Relationship of Pulmonary Vascular Structure and Function With Exercise Capacity in Health and COPD.

Background: Although it is generally accepted that aerobic exercise training does not change lung structure or function, some work suggests that greater pulmonary vascular structure and function are associated with higher exercise capacity (peak rate of oxygen consumption [V˙o ₂ peak]).
Research Question: Is there a cross-sectional association between the pulmonary vasculature and V˙o ₂ peak? We hypothesized that those with higher CT blood vessel volumes and pulmonary diffusing capacity for carbon monoxide (Dlco) would have higher V˙o ₂ peak, independent of airflow limitation.
Study Design and Methods: Participants from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study were categorized as follows: participants with normal spirometry who had never smoked (n = 263), participants with normal spirometry who had ever smoked (n = 407), and COPD: individuals with spirometric airflow obstruction (n = 334). Total vessel volume (TVV), volume for vessels < 5 mm ² in cross-sectional area (BV5), and volume for vessels between 5 and 10 mm ² in cross-sectional area (BV5-10) were generated from CT scans and used as indices of pulmonary vascular structure. Dlco was used as an index of pulmonary microvascular function. V˙o ₂ peak was evaluated via incremental cardiopulmonary exercise testing.
Results: General linear regression models revealed that even after controlling for FEV ₁ , emphysema severity, and body morphology, Dlco, TVV, BV5, and BV5-10, were independently associated with V˙o ₂ peak. Interaction effects were observed between COPD and TVV, BV5, and BV5-10, indicating a weaker association between pulmonary vascular volumes and V˙o ₂ peak in COPD.
Interpretation: Our results suggest that pulmonary vascular structure and Dlco are independently associated with V˙o ₂ peak, regardless of severity of airflow limitation and emphysema, suggesting that these associations are not limited to COPD.
Competing Interests: Financial/Nonfinancial Disclosures The authors have reported to CHEST the following: M. K. reports consulting fees related to the content of the manuscript from VIDA Diagnostics Inc (Coralville, IA). W. T. reports support from the Canadian Institute of Heath Research (CIHR/Rx&D Collaborative Research Program Operating Grants 93326) with industry partners Astra Zeneca Canada Ltd, Boehringer-Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Merck, Novartis Pharma Canada Inc, Nycomed Canada Inc, and Pfizer Canada Ltd for conducting the longitudinal population-based Canadian Cohort of Obstructive Lung Disease (CanCOLD) study on COPD. J. B. reports grants or contracts from CIHR, Réseau en santé respiratoire du FRQS, McGill University, McGill University Health Centre Foundation, AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Grifols, Novartis, Sanofi, and Trudell Canada Ltd, paid to his institution; and payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing, or educational events from AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Trudell Canada Ltd, Pfizer Canada Ltd, and COVIS Pharma Canada Ltd. S. S. reports grants from the ATS as chair for ATS/ERS Updated Technical Standard on PFT interpretation; reports consulting fees from Chiesi Pharmaceuticals; reports speaker fees from Vyaire Medical; holds a leadership position at the American Thoracic Society and European Respiratory Society; is on a medical advisory board at Ndd Technologies; and is statistical editor at Thorax, an editorial board member at the European Respiratory Journal, and associate editor at Canadian Journal of Respiratory, Critical Care and Sleep Medicine, outside the submitted work. None declared (S. É. C., B. M. S., S. T., S. D., D. J. M. K. S.).
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