Pulmonary capillary blood volume and diffusing membrane capacity during exercise in humans: role of pulmonary artery pressure
During exercise, lung diffusing capacity for carbon monoxide (DL<sub>CO</sub>), pulmonary capillary blood volume (V<sub>c</sub>), and diffusing membrane capacity (D<sub>M</sub>) increase secondary to a rise in pulmonary artery pressure (PAP) and central blood volume mobilization. Although the role of central blood volume on DL<sub>CO</sub> is well established, the impact of PAP on DL<sub>CO</sub>, V<sub>c</sub>, and D<sub>M</sub> during exercise is less clear. Based on previous work, we tested the hypothesis that acute increases in PAP will potentiate exercise DL<sub>CO</sub> via increases in D<sub>M</sub>. Fifteen healthy young adults (7 females; age: 24 ± 4 yr) completed two bouts of cycling exercise at 60 W, with (CUFF) or without (CON) bilateral thigh cuff inflation pressurized to 90 mmHg. The multiple fractions of the inspired O<sub>2</sub>-DL<sub>CO</sub> method were used to determine DL<sub>CO</sub>, V<sub>c</sub>, and D<sub>M</sub> at baseline and during both exercise conditions alongside estimates of cardiac output (Q̇<sub>c</sub>; impedance cardiography) and right ventricular systolic pressure (RVSP; echocardiography). CUFF exercise resulted in a larger increase in RVSP (CUFF: 44.7 ± 6.1 vs. CON: 38.9 ± 5.5 mmHg; <i>P</i> = 0.036) but not Q̇<sub>c</sub> (<i>P</i> = 0.644) or V̇o<sub>2</sub> (<i>P</i> = 0.976) compared with CON. DL<sub>CO</sub> was higher during the CUFF exercise (CUFF: 41 ± 6 vs. CON: 38 ± 6 mL/min/mmHg; <i>P</i> = 0.001) and was mediated by increases in D<sub>M</sub> (CUFF: 138 ± 55 vs. CON: 90 ± 39 mL/min/mmHg; <i>P</i> = 0.032), not V<sub>c</sub> (CUFF: 85 ± 18 vs. CON: 98 ± 27 mL/min/mmHg; <i>P</i> = 0.820). Increases in RVSP were positively related to D<sub>M</sub> (<i>r</i><sub>rm</sub> = 0.82; <i>P</i> = 0.024) but inversely related to V<sub>c</sub> (<i>r</i><sub>rm</sub> = -0.80, <i>P</i> = 0.029). Collectively, these data indicate that PAP primarily contributes to DL<sub>CO</sub> during low-intensity exercise via increases in capillary recruitment (i.e., D<sub>M</sub>).<b>NEW & NOTEWORTHY</b> Pulmonary artery pressure contributes to DL<sub>CO</sub> recruitment during exercise. However, it is unclear how pulmonary artery pressure impacts the pulmonary microcirculatory adjustments that comprise DL<sub>CO</sub>, namely V<sub>c</sub> and D<sub>M</sub>. Using subsystolic occlusion of the locomotor muscles during exercise to induce increases in pulmonary artery pressure, without changes in cardiac output or metabolic demand, we demonstrate that pulmonary artery pressure contributes to DL<sub>CO</sub> during exercise via heightened capillary recruitment (D<sub>M</sub>).
Authors
- Michael K. Stickland (ORCID: https://orcid.org/0000-0001-8234-4760)
- Jason Weatherald (ORCID: https://orcid.org/0000-0002-0615-4575)
- E. Bok
- Andrew W. D’Souza (ORCID: https://orcid.org/0000-0001-7024-0446)
- Sean van Diepen (ORCID: https://orcid.org/0000-0002-6688-828X)
- Andrew R. Brotto (ORCID: https://orcid.org/0000-0002-8644-5013)
- B.J. Hicks
Institutions
- University of Alberta (CA)
- Covenant Health (CA)
Publication Details
- Journal
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Published
- 2025-03-20
- DOI
- https://doi.org/10.1152/ajplung.00358.2024
- Citations
- 1
- Primary Topic
- Cardiovascular and exercise physiology
- Type
- article
- Field-Weighted Citation Impact
- 2.38
Funders
- Natural Sciences and Engineering Research Council of Canada