The effect of sustained heavy exercise on the development of pulmonary edema in trained male cyclists

Abstract

To determine whether intense, prolonged activity can induce transient pulmonary edema, eight highly trained male cyclists (mean ± S.D.: age, 26.9 ± 3.0 years; height, 179.9 ± 5.7 cm; weight, 76.1 ± 6.5 kg) performed a 45-min endurance cycle test (ECT). ${\dot{V}}_{{\text{O}}_2\text{,max}}$ was determined (4.84 ± 0.4 L min⁻¹, 63.7 ± 2.6  ml min⁻¹ g⁻¹) and the intensity of exercise for the ECT was set at 10% below ventilatory threshold (∼76% ${\dot{V}}_{{\text{O}}_2\text{,max}}$ 300 ± 25 W). Pre- and post-exercise pulmonary diffusion (DL_CO) measurements and magnetic resonance imaging of the lung were made. DL_CO and pulmonary capillary blood volume (VC) decreased 1 h post-exercise by 12% (P = 0.004) and 21% (P = 0.017), respectively, but no significant change in membrane diffusing capacity (DM) was found. The magnetic resonance scans demonstrated a 9.4% increase (P = 0.043) in pulmonary extravascular water 90 min post-exercise. These data support the theory that high intensity, sustained exercise in well-trained athletes can result in transient pulmonary edema.

Introduction

Exercise-induced hypoxemia (EIH) occurs frequently in healthy, fit subjects exercising at sea level. The proposed mechanisms include ventilation–perfusion $\dot{V}\text{/}\dot{Q}$ inequality, relative alveolar hypoventilation, right to left shunts and diffusion limitation (Dempsey, 1986, Dempsey and Wagner, 1999). An inadequate ventilatory response to maximal exercise in some athletes with high aerobic capacities results in a decreased alveolar $P_{{\text{O}}_2}$ (Dempsey et al., 1984, Wagner, 1992). $\dot{V}\text{/}\dot{Q}$ inequality can contribute to EIH and can explain more than 60% of the observed increase in $\text{A-a}{\text{D}}_{{\text{O}}_2}$ in well-trained subjects (Hopkins et al., 1994). Diffusion limitation represents a significant contribution to increases in $\text{A-a}{\text{D}}_{{\text{O}}_2}$ at sea level (Wagner et al.,1986) and a reduction in diffusing capacity of the lung (DL) following exercise has been reported by numerous authors (Hanel et al., 1994, Manier et al., 1993, McKenzie et al., 1999, Sheel et al., 1998). This may be attributed to an incomplete equilibration of O₂ in the pulmonary capillaries due to a short red blood cell transit time and/or an accumulation of pulmonary extravascular water (EW) secondary to increased capillary permeability, increased capillary surface area, increased capillary hydrostatic pressure or lymphatic insufficiency. The presence of EW in highly trained aerobic athletes has also been suggested by $\dot{V}\text{/}\dot{Q}$ mismatch, which persisted during 20 min of recovery from hypoxic exercise (Schaffartzik et al., 1993).

Measurement of the diffusing capacity of the lung for carbon monoxide (DL_CO), after maximal exercise, has yielded indirect evidence of a diffusion limitation relating to the pulmonary membrane (Manier et al., 1993). A more recent study using computed tomography (CT) to measure changes in EW following endurance activities, corroborated the presence of EW by the visual inspection of the images for linear and polygonal opacities, as well as computing lung density (Caillaud et al., 1995). These authors reported an increase in the number of opacities, and an increase in lung density (P < 0.001 and 0.0001, respectively). Currently, technical advances in the use of magnetic resonance imaging (MR) have resulted in a more sensitive method of detecting changes in EW (Estilaei et al., 1999). The present study investigated the changes in EW following 45 min of heavy exercise in endurance-trained cyclists using MR imaging of the lung. It was our contention that this exercise task would result in transient pulmonary edema in these subjects.