Key points
Endurance trained athletes exhibit enhanced cardiovascular function compared to non‐athletes, although it is considered that exercise training does not enhance lung structure and function.An increased pulmonary capillary blood volume at rest is associated with a higher V˙O2 max .In the present study, we compared the diffusion capacity, pulmonary capillary blood volume and diffusing membrane capacity responses to exercise in endurance‐trained males compared to non‐trained males.Exercise diffusion capacity was greater in athletes, secondary to an increased membrane diffusing capacity, and not pulmonary capillary blood volume.Endurance‐trained athletes appear to have differences within the pulmonary membrane that facilitate the increased O2 demand needed for high‐level exercise.
AbstractEndurance‐trained athletes exhibit enhanced cardiovascular function compared to non‐athletes, allthough it is generally accepted that exercise training does not enhance lung structure and function. Recent work has shown that an increased resting pulmonary capillary blood volume (V
C) is associated with a higher maximum oxygen consumption (V˙O2 max ), although there have been no studies to date examining how aerobic fitness affects the V
C response to exercise. Based on previous work, we hypothesized that endurance‐trained athletes will have greater V
C compared to non‐athletes during cycling exercise. Fifteen endurance‐trained athletes (HI: V˙O2 max 64.6 ± 1.8 ml kg−1 min−1) and 14 non‐endurance trained males (LO: V˙O2 max 45.0 ± 1.2 ml kg−1 min−1) were matched for age and height. Haemoglobin‐corrected diffusion capacity (DLCO), V
C and diffusing membrane capacity (D
M) were determined using the Roughton and Forster (1957) multiple fraction of inspired O2 (FIO2)‐DLCO method at baseline and during incremental cycle exercise up to 90% of peak O2 consumption. During exercise, both groups exhibited increases in DLCO, D
M and V
C with exercise intensity. Athletes had a greater DLCO and greater D
M at 80 and 90% of V˙O2 max compared to non‐athletes. However, V
C was not different between groups during exercise. In contrast to our hypothesis, exercise V
C was not greater in endurance‐trained subjects compared to controls; rather, the increased DLCO in athletes at peak exercise was secondary to an enhanced D
M. These findings suggest that endurance‐trained athletes appear to have differences within the pulmonary membrane that facilitate the increased O2 demand needed for high‐level exercise.