PULMONARY GAS-EXCHANGE AND BREATHING PATTERN DURING AND AFTER EXERCISE IN HIGHLY TRAINED ATHLETES

Highly trained athletes (HT) have been found to show arterial hypoxaemia during strenuous exercise. A lack of compensatory hyperpnoea and/or a limitation of pulmonary diffusion by pulmonary interstitial oedema have been suggested as causes, but the exact role of each is not clear. It is known, however, that interstitial pulmonary oedema may result in rapid shallow breathing (RSB). The purpose of this study was therefore twofold:firstly, to determine the exact role of a lack of compensatory hyperpnoea versus a widened in ideal alveolar minus arterial oxygen partial pressure difference [P-A(i-a)O-2] in the decrease in partial pressure of oxygen in arterial blood (PaO2) and, secondly, to detect RSB during recovery in HT. Untrained subjects (UT) and HT performed exhausting incremental exercise. During rest, exercise testing, and recovery, breathing pattern, respiratory gas exchange, and arterial blood gases were measured. The P-A(i-a)O-2 and the difference in tidal volume (V-T) between exercise and recovery for the same level of ventilation, normalized to vital capacity of the subject [Delta V-T(%VC)], were then calculated. A large positive Delta V-T(%VC) was considered to be the sign of RSB. HT showed a marked hypoxaemia (F=11.6, P<0.0001), higher partial pressure of carbon dioxide in arterial blood (F=3.51, P<0.05), and lower ideal partial pressure of oxygen in alveolar gas (P<0.001). The relationship between P-A(i-a)O-2 and oxygen consumption was the same for the two groups. The widening P-A(i-a)O-2 persisted throughout recovery for both HT and UT. The RSB was observed in HT during recovery. These results would suggest that the lack of compensatory hyperpnoea in HT during submaximal exercise was the major factor in the decrease in PaO2. The RSB and the widening P-A(i-a)O-2 during recovery would suggest that interstitial pulmonary oedema was involved during the strenuous exercise in the case of HT. Lastly, the wide P-A(i-a)O-2 observed in UT during recovery would suggest that an increase in extravascular pulmonary water may also have been involved for these subjects, although to a lesser extent.