Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema

Abstract

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (Vo2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 +/- 7.4 and 100.7 +/- 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 +/- 9.5% Vo2 max) and 55.5 +/- 9.8 and 104.3 +/- 9.1 min following 60 min cycling exercise in H (intensity = 65.4 +/- 7.1% hypoxic Vo2 max), where Vo2 max = 65.0 +/- 7.5 ml x kg(-1) x min(-1) (N) and 54.1 +/- 7.0 ml x kg(-1) x min(-1) (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 +/- 1.1%) as measured noninvasively during the Vo2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 +/- 0.019, 0.181 +/- 0.019, and 0.173 +/- 0.019 g/ml (N) and 0.178 +/- 0.021, 0.174 +/- 0.022, and 0.176 +/- 0.019 g/ml (H), respectively. No significant differences (P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.

Early subclinical increase in pulmonary water content in athletes performing sustained heavy exercise at sea level: ultrasound lung comet-tail evidence

“…Hodges et al (18) showed no changes in pulmonary density, which increases in the presence of extravascular lung water, following normoxic and hypoxic midintensive exercise. Conversely, Hopkins (19) demonstrated the presence of red cells, proteins, and leukotriene B4 in the bronchoalveolar lavage after brief maximal sea level exercise, suggesting the occurrence of transient increase in pulmonary blood-gas barrier permeability.…”

“…pulmonary edema EVEN IN HEALTHY SUBJECTS EXTREMELY demanding endurance exercise leads to functional and structural cardiac and pulmonary changes, along with local and systemic responses, reflecting oxidative, metabolic, hormonal, and thermal stress, besides immunomodulation and inflammatory reaction (4,30,32,40,41,46). Whether interstitial pulmonary edema occurs in athletes performing heavy sea level exercise is debated (2,6,12,18,19,27,28,44,56). Interstitial pulmonary edema has been documented in endurance athletes performing heavy sea level exercise, using imaging techniques such as chest X-ray, magnetic resonance, computed tomography, and scintigraphy (17,36,56).…”

“…letes performing heavy sea level exercise is debated (2,6,12,18,19,27,28,44,56). Interstitial pulmonary edema has been documented in endurance athletes performing heavy sea level exercise, using imaging techniques such as chest X-ray, magnetic resonance, computed tomography, and scintigraphy (17,36,56).…”

Lung injury related to extreme environments

“…While some controversy exists on the presence of exercise-induced pulmonary oedema [24][25][26], numerous case reports demonstrate the presence of pulmonary oedema after prolonged or high-intensity exercise [27], which, upon further evaluation, appears to be unrelated to abnormal cardiac function. Evidence for pulmonary oedema has been shown in competitive rowers [28], during exertion in dry cold environments and in cases of emotional stress and sexual intercourse [29], in addition to long distance runners and triathletes [30][31][32][33][34][35][36][37][38][39][40] and competitive cyclists [41,42].…”

Genetic variation of αENaC influences lung diffusion during exercise in humans

“…Given similar clinical and environmental parameters, exposure to intense prolonged exercise, exposure to high altitude, or development of heart failure can all lead to pulmonary edema in some, but not all, individuals (Caillaud et al, 1995; Hopkins et al, 1997). However, not all sojourners to high altitude, athletes, or patients with heart failure show evidence for pulmonary edema, suggesting a genetic component to one’s susceptibility to pulmonary edema formation (Guenette et al, 2007; Hodges et al, 2007; Hopkins et al, 1997; McKenzie et al, 2005). While lung fluid accumulation is primarily passive and follows Starling’s law, lung fluid clearance is an active process involving several pathways including activation of the amiloride sensitive epithelial sodium channel (ENaC).…”