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Sleep and physical activity in relation to all-cause, cardiovascular disease and cancer mortality risk
  1. Bo-Huei Huang1,
  2. Mitch J Duncan2,3,
  3. Peter A Cistulli4,
  4. Natasha Nassar4,
  5. Mark Hamer5,
  6. Emmanuel Stamatakis1
  1. 1 Charles Perkins Centre, School of Health Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia
  2. 2 Priority Research Centre for Physical Activity and Nutrition, The University of Newcastle, Callaghan, New South Wales, Australia
  3. 3 School of Medicine & Public Health, Faculty of Health and Medicine, The University of Newcastle, Callaghan, New South Wales, Australia
  4. 4 Charles Perkins Centre, Sydney Medical School, Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia
  5. 5 Institute Sport Exercise Health, Division of Surgery and Interventional Science, University College London, London, UK
  1. Correspondence to Dr Emmanuel Stamatakis, Charles Perkins Centre, School of Health Sciences, Faculty of Medicine and Health, the University of Sydney, Camperdown, Australia; emmanuel.stamatakis{at}sydney.edu.au

Abstract

Objectives Although both physical inactivity and poor sleep are deleteriously associated with mortality, the joint effects of these two behaviours remain unknown. This study aimed to investigate the joint association of physical activity (PA) and sleep with all-cause and cause-specific mortality risks.

Methods 380 055 participants aged 55.9 (8.1) years (55% women) from the UK Biobank were included. Baseline PA levels were categorised as high, medium, low and no moderate-to-vigorous PA (MVPA) based on current public health guidelines. We categorised sleep into healthy, intermediate and poor with an established composited sleep score of chronotype, sleep duration, insomnia, snoring and daytime sleepiness. We derived 12 PA–sleep combinations, accordingly. Mortality risks were ascertained to May 2020 for all-cause, total cardiovascular disease (CVD), CVD subtypes (coronary heart disease, haemorrhagic stroke, ischaemic stroke), as well as total cancer and lung cancer.

Results After an average follow-up of 11.1 years, sleep scores showed dose-response associations with all-cause, total CVD and ischaemic stroke mortality. Compared with high PA-healthy sleep group (reference), the no MVPA-poor sleep group had the highest mortality risks for all-cause (HR (95% CIs), (1.57 (1.35 to 1.82)), total CVD (1.67 (1.27 to 2.19)), total cancer (1.45 (1.18 to 1.77)) and lung cancer (1.91 (1.30 to 2.81))). The deleterious associations of poor sleep with all outcomes, except for stroke, was amplified with lower PA.

Conclusion The detrimental associations of poor sleep with all-cause and cause-specific mortality risks are exacerbated by low PA, suggesting likely synergistic effects. Our study supports the need to target both behaviours in research and clinical practice.

  • cohort study
  • risk factor
  • sleep

Data availability statement

Due to the personal nature of the health data collected from participants, no data are available to be shared.

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Data availability statement

Due to the personal nature of the health data collected from participants, no data are available to be shared.

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Footnotes

  • Twitter @BoHuei_Huang, @mitchjduncan, @ma_hamer, @M_Stamatakis

  • Contributors MJD, PC, NN, MH and ES contributed to the conception and design of the work. B-HH performed all analyses and drafted and re-drafted the manuscript several times. ES re-drafted parts of the manuscript and supervised all aspects of the project. All authors revised the manuscript critically and approved the final version to be submitted.

  • Funding ES is funded by a National Health and Medical Research Council (NHMRC) Leadership 2 Fellowship (APP1194510). MJD is supported by a Career Development Fellowship (APP1141606).

  • Disclaimer The funding sources had no involvement in study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.

  • Competing interests None declared.

  • 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.

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