34%)
Although reduced blood lactate concentrations ([lac(-)](B)) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction.
After 6 weeks, increases in [lac(-)](B) during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac(-)](B) during volitional hyperpnoea was reduced by 17 +/- 37% and 25 +/- 34% following 8 and 10 min, respectively (P < 0.05).
These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac(-)](B), often observed during whole-body exercise.
Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise.
Den andre viser til en 15% laver melkesyrekonsentrasjon og at årsaken er pustemusklenes evne til å fjerne det.
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.