Gnaiger 2020 PaduaMuscleDays

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Gnaiger E (2020) Body mass excess, muscle mass, obesity and mitochondrial fitness. PaduaMuscleDays.

Link: Padova Muscle Days

Gnaiger E (2020)

Event: 2020 PaduaMuscleDays Padova IT

Skeletal muscle is the driver of whole-body aerobic capacity measured by spiroergometry as VO2max/M [mL O2∙min-1∙kg-1]. Obesity is defined as accumulation of excess fat tissue mass, MFE=MF-MF° [kg/x]. MF° is the fat mass [kg] per individual [x] in the healthy reference population at a given height and total body mass M° without overweight [1]. Body fat excess, BFE=MFE/M°, is directly related to total body mass excess, BME=ME/M°, where ME=M-M°. In model 1, BFE does not reduce VO2max [mL O2∙min-1∙x-1], but BFE lowers VO2max/M by increasing M. Experimentally, however, VO2max/M declines with BME much steeper than predicted by model 1. The more pronounced loss of ergometric fitness is due to the decline of mitochondrial respiratory capacity per muscle mass, mM [2,3], as a function of BME. Yet this model 2 predicts an even lower VO2max/M at overweight. Finally, model 3 includes the well-known ‘weight-lifting’ effect of obesity on increasing muscle mass with low mitochondrial density, providing a quantitatively complete link between low mitochondrial and whole body aerobic fitness in obesity before onset of sarcopenia. The decline of muscular mitochondrial fitness in overweight states is a biomarker of the systemic mitObesity syndrome: Compromised mitochondrial fitness across metabolically active organs provides the mechanistic link between obesity and comorbidities such as diabetes, cardiovascular and neurodegenerative diseases and various types of cancer bound to redox imbalance, inflammation, oxidative stress and insulin resistance. Today mitObesity is the world-wide leading cause of deaths and early aging, which can be prevented by an active lifestyle and improvement of the quality of life by exercise and caloric balance.

Keywords: mitochondrial respiratory capacity, BME, VO2max, mitObesity, comorbidities, early aging Bioblast editor: Plangger M O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck MitoFit, AT Innsbruck Oroboros


Affiliations and support

Erich Gnaiger (1,2)
  1. D Swarovski Research Lab, Dept Visceral, Transplant Thoracic Surgery, Med Univ Innsbruck
  2. Oroboros Instruments, Innsbruck; Austria. - erich.gnaiger@oroboros.at
Supported by project NextGen-O2k which has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 859770. Contribution to COST Action CA15203 MitoEAGLE funded by the Horizon 2020 Framework Programme of the European Union.

References

  1. Gnaiger E (2019) OXPHOS capacity in human muscle tissue and body mass excess – the MitoEAGLE mission towards an integrative database. Mitochondrial Physiology Conference, Belgrade. https://www.mitophysiology.org/index.php/Gnaiger_2019_MiP2019 (Version 6; 2020-01-12).
  2. Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41:1837-45.
  3. Gnaiger E, Boushel R, Søndergaard H, Munch-Andersen T, Damsgaard R, Hagen C, Díez-Sánchez C, Ara I, Wright-Paradis C, Schrauwen P, Hesselink M, Calbet JA, Christiansen M, Helge JW, Saltin B (2015) Mitochondrial coupling and capacity of oxidative phosphorylation in skeletal muscle of Inuit and caucasians in the arctic winter. Scand J Med Sci Sports 25(Suppl 4):126–34.


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