Abstract
Background Cardiorespiratory fitness is not limited by pulmonary mechanical reasons in the majority of adults. However, the degree to which lung function contributes to exercise response patterns among ostensibly healthy individuals remains unclear.
Methods We examined 2314 Framingham Heart Study participants who underwent cardiopulmonary exercise testing (CPET) and pulmonary function testing. We investigated the association of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC and diffusing capacity of the lung for carbon monoxide (DLCO) with the primary outcome of peak oxygen uptake (V′O2) along with other CPET parameters using multivariable linear regression. Finally, we investigated the association of total and peripheral pulmonary blood vessel volume with peak V′O2.
Results We found lower FEV1, FVC and DLCO were associated with lower peak V′O2. For example, a 1 L lower FEV1 and FVC was associated with a 7.1% (95% CI 5.1–9.1%) and 6.0% (95% CI 4.3–7.7%) lower peak V′O2, respectively. By contrast, FEV1/FVC was not associated with peak V′O2. Lower lung function was associated with lower oxygen uptake efficiency slope, oxygen pulse slope, V′O2 at anaerobic threshold (AT), minute ventilation (V′E) at AT and breathing reserve. In addition, lower total and peripheral pulmonary blood vessel volume were associated with lower peak V′O2.
Conclusions In a large, community-based cohort of adults, we found lower FEV1, FVC and DLCO were associated with lower exercise capacity, as well as oxygen uptake efficiency slope and ventilatory efficiency. In addition, lower total and peripheral pulmonary blood vessel volume were associated with lower peak V′O2. These findings underscore the importance of lung function and blood vessel volume as contributors to overall exercise capacity.
Abstract
Lower FEV1, FVC and DLCO were associated with lower exercise capacity, as well as oxygen uptake efficiency slope and ventilatory efficiency. In addition, lower total and peripheral pulmonary blood vessel volume were associated with lower peak V′O2. https://bit.ly/31VVpsu
Footnotes
Conflict of interest: J. McNeill has nothing to disclose.
Conflict of interest: A. Chernofsky has nothing to disclose.
Conflict of interest: M. Nayor reports grants from the NIH, during the conduct of the study.
Conflict of interest: F.N. Rahaghi has nothing to disclose.
Conflict of interest: R. San Jose Estepar has contracts with Lung Biotechnology, Insmed and Boehringer Ingelheim, receives consulting fees from Leuko Labs, and has stock options in Quantitative Imaging Solutions.
Conflict of interest: G. Washko reports grants from the NIH, DoD, Boehringer Ingelheim, Janssen Pharmaceuticals, BTG Therapeutics, Pulmonx, Lung Biotechnology and Insmed; participation in advisory boards and consultancies for Boehringer Ingelheim, CSL Behring, Novartis, Phillips and Vertex Pharmaceuticals; is a co-founder and equity shareholder in Quantitative Imaging Solutions, a company that provides consulting services for image and data analytics; finally, the author's spouse works for Biogen.
Conflict of interest: A. Synn reports grants from the American Lung Association and NHLBI, outside the submitted work.
Conflict of interest: R.S. Vasan has nothing to disclose.
Conflict of interest: G. O'Connor has nothing to disclose.
Conflict of interest: M.G. Larson has nothing to disclose.
Conflict of interest: J.E. Ho reports grants from the NIH/NHLBI, during the conduct of the study; research support from Gilead Sciences and Bayer AG, and research supplies from EcoNugenics, outside the submitted work.
Conflict of interest: G.D. Lewis reports grants from Amgen, Cytokinetics, AstraZeneca, Applied Therapeutics and Sonivie, personal fees and other for advisory board work from American Regent, outside the submitted work.
Support statement: This work was supported by the National Heart, Lung, and Blood Institute's Framingham Heart Study (contracts N01-HC-25195, HHSN268201500001I and 75N92019D00031), National Institutes of Health grants F32 HL143819 (A. Synn), K23 HL138260 (M. Nayor), K23 HL136905 (F.N. Rahaghi), R01 HL134893 (J.E. Ho), R01 HL140224 (J.E. Ho), K24 HL153669 (J.E. Ho), 1R01 HL131029 (R.S. Vasan and G.D. Lewis) and R01 HL151841 (G.D. Lewis), and American Heart Association grant 15GPSGC24800006 (G.D. Lewis). R.S. Vasan is supported in part by the Evans Medical Foundation and the Jay and Louis Coffman Endowment from the Dept of Medicine, Boston University School of Medicine (Boston, MA, USA). A. Synn is supported by the American Lung Association. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received June 29, 2021.
- Accepted December 6, 2021.
- Copyright ©The authors 2022. For reproduction rights and permissions contact permissions{at}ersnet.org
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