Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Abstract

A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.

Evidence of Exercise-Induced Arterial Hypoxemia in Prepubescent Trained Children

“…In the H group, SaO 2 was lower than in the NH group from 25% up to 100% of maximal power and was significantly decreased from resting values from 75%, which is in agreement with previous studies in adults (26,27). Indeed, Rice et (27) reported significantly higher values of alveolar to arterial difference in oxygen pressure from 30% V O 2max in subjects who exhibited gas exchange disturbance than in control subjects.…”

“…A major mechanism in EIAH in adults is a ventilatory limitation during exercise, termed relative hypoventilation (5,7). In adults, the submaximal decrease in SaO 2 seems explained by a relative hypoventilation associated with a V A/Q c mismatch (26,27) V A/Q c mismatch was not measured in the present study; however, we found lower values of ⌬V E /⌬V CO 2 during submaximal exercise in hypoxemic children (Fig. 2).…”

“…V E , VT, f), PetO 2 , and PetCO 2 during exercise, which led us to be very cautious with the interpretation of the lower ⌬V E /⌬V CO 2 in hypoxemic subjects during submaximal exercise. In addition, this suggests that other mechanisms as V A/Q c mismatch, which increases with low lung capacity (9), could be involved in early onset of the differences in SaO 2 between hypoxemic and nonhypoxemic children (26,27). Obviously, these speculations need further investigation.…”

Inspiratory muscle warm-up does not improve cycling time-trial performance

“…This participant also experienced marked increases in PCO 2 (sometimes reaching 60 mm Hg), indicative of inadequate hyperventilation. Indeed, desaturation during submaximal (40% 2 O V  max) exercise has been reported previously in trained cyclists and is attributed to an inadequate hyperventilatory response (Rice et al 1999). …”

Exercise-induced arterial hypoxemia in aerobic and anaerobic trained athletes during incremental exercise

“…Studies examining EIAH have primarily focused on aerobic trained individuals [4,8,[12][13][14][15][16][17][18]. Interestingly, no studies have examined the EIAH in anaerobic trained athletes.…”