Article Text

Device-measured physical activity, adiposity and mortality: a harmonised meta-analysis of eight prospective cohort studies
  1. Jakob Tarp1,
  2. Morten W Fagerland1,
  3. Knut Eirik Dalene1,
  4. Jostein Steene Johannessen1,
  5. Bjørge H Hansen1,2,
  6. Barbara J Jefferis3,
  7. Peter H Whincup4,
  8. Keith M Diaz5,
  9. Steven Hooker6,
  10. Virginia J Howard7,
  11. Ariel Chernofsky8,
  12. Martin G Larson8,
  13. Nicole L Spartano9,
  14. Ramachandran S Vasan10,
  15. Ing-Mari Dohrn11,
  16. Maria Hagströmer11,12,
  17. Charlotte Edwardson13,14,
  18. Thomas Yates13,14,
  19. Eric J Shiroma15,
  20. Paddy C Dempsey16,17,
  21. Katrien Wijndaele16,
  22. Sigmund A Anderssen1,
  23. I-Min Lee18,19,
  24. Ulf Ekelund1,20
  1. 1 Department of Sports Medicine, Norwegian School of Sports Sciences, Oslo, Norway
  2. 2 Department of Sport Science and Physical Education, University of Agder, Kristiansand, Norway
  3. 3 Primary Care and Population Health, University College London, London, UK
  4. 4 Population Health Research Institute, St George's University of London, London, UK
  5. 5 Department of Medicine, Center for Behavioral Cardiovascular Health, Columbia University Medical Center, New York, New York, USA
  6. 6 College of Health and Human Services, San Diego State University, San Diego, California, USA
  7. 7 Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, USA
  8. 8 Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, USA
  9. 9 Department of Endocrinology, Diabetes, Nutrition and Weight Management, Boston University School of Medicine, Boston, Massachusetts, USA
  10. 10 Departments of Medicine and Epidemiology, Boston University School of Medicine and Boston University School of Public Health, Boston, Massachusetts, USA
  11. 11 Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
  12. 12 Academic Primary Health Care Centre, Region Stockholm, Stockholm, Sweden
  13. 13 Diabetes Research Centre, College of Life Sciences, University of Leicester, Leicester, UK
  14. 14 NIHR Leicester Biomedical Research Centre, University Hospitals of Leicester NHS Trust, Leicester, UK
  15. 15 Laboratory of Epidemiology and Population Sciences, National Institute on Aging, Bethesda, Maryland, USA
  16. 16 MRC Epidemiology Unit, University of Cambridge, Cambridge, UK
  17. 17 Physical Activity and Behavioural Epidemiology Laboratories, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
  18. 18 Department of Epidemiology, Harvard T H Chan School of Public Health, Boston, Massachusetts, USA
  19. 19 Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
  20. 20 Department of Chronic Diseases and Ageing, Norwegian Institute of Public Health, Oslo, Norway
  1. Correspondence to Dr Jakob Tarp, Department of Sports Medicine, Norwegian School of Sports Sciences, Oslo 0806, Norway; jtarp{at}clin.au.dk

Abstract

Background The joint associations of total and intensity-specific physical activity with obesity in relation to all-cause mortality risk are unclear.

Methods We included 34 492 adults (72% women, median age 62.1 years, 2034 deaths during follow-up) in a harmonised meta-analysis of eight population-based prospective cohort studies with mean follow-up ranging from 6.0 to 14.5 years. Standard body mass index categories were cross-classified with sample tertiles of device-measured total, light-to-vigorous and moderate-to-vigorous physical activity and sedentary time. In five cohorts with waist circumference available, high and low waist circumference was combined with tertiles of moderate-to-vigorous physical activity.

Results There was an inverse dose–response relationship between higher levels of total and intensity-specific physical activity and mortality risk in those who were normal weight and overweight. In individuals with obesity, the inverse dose–response relationship was only observed for total physical activity. Similarly, lower levels of sedentary time were associated with lower mortality risk in normal weight and overweight individuals but there was no association between sedentary time and risk of mortality in those who were obese. Compared with the obese-low total physical activity reference, the HRs were 0.59 (95% CI 0.44 to 0.79) for normal weight-high total activity and 0.67 (95% CI 0.48 to 0.94) for obese-high total activity. In contrast, normal weight-low total physical activity was associated with a higher risk of mortality compared with the obese-low total physical activity reference (1.28; 95% CI 0.99 to 1.67).

Conclusions Higher levels of physical activity were associated with lower risk of mortality irrespective of weight status. Compared with obesity-low physical activity, there was no survival benefit of being normal weight if physical activity levels were low.

  • exercise
  • body mass index
  • observational study

Data availability statement

Data ara available on reasonable request. The study-specific summary data included in the meta-analyses can be obtained from the corresponding authors; jtarp@clin.au.dk.

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This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Data availability statement

Data ara available on reasonable request. The study-specific summary data included in the meta-analyses can be obtained from the corresponding authors; jtarp@clin.au.dk.

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Footnotes

  • Twitter @PARG3, @PC_Dempsey

  • Contributors JT, UE and MWF had full access to the cohort-specific data and take full responsibility for the integrity of the data and the accuracy of the meta-analyses. Study concept and design: JT, UE, MWF, I-ML. Acquisition of data: all authors. Analysis and interpretation of pooled data: JT, UE, KED, BHH, MWF, JSJ, SAA, I-ML. Drafting of the manuscript: JT, UE. Critical revision of the manuscript for important intellectual content: all authors. Statistical analysis of pooled data: MWF, JT. Statistical analysis of individual studies: JT, BJJ, PCD, AC, KMD, I-MD. Study supervision: UE. JT is the study guarantor.

  • Funding The ABC study was funded by the Stockholm County Council, the Swedish National Centre for Research in Sports and the project ALPHA, which received funding from the European Union in the framework of the Public Health Programme and Folksam Research Foundation, Sweden. The British Regional Heart Study was funded by project and programme grants from the British Heart Foundation (PG/13/86/30546, RG/13/16/30528). The EPIC-Norfolk study has received funding from the UK Medical Research Council (MR/N003284/1), Cancer Research UK (C864/A14136) and the NIHR Biomedical Research Centre in Cambridge (IS-BRC-1215-20014). PCD is supported by a National Health and Medical Research Council of Australia Research Fellowship (1142685), and PCD and KW by the UK Medical Research Council (MC_UU_12015/3, MC_UU_00006/4, MC_UU_12015/3). The Framingham Heart Study’s data collection and analysis was funded by the National Institutes of Health (NIH), the National Heart, Lung, and Blood Institute (NHLBI) (N01-HC25195, HHSN268201500001I, 75N92019D00031) and grant from the National Institute on Aging (R01AG047645), Health and Human Services (HHS) (N268201500001I, R01-AG047645, R01-HL131029) and the American Heart Association (15GPSGC24800006). The Norwegian National Physical Activity Surveillance Study was supported by the Norwegian Directorate for Public Health and the Norwegian School of Sport Sciences. JT is funded by the Research Council of Norway (249932/F20). The REGARDS study was supported by a cooperative agreement (U01-NS041588) cofunded by the National Institute of Neurological Disorders and Stroke and the National Institute on Aging of the NIH. Additional funding was provided by an investigator-initiated grant (R01-NS061846) from the National Institute of Neurological Disorders and Stroke of the NIH and an unrestricted research grant from the Coca-Cola. The Women’s Health Study was funded by the NIH grants (CA154647, CA047988, CA182913, HL043851, HL080467, HL099355). EJS was supported by the intramural research programme at the National Institute on Aging.

  • Competing interests None declared.

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

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