Evidence map›Paper›PMID 42163317›Full record

Observational studyBMC medicine2026

Cardiorespiratory fitness, genetic susceptibility, and the risk of chronic obstructive pulmonary disease: findings from observational and two-sample bidirectional Mendelian randomisation analyses.

Ziyuan Chen, Paul James Collings, Qiaoxin Shi, Shiu Lun Au Yeung, Shan Luo, Chenxi Li, Tomas Gonzales, Soren Brage, Youngwon Kim

Abstract readObservational Study
In one paragraph

Observational study in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

9 authors.

Ziyuan ChenSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China.
Paul James CollingsSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China.
Qiaoxin ShiSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China.
Shiu Lun Au YeungSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China.
Shan LuoSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China.
Chenxi LiSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China.
Tomas GonzalesMRC Epidemiology Unit, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
Soren BrageMRC Epidemiology Unit, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
Youngwon KimSchool of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, Pokfulam, China. youngwon.kim@hku.hk.

Funding

General Research Fund of the Hong Kong Research Grants Council 17115422Health and Medical Research Fund (HMRF) Research Fellowship 06200087
6 · The paper itself

Abstract

backgroundCardiorespiratory fitness (CRF) is a common risk factor for cardiometabolic diseases, but the causal relation of CRF with chronic obstructive pulmonary disease (COPD) and its interplay with genetic risk remain unknown. We integrated genetic susceptibility and causal inference methods to evaluate the protective roles of CRF in COPD development.

methodsWe included 68,288 White British individuals from the UK Biobank (aged 40-79 years) without prevalent COPD at the baseline (2006-13). CRF was assessed using heart rate responses to submaximal bike tests. Genetic risk for COPD was quantified using a polygenic risk score constructed from 71 uncorrelated single nucleotide polymorphisms. Cox regression was used to estimate the hazard of COPD. Causal inference was evaluated via two-sample Mendelian randomisation (MR). Potential reverse causation was assessed using a bidirectional MR.

resultsWithin an MR framework, we found that higher genetically predicted CRF is causally associated with lower risk of COPD. Observational analysis found: (1) compared with low CRF (bottom tertile), hazard ratios (95% CI) of COPD were 0.80 (0.72-0.89) and 0.71 (0.64-0.80) for medium and high CRF, respectively; (2) compared to the high CRF-low genetic risk group, COPD hazards were higher for individuals who had medium or high genetic risk combined with low or medium CRF but not for those who had medium genetic risk but high CRF; (3) low CRF combined with any levels of genetic risk showed consistently higher COPD hazards relative to high CRF and low genetic risk combination.

conclusionsBeing more aerobically fit may prevent or delay the onset of COPD. Improving CRF has the potential to attenuate the increased risk of COPD associated with elevated genetic risk. Public health initiatives should prioritise making measurable improvements in cardiorespiratory fitness (beyond merely being active or exercising more) as a promising intervention target for reducing the risk of COPD.

Indexed as

Cardiorespiratory FitnessGenetic Predisposition to DiseasePulmonary Disease, Chronic ObstructiveAdultAgedFemaleGenetic Risk ScoreHumansMaleMendelian Randomization AnalysisMiddle AgedPolymorphism, Single NucleotideRisk FactorsUnited KingdomCardiorespiratory fitnessChronic obstructive pulmonary diseaseGene-environment interactionGeneticsMendelian randomisation

Identifiers

PMID42163317
PMCPMC13480046

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.