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.

Previous work suggests that women may exhibit a greater respiratory limitation in exercise compared with height-matched men. Diffusion capacity (Dl) increases with incremental exercise, and the smaller lungs of women may limit membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) in response to the increased oxygen demand. We hypothesized that women would have lower Dl, Dl relative to cardiac output (Dl/Q̇), Dm, Vc, and pulmonary transit time, secondary to lower Vc at peak exercise. Sixteen women (112 ± 12% predicted relative V̇o) and sixteen men (118 ± 22% predicted relative V̇o) were matched for height and weight. Hemoglobin-corrected diffusing capacity (Dl), Vc, and Dm were determined via the multiple-[Formula: see text] Dl technique at rest and during incremental exercise up to 90% of V̇o Both groups increased Dl, Vc, and Dm with exercise intensity, but women had 20% lower Dl ( < 0.001), 18% lower Vc ( = 0.002), and 22% lower Dm ( < 0.001) compared with men across all workloads, and neither group exhibited a plateau in Vc. When expressed relative to alveolar volume (Va), the between-sex difference was eliminated. The drop in Dl/Q̇ was proportionally less in women than men, and mean pulmonary transit time did not drop below 0.3 s in either group. Women demonstrate consistently lower Dl, Vc, and Dm compared with height-matched men during exercise; however, these differences disappear with correction for lung size. These results suggest that after differences in lung volume are accounted for there is no intrinsic sex difference in the Dl, Vc, or Dm response to exercise. Women demonstrate lower diffusing capacity-to-cardiac output ratio (Dl/Q̇), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (Dm) compared with height-matched men during exercise. However, these differences disappear after correction for lung size. The drop in Dl/Q̇ was proportionally less in women, and pulmonary transit time did not drop below 0.3 s in either group. After differences in lung volume are accounted for, there is no intrinsic sex difference in Dl, Vc, or Dm response to exercise.

Key pointsr At rest, dopamine induces recruitment of intrapulmonary arteriovenous anastomoses (IPAVA) and increases venous admixture (i.e.Q s /Q t ).r Dopamine increases during exercise, and may be partly responsible for exercise-induced IPAVA recruitment.r In this study, we antagonized dopamine receptors with metoclopramide, and observed improved pulmonary gas exchange but no difference in IPAVA recruitment during exercise.r Dopamine blockade decreased cardiac output at peak exercise, resulting in decreased exercise performance.r Increasing endogenous dopamine is important for the normal healthy response to exercise. Abstract Pulmonary gas exchange, as evaluated by the alveolar-arterial oxygen difference (A-aD O 2 ), is impaired during intense exercise, and has been correlated with recruitment of intrapulmonary arteriovenous anastomoses (IPAVA) as measured by agitated saline contrast echocardiography. Previous work has shown that dopamine (DA) recruits IPAVA and increases venous admixture (Q s /Q t ) at rest. As circulating DA increases during exercise, we hypothesized that A-aD O 2 and IPAVA recruitment would be decreased with DA receptor blockade. Twelve healthy males (age: 25 ± 6 years,V O 2 max : 58.6 ± 6.5 ml kg −1 min −1 ) performed two incremental staged cycling exercise sessions after ingestion of either placebo or a DA receptor blocker (metoclopramide 20 mg). Arterial blood gas, cardiorespiratory and IPAVA recruitment (evaluated by agitated saline contrast echocardiography) data were obtained at rest and during exercise up to 85% ofV O 2 max . On different days, participants also completed incremental exercise tests and exercise tolerance (time-to-exhaustion (TTE) at 85% ofV O 2 max ) with or without dopamine blockade. Compared to placebo, DA blockade did not change O 2 consumption, CO 2 production, or respiratory exchange ratio at any intensity. At 85%V O 2 max , DA blockade decreased A-aD O 2 , increased arterial O 2 saturation and minute ventilation, but did not reduce IPAVA recruitment, suggesting that positive saline contrast is unrelated to A-aD O 2 . Compared to placebo, DA blockade decreased maximal cardiac output,V O 2 max and TTE. Despite improving pulmonary gas exchange, blocking dopamine receptors appears to be detrimental to exercise performance. These findings suggest that endogenous dopamine is important to the normal cardiopulmonary response to exercise and is necessary for optimal high-intensity exercise performance.

Impaired pulmonary gas exchange during heavy exercise, manifested as an increase in the alveolar‐arterial oxygen difference (A‐aDO2), may be due to anatomical intrapulmonary (IP) shunt recruitment. Dopamine (DA) has been shown to recruit IP shunts at rest and circulating DA increases with exercise, and thus may contribute to the increased A‐aDO2 during exercise. We hypothesized that gas exchange impairment during exercise will decrease with DA receptor blockade. Ten healthy males (Age: 25±6 yrs, VO2max: 56.3±6.6 ml∙kg‐1∙min‐1) performed two incremental staged cycling exercise sessions after ingestion of either placebo (P) or DA blockade (B) (Metoclopramide 20mg). Arterial blood gas sampling and cardiorespiratory data were obtained at rest and during 4 exercise intensities (30%, 50%, 75% and 90% of previously determined VO2max). At 90% VO2max, DA blockade decreased A‐aDO2 (P: 19.3±8.5 torr, B: 14.8±6.8 torr, p=0.038 and increased arterial O2 saturation (P: 95.4±1.0%, B: 96.2±0.9%, p=0.004). Blood gases were similar between the two groups at rest, 30%, 50% and 75% of VO2max. Compared to placebo, DA blockade did not change O2 consumption, CO2 production, or respiratory exchange ratio at any intensity. Administration of a DA receptor blockade decreased A‐aDO2 during near‐maximal exercise, suggesting that endogenous DA affects affects pulmonary gas exchange during exercise. Grant Funding Source: Supported by The National Sciences and Engineering Research Council of Canada