Lung Diffusion in a 14-Day Swimming Altitude Training Camp at 1850 Meters

Abstract

Swimming exercise at sea level causes a transient decrease in lung diffusing capacity for carbon monoxide (DL_CO). The exposure to hypobaric hypoxia can affect lung gas exchange, and hypoxic pulmonary vasoconstriction may elicit pulmonary oedema. The purpose of this study is to evaluate whether there are changes in DL_CO during a 14-day altitude training camp (1850 m) in elite swimmers and the acute effects of a combined training session of swimming in moderate hypoxia and 44-min cycling in acute normobaric severe hypoxia (3000 m). Participants were eight international level swimmers (5 females and 3 males; 17-24 years old; 173.5 ± 5.5 cm; 64.4 ± 5.3 kg) with a training volume of 80 km per week. The single-breath method was used to measure the changes in DL_CO and functional gas exchange parameters. No changes in DL_CO after a 14-day altitude training camp at 1850 m were detected but a decrease in alveolar volume (VA; 7.13 ± 1.61 vs. 6.50 ± 1.59 L; p = 0.005; d = 0.396) and an increase in the transfer coefficient of the lung for carbon monoxide (K_CO; 6.23 ± 1.03 vs. 6.83 ± 1.31 mL·min^-1·mmHg^-1·L^-1; p = 0.038; d = 0.509) after the altitude camp were observed. During the acute hypoxia combined session, there were no changes in DL_CO after swimming training at 1850 m, but there was a decrease in DL_CO after cycling at a simulated altitude of 3000 m (40.6 ± 10.8 vs. 36.8 ± 11.2 mL·min^-1·mmHg^-1; p = 0.044; d = 0.341). A training camp at moderate altitude did not alter pulmonary diffusing capacity in elite swimmers, although a cycling session at a higher simulated altitude caused a certain degree of impairment of the alveolar-capillary gas exchange.

Keywords: DLCO; SIPO; altitude training; pulmonary diffusing capacity; swimming.

Figure 1

Schematic representation of external stimuli for the development of environmental-induced pulmonary oedema in healthy individuals. At high altitude, mountaineers are exposed to the effects of hypoxic pulmonary vasoconstriction, and increased pulmonary blood flow during exercise, thus developing the risk for high-altitude pulmonary oedema. Breath-holding divers suffer the simultaneous effects of hypoxia, central blood-shift, and chest compression. Swimmers experience hemodynamic changes in pulmonary circulation during exercise, due to regular breath-holding pattern and chest compression. SATC (swimming altitude training camp) combines all three forms of environmental stress that can elicit sub-clinical pulmonary oedema. Based on Marabotti et al. [2].