Effect of respiratory muscle training on maximum aerobic power in normoxia and hypoxia

Multifactorial models of maximal oxygen consumption (VO2max) limitation imply that O2 transfer from ambient air to the alveoli, setting the ventilatory resistance (RV) to O2 flow, does not limit VO2max in normoxia in non-athletic healthy subjects. By contrast, in hypoxia RV may play a significant role in limiting VO2max. PURPOSE: To assess the effects of respiratory muscle training (RMT), as a means to reduce RV, on VO2max in normoxia and hypoxia. METHODS: Nine 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 = 0.11), before and after 8 weeks of RMT (5 days/week). During each test, gas exchange variables were measured breath-by-breath by a metabolimeter. RESULTS: 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 (VE and VA, respectively) at maximal exercise were significantly higher than pre-training condition (+12 and +13%, respectively; P<0.05). Accordingly, alveolar O2 partial pressure (PAO2) after RMT significantly increased by ~10%. Nevertheless, arterial PO2 and VO2max did not change with respect to pre-training condition. CONCLUSION: RMT ameliorated respiratory function but did not have any effect on VO2max, neither under normoxic nor hypoxic condition. In hypoxia, the significant increase in VE and VA at maximum exercise after training lead to higher and alveolar but not arterial PO2 values, suggesting an increased A-a gradient. This result, according to the theoretical models of VO2max limitation, seems to contradict the lack of VO2max increase in hypoxia, suggesting a possible role of increased ventilation-perfusion mismatch. Grant: Centro di Ricerca Alta Valtellina (CRAV), University of Milan, Italy.