Persistence of expiratory flow limitations between normoxia and hypoxia

Introduction Expiratory flow limitation (EFL) refers to the inability to generate higher airflow despite greater respiratory effort and is common in both men and women. In normoxic condition, EFL is contingent upon an imbalance between ventilatory demands and capacity. Since hypoxia is known to alter ventilatory drive and pattern, it may influence the development of EFL. Therefore, the aim of this study was to investigate the origin of EFL in hypoxia and its repeatability and persistence during exercise in hypoxia. Method Fifty-one healthy active individuals (27 men and 24 women) performed a lung function test and a maximal incremental exercise test on a cycle-ergometer in normoxia and hypoxia (inspired oxygen fraction = 0.14) on two separate visits. Ventilatory capacity, assessed using the slope ratio (SR), were evaluated from maximal flow volume curve analyses. Results During exercise in normoxia, 28 participants exhibited EFL (55%). Another set of 28 participants exhibited EFL in hypoxia but they were not all the same individuals as those in normoxia. In normoxia, both SR and maximum minute ventilation (V̇E) were higher in the EFL group than the non-EFL group (p = 0.029 and p <0.001; respectively). However, in hypoxia, only maximum V̇E was higher in the EFL group compared to non-EFL group (p = 0.006). Participants were then classified into 4 groups according to the occurrence of EFL in both normoxia and hypoxia: non-EFL in both conditions (non-EFLN/H, n = 18), EFL in both conditions (EFLN/H, n = 23), EFL developed only in normoxia (EFLN+/H-, n = 5), EFL developed only in hypoxia (EFLN-/H+, n = 5). The EFLN+/H- group showed different V̇E changes between normoxia and hypoxia (-13.5 ± 7.8%) compared to the EFLN-/H+ (+6.7 ± 6.3%) and the non-EFLN/H groups (+5.1 ± 10.3%; p = 0.004 and p < 0.001, respectively). The difference with the EFLN/H (-1.7 ± 8.0%) did not reach significance (p = 0.057). Breathing frequency changes between normoxia and hypoxia were different between the EFLN-/H+ group (+4.6 ± 12.9%) and the EFLN+/H- group (-11.7 ± 13.1%) (p = 0.039). Normoxia to hypoxia decrease in maximal oxygen uptake was not significantly larger in the EFL N+/H- group (-18.4 ± 3.4%) than in the EFL EFLN-/H+ group (-10.3 ± 5.4%; p = 0.087). Discussion/Conclusion Hypoxia altered EFL development since there was a shift in the individuals who exhibited flow limitation between normoxia and hypoxia. This can be attributed to the extent of ventilatory reserve utilization. Specifically, those who developed EFL exclusively in hypoxia exhibited a significant increase in V̇E whereas those with EFL only in normoxia experienced a significant decrease in V̇E. Notably in hypoxia, the ventilatory capacity did not differ between individuals with EFL and those without. This observation suggests that in hypoxia, the development of EFL relied more on ventilatory demands than on ventilatory capacity.