The purpose of the present study was to clarify longitudinally the effects of exercise training on arterial O2 saturation (Sa(O)2) and ventilation during heavy exercise. A group of six subjects (training group) volunteered to train four times a week for 12 weeks. Each training session consisted of five 3-min periods of exercise on a cycle ergometer at a power output of 100% maximal O2 uptake (V̇O(2 max)), interspersed with 2 min recovery period cycling at 50% V̇O(2 max). During the training, V̇O(2 max), Sa(O)2, the ventilatory equivalent for oxygen (V̇E/V̇O2), and the end- tidal partial pressure of O2 (PET(O)2) during heavy exercise were measured periodically. The same parameters were measured simultaneously in another group of five subjects (control group) who led normal lives. Maximal interval training increases V̇O(2 max), with little change in V̇E(max) and pulmonary functions at rest. The training decreased PET(O)2, V̇E/V̇O2, and Sa(O)2 during heavy exercise. Sa(O)2 is significantly related to V̇E/V̇O2 (r2 = 0.49). These results suggest that less hyperventilatory response to exercise occurs with progress in physical training because the adaptability of ventilatory capacity is less than that of aerobic work capacity, which half induces arterial O2 desaturation during heavy exercise. PET(O)2 as well as V̇E/V̇O2 and V̇O(2 max) did not change anymore after the 6th week, nevertheless Sa(O)2 kept decreasing up to the last 2 weeks. In addition, when the Sa(O)2-V̇E/V̇O2 plot was compared between the two groups, the regression line of the training group was steeper than that of the control groups; i.e., compared at a lower level of V̇E/V̇O2 (~30 ml · ml-1), the Sa(O)2 of the trained subjects exercising at a higher V̇O2 level was lower than that of the control subjects. Predominance of less hyperventilation and another factor, increased A-aDO2, in the genesis of arterial hypoxemia and O2 desaturation may be dependent upon V̇O2 levels in heavy exercise and the state of training.
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