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Long-term leisure-time physical activity and risk of all-cause and cardiovascular mortality: dose–response associations in a prospective cohort study of 210 327 Taiwanese adults
  1. David Martinez-Gomez1,2,3,
  2. Veronica Cabanas-Sanchez3,
  3. Tsung Yu4,
  4. Fernando Rodriguez-Artalejo1,2,3,
  5. Ding Ding5,
  6. I-Min Lee6,7,
  7. Ulf Ekelund8,9
  1. 1Preventive Medicine and Public Health, Universidad Autonoma de Madrid, Madrid, Spain
  2. 2CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain
  3. 3IMDEA Food Institute, CEI UAM+CSIC, Madrid, Spain
  4. 4Department of Public Health, College of Medicine, National Cheng Kung University, Taipei, Taiwan
  5. 5Sydney School of Public Health, The University of Sydney, Sydney, New South Wales, Australia
  6. 6Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
  7. 7Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
  8. 8Department of Sports Medicine, Norwegian School of Sports Sciences, Oslo, Norway
  9. 9Department of Chronic Diseases and Ageing, Norwegian Institute of Public Health, Oslo, Norway
  1. Correspondence to Dr David Martinez-Gomez, Preventive Medicine and Public Health, Universidad Autonoma de Madrid, Madrid 28049, Spain; d.martinez{at}uam.es

Abstract

Objectives We aimed to investigate the dose–response associations of long-term leisure-time physical activity (LTPA) obtained from repeated measures with all-cause and cardiovascular disease (CVD) mortality outcomes in Taiwanese adults.

Methods We included 210 327 participants with self-reported LTPA at least in two medical examinations (867 968 data points) for up to 20 years (median, IQR: 4.8 years, 2.3–9.0). Dose–response relationships were modelled with restricted cubic spline functions and Cox regressions HRs (95% CIs) adjusted for main covariates.

Results During up to 23 years of follow-up (3 655 734 person-years), 10 539 participants died, of which 1919 of CVD. We observed an inverse, non-linear dose–response association between long-term LTPA and all-cause and CVD mortality. Compared with the referent (0 metabolic equivalent of task (MET) hours/week), insufficient (0.01–7.49 MET hours/week), recommended (7.50–15.00 MET hours/week) and additional (>15 MET hours/week) amounts of LTPA had a lower mortality risk of 0.74 (0.69–0.80), 0.64 (0.60–0.70) and 0.59 (0.54–0.64) for all-cause mortality and 0.68 (0.60–0.84), 0.56 (0.47–0.67) and 0.56 (0.47–0.68) for CVD mortality. When using only baseline measures of LTPA, the corresponding mortality risk was 0.88 (0.84–0.93), 0.83 (0.78–0.88) and 0.78 (0.73–0.83) for all-cause and 0.91 (0.81–1.02), 0.78 (0.68–0.89) and 0.80 (0.70–0.92) for CVD mortality.

Conclusion Long-term LTPA was associated with lower risks of all-cause and CVD mortality. The magnitude of risk reductions was larger when modelling repeated measures of LTPA compared with one measure of LTPA at baseline.

  • Epidemiology
  • Cohort Studies
  • Physical activity
  • Death
  • Cardiovascular Diseases

Data availability statement

Data may be obtained from a third party and are not publicly available. The data of this study can be requested from the MJ Health Research Foundation (http://www.mjhrf.org).

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Data availability statement

Data may be obtained from a third party and are not publicly available. The data of this study can be requested from the MJ Health Research Foundation (http://www.mjhrf.org).

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Footnotes

  • DD, IL and UE are joint senior authors.

  • Twitter @DrMelodyDing

  • Correction notice This article has been corrected since it published Online First. The abstract has been corrected and affiliations updated.

  • Contributors DMG conceived and designed the study. DMG, FR-A and TY acquired the data. DMG and VC-S analysed and interpreted the data. DMG and FR-A obtained the funding. DMG drafted the first version of this article. All authors critically revised and edited the article. DD, I-ML and UE supervised this work. DMG was the guarantor.

  • Funding This work was supported by FIS grants (State Secretary of R+D+I and FEDER/FSE; 16/609, 16/1512, 18/287, 19/319, 20/00657). DMG was supported by a ‘Ramon y Cajal’ contract (RYC2016-20546) and DD by a Heart Foundation Australia Future Leader Fellowship (no. 101234) while contributing to this work. A preliminary version of this work was awarded the 2020 National Sports Medicine Award (University of Oviedo, Oviedo, Spain).

  • Disclaimer The funders had no role in study design, data collection, data analysis, data interpretation or writing of the report. Any interpretation or conclusion related to this article does not represent the views of MJ Health Research Foundation.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.