EFFECTS OF 2 SUCCESSIVE MAXIMAL EXERCISE TESTS ON PULMONARY GAS-EXCHANGE IN ATHLETES

Citation
Cf. Caillaud et al., EFFECTS OF 2 SUCCESSIVE MAXIMAL EXERCISE TESTS ON PULMONARY GAS-EXCHANGE IN ATHLETES, European journal of applied physiology and occupational physiology, 74(1-2), 1996, pp. 141-147
Citations number
26
Categorie Soggetti
Physiology
ISSN journal
03015548
Volume
74
Issue
1-2
Year of publication
1996
Pages
141 - 147
Database
ISI
SICI code
0301-5548(1996)74:1-2<141:EO2SME>2.0.ZU;2-G
Abstract
Pulmonary extravascular water accumulation may be involved in exercise -induced hypoxaemia in highly aerobically trained athletes. We hypothe sized that if such an alteration were present in elite athletes perfor ming a maximal exercise test, the impairment of gas exchange would be worse during a second exercise test following the first one. Eight mal e athletes performed two incremental exercise tests separated by a 30- min recovery period. Pulmonary gas exchange and ventilatory data were measured during exercise tests performed in normoxia. Arterial blood s amples were drawn each minute during rest, exercise, and recovery. Pul monary diffusing capacity for CO (DLCO) was measured at rest, after th e first (T1) and the second (T2) test. All the subjects underwent a sp irometric test at rest and after T2. Maximal and recovery data for O-2 uptake and minute ventilation were not statistically different betwee n T1 and T2. Partial pressure of arterial O-2 (PaO2) decreased during both tests but was lower during T2 for rest, 60 W, and 120 W (P <0.02) . Alveolar-arterial difference in partial pressure of O-2 (PA-aO2) inc reased during both the tests but was significantly larger during T2 fo r rest, 60 W, and 120 W (P <0.01). The PaO2 and PA-aO2 data at maximal exercise were not significantly different between T1 and T2. Compared to rest, PA-aO2 remained significantly larger during recovery for bot h T1 and T2 (P <0.0001). The PA-aO2 during T2 recovery was larger than T1 recovery (P <0.008). Spirometric data did not change. The DLCO mea surements after T1 and T2 were not significantly different from rest. These results showed an alteration of PaO2 and PA-aO2 during T1, which tended to be worse during and after T2: however, these data do not al low us to make a definitive statement as to the cause of the hypoxaemi a. Our study confirmed that exhausting exercise caused hypoxaemia. It also demonstrated that the disturbance in pulmonary gas exchange persi sted for at least 30 min following the end of the exercise period and became worse during submaximal intensities of the following incrementa l exercise test.