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Low cardiorespiratory and mitochondrial fitness as risk factors in viral infections: implications for COVID-19
  1. Johannes Burtscher1,2,
  2. Grégoire P Millet2,
  3. Martin Burtscher3
  1. 1 Department of Biomedical Sciences, University of Lausanne Faculty of Biology and Medicine, Lausanne, Switzerland
  2. 2 Institute of Sport Sciences, University of Lausanne, Lausanne, VD, Switzerland
  3. 3 Sport Science, Medical Section, University of Innsbruck, Innsbruck, Austria
  1. Correspondence to Professor Grégoire P Millet, Institute of Sport Sciences, University of Lausanne, Lausanne, VD, Switzerland; gregoire.millet{at}

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Physical activity (PA) modulates immune system functions.1 Susceptibility to viral infection thereby depends on the volume and intensity of PA: regular moderate PA (up to 60% of maximal oxygen uptake for no more than 1 hour/session) and an associated high cardiovascular fitness (CRF) boost immune system capacity and reduce inflammation, whereas exhausting PA transiently suppresses immune functions.1

It seems reasonable that the beneficial effects of regular PA on immune function are at least partly mediated by mitochondrial fitness, as outlined further. Both low mitochondrial fitness and low CRF may be important risk factors for the ongoing COVID-19 pandemic, possibly representing a link between established risk factors like age and various chronic diseases, such as obesity and diabetes mellitus.

Energetic bug busters: mitochondria

Mitochondria are cellular power generators and regulators of metabolism and are critically involved in the antiviral host response.2 One important component in the innate immune defence is the mitochondrial antiviral signalling (MAVS) complex, a large protein complex localised on the outer mitochondrial membrane. MAVS gets activated by a family of pathogen-detecting receptors, the retinoic acid inducible gene-like receptors (RLRs), and induces a response that includes the transcription of class 1 interferons, which serve as central molecules in the cellular defence …

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  • Twitter @JohBurtscher, @GregoireMillet1

  • Contributors All authors contributed to the preparation and writing of the manuscript. All authors read and approved the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

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