Effect of Ultramarathon Trail Running at Sea Level and Altitude on Alveolar-Capillary Function and Lung Diffusion

Introduction Endurance exercise at altitude can increase cardiac output and pulmonary vascular pressure to levels that may exceed the stress tolerability of the alveolar-capillary unit. This study examined the effect of ultramarathon trail racing at different altitudes (ranging from <1000 m to between 1500 and 2700 m) on alveolar-capillary recruitment and lung diffusion. Methods Cardiac and lung function were examined before and after an ultramarathon in 67 runners (age: 41 ± 9 yr, body mass index: 23 ± 2 kg·m-2, 10 females), and following 12-24 h of recovery in a subset (n = 27). Cardiac biomarkers (cTnI and BNP) were assessed from whole blood, whereas lung fluid accumulation (comet tails), stroke volume (SV), and cardiac output (Q) were quantified via echocardiography. Lung diffusing capacity for carbon monoxide (DLco) and its components, alveolar membrane conductance (Dm) and capillary blood volume (Vc), were determined via a single-breath method at rest and during three stages of submaximal semirecumbent cycling (20, 30, and 40 W). Results Average race time was 25 ± 12 h. From pre- to post-race, there was an increase in cardiac biomarkers (cTnI: 0.04 ± 0.02 vs 0.13 ± 0.03 ng·mL-1, BNP: 20 ± 2 vs 112 ± 21 pg·mL-1; P < 0.01) and lung comet tails (2 ± 1 vs 7 ± 6, P < 0.01), a decrease in resting and exercise SV (76 ± 2 vs 69 ± 2 mL, 40 W: 93 ± 2 vs 88 ± 2 mL; P < 0.01), and an elevation in Q at rest (4.1 ± 0.1 vs 4.6 ± 0.2 L·min-1, P < 0.01; 40 W: 7.3 ± 0.2 vs 7.4 ± 0.3 L·min-1, P = 0.899). Resting DLco and Vc decreased after the race (P < 0.01), whereas Dm was unchanged (P = 0.465); however, during the three stages of exercise, DLco, Vc, and Dm were all reduced from pre- to post-race (40 W: 36.3 ± 0.9 vs 33.0 ± 0.8 mL·min-1·mm Hg-1, 83 ± 3 vs 73 ± 2 mL, 186 ± 6 vs 170 ± 7 mL·min-1·mm Hg-1, respectively; P < 0.01). When corrected for alveolar volume and Q, DLco decreased from pre- to post-race (P < 0.01), and changes in DLco were similar for all ultramarathon events (P > 0.05). Conclusions Competing in an ultramarathon leads to a transient increase in cardiac injury biomarkers, mild lung-fluid accumulation, and impairments in lung diffusion. Reductions in DLco are predominantly caused by a reduced Vc and possible pulmonary capillary de-recruitment at rest. However, impairments in alveolar-capillary recruitment and Dm both contribute to a fall in exertional DLco following an ultramarathon. Perturbations in lung diffusion were evident across a range of event distances and varying environmental exposures.