Inspiratory muscle training lowers the oxygen cost of voluntary hyperpnea

Nevner at innpustmuskel trening gir mindre oksygenbehov under trening og dermed mer utholdenhet. Innpustmuskler bruker opp mye av oksygenet kroppen trenger under trening så med svak pustefunksjon blir man fort sliten. Under maksimal trening krever pustemusklene 15% av oksygenet, men med pustetrening synker det til 8%. Den nevner at diafragma og pustemuskler blir sterkere og større. Den henviser også til studier som nevner at det gir mindre melkesyre. Noe av effekten kommer også av at man får en større reserve i lungene ved å øke inn- og utpust styrken.

IMT significantly reduced the O2 cost of voluntary hyperpnea, which suggests that a reduction in the O2 requirement of the respiratory muscles following a period of IMT may facilitate increased O2 availability to the active muscles during exercise. These data suggest that IMT may reduce the O2cost of ventilation during exercise, providing an insight into mechanism(s) underpinning the reported improvements in whole body endurance performance; however, this awaits further investigation.

THE OXYGEN COST of breathing or energy requirement of the respiratory muscles are shown to increase relative to the level of ventilation (V̇E) and the work of breathing (Wb) (1, 8). During moderate-intensity exercise the respiratory musculature requires ∼3–6% of total oxygen consumption (V̇O2T), increasing to ∼10–15% at maximal exercise (1, 3).

Inspiratory muscle training (IMT) is an intervention that has been associated with improvements in whole body exercise performance (24, 31, 34), enhanced pulmonary oxygen uptake kinetics (5), reduced blood lactate concentrations (6, 24), diaphragmatic fatigue, and cardiovascular responsiveness (37).

The oxygen cost of voluntary hyperpnea (V̇O2RM) and V̇O2RM expressed as a percentage of total oxygen consumption (V̇O2T) graphed against V̇E at low (50% V̇O2 max), moderate (75% V̇O2 max), and high (100% V̇O2 max) exercise intensities for both IMT (A) and CON (B) groups, pre- and post-training (means ± SE).
•, Pre-IMT;
○, post-IMT;
▴, pre-CON;
Δ, post-CON.

To our knowledge this study is the first to investigate the influence of IMT on the oxygen cost of voluntary hyperpnea. The main findings of the present study are that the relationship between increasing ventilatory workloads and the O2 cost of voluntary hyperpnea is curvilinear in trained cyclists and that 6 wk of pressure threshold IMT significantly reduced the O2 cost of V̇E at high ventilatory workloads. Importantly, the finding that V̇O2RM is reduced at a V̇E above 50% V̇O2 max suggests that IMT may reduce the energy requirements of the respiratory musculature in maintaining a given V̇E.

The increase in energy expenditure as V̇E increases can be attributed to a variety of sources of respiratory muscle work, including the elastic recoil of the chest and lung wall, airway resistance (4,15), increased EELV (9), and high muscle shortening velocities (19, 23). It has been suggested that as tidal breathing approaches the maximal limits for inspiratory muscle pressure development and expiratory flow rates, energy expenditure may increase to overcome the additional respiratory muscle work (3). Conversely, if one or more of the additional sources of respiratory muscle work are reduced as a result of IMT, it is reasonable to suggest that the increase in the O2 cost maybe attenuated.

In the present study, following 6 wk of IMT, V̇O2RM was significantly reduced from pretraining values at submaximal and maximal levels of ventilation. The O2 cost of voluntary hyperpnea expressed as a percentage of V̇O2T was reduced by 1.5% at a V̇Ecorresponding to 75% V̇O2max following IMT. The greatest reduction in the O2 cost of voluntary hyperpnea was observed at V̇O2 max, where V̇O2RM was significantly reduced from 11% of V̇O2T to 8% V̇O2T following IMT.

Increased ventilatory demand was previously shown to elicit a sympathetically mediated metaboreflex (33), which increases heart rate and mean arterial pressure (MAP), reducing blood flow to the limb locomotor muscles during exercise (16) and potentially reducing whole body endurance performance (18). Furthermore, Witt et al. (37) showed that IMT attenuates this increase in HR and MAP, presumably by reducing or delaying the sympathetically mediated reflex.

The 22% increase in respiratory muscle strength shown in the present study is similar in magnitude to those previously reported using pressure-threshold IMT (11, 22, 30, 32, 37). Respiratory muscle structure has also been shown to change following IMT, with an increase in diaphragm thickness (11, 12) and hypertrophy of type II muscle fibers of the external intercostal muscles (27) being reported.

Aaron et al. (3) demonstrated that individuals who reached their reserve for expiratory flow and inspiratory muscle pressure development required 13–15% of V̇O2T compared with ∼10% of V̇O2T for non-flow-limited individuals. Thus, an increase in maximal expiratory flow rates or inspiratory pressure development would increase the ventilatory reserve, thereby increasing the maximal limits for ventilation.

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