2] values in the OWAS group, judged from a clinical basis, were either elevated (TM trial) or borderline elevated (Sit CE trial) (50).
However, in general, since we observed no marked evidence of altered ventilation variables with submaximal (Table 2) or maximal exercise (Table 3), inappropriate dyspnea, or observable cyanosis, we conclude that there was no evidence of an increased work of breathing or gas exchange impairment in the OWAS group (40,50).
Consistent with the lack of exercise ventilation impairments in the OWAS group was that the post exercise spirometry values (Figure 3), notably the FEV1.
Thus, a few members of our OWAS group should have demonstrated EIB.
2] pulse of the NWNL group were substantially and consistently greater than the OWAS group (Figure 1 & Table 3).
Mathematically, in support of the OWAS having decreased aerobic fitness, their composite V[O.
2] max findings between these last two cited studies and our study are due to our OWAS subjects being more deconditioned.
The steady-state submaximal trial (Figure 2) illustrates that the oxygen kinetics (23) of the OWAS group was parallel to, but simply lower in magnitude, than the NWNL group throughout the trial.
It would have been of great value to know if the OWAS airway inflammation level was similar to the NWNL values and also to determine if GXT increased airway inflammation in the OWAS over the NWNL (8).