Pulmonary oedema following exercise in humans

Abstract

Sub-clinical transient pulmonary oedema has been observed following exercise in both animals and, to some degree, humans. It has been proposed that transient pulmonary oedema, resulting from either pulmonary capillary leakage or capillary stress failure, may limit diffusion in the lung during and after exercise. Initially, to determine the minimal tolerable FIO2 for subsequent work in hypoxia, 10 aerobically trained males (VO2 max, 57.2 ± 7.95 mL·kg–1·min–1; age, 29.6 ± 5.8 y; height, 181.1 ± 8.3 cm; mass, 79.4 ± 5.6 kg) performed graded cycling work to maximal effort under 4 conditions of varying FIO2 (21%, 18%, 15%, and 12%) in a randomized blinded fashion. VO2 max and minimal SaO2 were significantly reduced while breathing 15% and 12% oxygen (VO2 max, 48.2 ± 7.9 and 31.5 ± 7.4 mL·kg–1·min–1, respectively). In the 12% oxygen condition, the majority of the subjects were not able to complete maximal exercise without SaO2 falling below 70%. Subsequently, to determine if transient pulmonary oedema occurs after sustained exercise, 10 highly trained male athletes (VO2 max, 65.0 ± 7.5 mL·kg–1·min–1; age, 25.9 ± 4.7 y; height, 184.1 ± 8.2 cm; mass, 79.4 ± 9.5 kg) underwent assessment of lung density by quantified magnetic resonance imaging before and 54.0 ± 17.2 and 100.7 ± 15.1 min after 60 min of cycling exercise (61.6% ± 9.5% VO2 max). The same 10 subjects underwent an identical measure before and 55.6 ± 9.8 and 104.3 ± 9.1 min after 60 min of cycling exercise (65.4% ± 7.1% hypoxic VO2 max) in hypoxia (FIO2 = 15.0%). Two subjects demonstrated mild exercise-induced arterial hypoxaemia (EIAH) (minSaO2 = 94.5% and 93.8%), and 7 demonstrated moderate EIAH (minSaO2 = 91.4% ± 1.1%) during a preliminary VO2 max test in normoxia. No significant differences (p < 0.05) were found in lung density after exercise in either condition. Mean lung densities, measured once pre- and twice post-exercise, were 0.177 ± 0.019, 0.181 ± 0.019, and 0.173 ± 0.019 g·mL–1 in the normoxic condition, and 0.178 ± 0.021, 0.174 ± 0.022, and 0.176 ± 0.019 g·mL–1 in the hypoxic condition. These results indicate that transient interstitial pulmonary oedema does not occur following sustained steady-state cycling exercise in normoxia or hypoxia. This diminishes the likelihood of pulmonary capillary leakage as a mechanism of transient pulmonary oedema, and, in turn, as a mechanism for changes in SaO2 during sustained exercise.