Short-term hypoxic exposure at rest and during exercise reduces lung water in healthy humans

Abstract

Hypoxia and hypoxic exercise increase pulmonary arterial pressure, cause pulmonary capillary recruitment, and may influence the ability of the lungs to regulate fluid. To examine the influence of hypoxia, alone and combined with exercise, on lung fluid balance, we studied 25 healthy subjects after 17-h exposure to 12.5% inspired oxygen (barometric pressure = 732 mmHg) and sequentially after exercise to exhaustion on a cycle ergometer with 12.5% inspired oxygen. We also studied subjects after a rapid saline infusion (30 ml/kg over 15 min) to demonstrate the sensitivity of our techniques to detect changes in lung water. Pulmonary capillary blood volume (Vc) and alveolar-capillary conductance (D(M)) were determined by measuring the diffusing capacity of the lungs for carbon monoxide and nitric oxide. Lung tissue volume and density were assessed using computed tomography. Lung water was estimated by subtracting measures of Vc from computed tomography lung tissue volume. Pulmonary function [forced vital capacity (FVC), forced expiratory volume after 1 s (FEV(1)), and forced expiratory flow at 50% of vital capacity (FEF(50))] was also assessed. Saline infusion caused an increase in Vc (42%), tissue volume (9%), and lung water (11%), and a decrease in D(M) (11%) and pulmonary function (FVC = -12 +/- 9%, FEV(1) = -17 +/- 10%, FEF(50) = -20 +/- 13%). Hypoxia and hypoxic exercise resulted in increases in Vc (43 +/- 19 and 51 +/- 16%), D(M) (7 +/- 4 and 19 +/- 6%), and pulmonary function (FVC = 9 +/- 6 and 4 +/- 3%, FEV(1) = 5 +/- 2 and 4 +/- 3%, FEF(50) = 4 +/- 2 and 12 +/- 5%) and decreases in lung density and lung water (-84 +/- 24 and -103 +/- 20 ml vs. baseline). These data suggest that 17 h of hypoxic exposure at rest or with exercise resulted in a decrease in lung water in healthy humans.

Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists

“…Subjects exercised and recovered in hypoxia in an attempt to heterogeneously elevate pulmonary artery pressures and increase the probability of stress failure and/or leakage in the pulmonary capillaries. However, recent work by Snyder and colleagues demonstrated that rest and exercise in normobaric hypoxia actually caused a decrease in lung density and lung water, possibly caused by hypoxic stimulation of lymph flow from the lung (Snyder et al 2006). If lymphatic clearance rates were elevated to equal or exceed the rate of EVLW accumulation then an increase in lung density would not be measurable even during or immediately following exercise.…”

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

“…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).…”

Variability in pulmonary function following rapid altitude ascent to the Amundsen–Scott South Pole station

“…Interestingly, the magnitude of the epinephrine response to altitude was six times larger in individuals with decreased FEF 25-75 versus individuals with increased FEF 25-75 . Catecholamine upregulation has been associated with stimulation of b 2 -adrenergic receptors leading to enhanced fluid clearance from the alveoli via the epithelial sodium channels and from the interstitial space via the lymph system (Berthiaume et al 1987;Sartori et al 2002;Snyder et al 2006bSnyder et al , 2007. It is possible that the greater epinephrine response to altitude in individuals with decreased FEF 25-75 may be in response to other mediators or to the accumulation of fluid in these individuals.…”

“…However, previous studies suggest that acute normobaric hypoxia may actually cause a decrease in extravascular lung water possibly due to catecholamine stimulation of b 2 -adrenergic receptors leading to an increase in alveolar fluid clearance through stimulation of epithelial sodium channels (Sartori et al 2002;Snyder et al 2006bSnyder et al , 2007. Also, it has been suggested that the lungs are more resistant to edema than other organs due to specific pulmonary vasculature properties such as a less permeable endothelium lining in the pulmonary capillaries as well as restricted movement of electrolytes and proteins (Effros and Parker 2009).…”