Effects of maximal interval training on arterial oxygen desaturation and ventilation during heavy exercise.
The purpose of the present study was to clarify longitudinally the effects of exercise training on arterial O(2) 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 O(2) uptake (V(.)(O(2 max))), interspersed with 2-min recovery period cycling at 50% V(.)(O(2 max)). During the training, V(.)(O(2 max)), Sa(O(2)), the ventilatory equivalent for oxygen (V(.)E/V(.)(O(2))), and the end-tidal partial pressure of O(2) (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 V(.)(O(2 max)), with little change in V(.)E(max) and pulmonary functions at rest. The training decreased PET(O(2)), V(.)E/V(.)(O(2)), and Sa(O(2)) during heavy exercise. Sa(O(2)) is significantly related to V(.)E/V(. )(O(2)) (r(2) = 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 O(2) desaturation during heavy exercise. PET(O(2)) as well as V(.)E/V(.)(O(2)) and V(.)(O(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))-V(.)E/V(.)(O(2)) 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 V(.)E/V(.)(O(2)) ( approximately 30 ml.ml(-1)), the Sa(O(2)) of the trained subjects exercising at a higher V(.)(O(2)) level was lower than that of the control subjects. Predominance of less hyperventilation and another factor, increased A-aDO(2), in the genesis of arterial hypoxemia and O(2) desaturation may be dependent upon V(.)(O(2)) levels in heavy exercise and the state of training.