Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2847698 | Respiratory Physiology & Neurobiology | 2010 | 5 Pages |
To assess the effects of respiratory muscle training (RMT) on maximum oxygen uptake (V˙O2max) in normoxia and hypoxia, 9 healthy males (age 24 ± 4 years; stature 1.75 ± 0.08 m; body mass 72 ± 9 kg; mean ± SD) performed on different days maximal incremental tests on a cycle ergometer in normoxia and normobaric hypoxia (FIO2=0.11FIO2=0.11), before and after 8 weeks of RMT (5 days/week). During each test, gas exchange variables were measured breath-by-breath by a metabolimeter. After RMT, no changes in cardiorespiratory and metabolic variables were detected at maximal exercise in normoxia. On the contrary, in hypoxia expired and alveolar ventilation (V˙E and V˙A, respectively) at maximal exercise were significantly higher than pre-training condition (+12 and +13%, respectively; P < 0.05). Accordingly, alveolar O2 partial pressure (PAO2PAO2) after RMT significantly increased by ∼10%. Nevertheless, arterial PO2PO2 and V˙O2max did not change with respect to pre-training condition. In conclusion, RMT improved respiratory function but did not have any effect on V˙O2max, neither under normoxic nor hypoxic condition. In hypoxia, the significant increase in V˙E and V˙A at maximum exercise after training lead to higher alveolar but not arterial PO2PO2 values, revealing an increased A-a gradient. This result, according to the theoretical models of V˙O2max limitation, seems to contradict the lack of V˙O2max increase in hypoxia, suggesting a possible role of increased ventilation-perfusion mismatch.