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Gnaiger 2012 Abstract-FEPS-Santiago de Compostela

From Bioblast
Gnaiger E (2012) Aging and mitochondrial physiology. The effect of exercise and caloric balance on oxidative phosphorylation (OXPHOS). Abstract FEPS, Santiago de Compostela, Spain. Symposium: Advances in Aging and Mitochondria Research. September 08-12.

Link: Joint FEPS and Spanish Physiol Soc Scientific Congress 2012

Gnaiger E (2012)

Event: Joint FEPS and Spanish Physiol Soc Scientific Congress

Aging implicates a progressive decline in muscle mass and strength (sarcopenia) which is counteracted by strength training, and a decline of aerobic performance (muscle fatigability, reduced aerobic capacity and loss of mitochondrial power or OXPHOS capacity in muscle tissue). OXPHOS capacity is increased or maintained high by a life style involving endurance exercise and strength training [1]. Life style changes from the age of 20-30 years to the elderly, but is subject to change and intervention. Depending on group selection in cross-sectional studies, OXPHOS capacity declines from the age of 20-30 years [2,3], or is independent of age up to 80 years [4,5]. Independent of age, there is a strong decline of OXPHOS capacity in human vastus lateralis from BMI of 20 to 30 [6]. The relationship between BMI, training and OXPHOS capacity is also observed in horse skeletal muscle [7]. At a BMI >30, a minimum OXPHOS capacity is reached in human v. lateralis that may be characteristic of a low-grade inflammatory state (‘mitochondrial fever’). Onset of degenerative diseases (diabetes 2, neuromuscular degeneration, various cancers) and mitochondrial dysfunction interact in an amplification loop progressing slowly with age, such that cause and effect of mitochondrial dysfunction cannot be distinguished. Diminished antioxidant capacity at low mitochondrial density is an important mechanistic candidate in the state of mitochondrial fever.

Contribution to K-Regio MitoCom Tyrol.

  1. Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans. Am J Physiol Regul Integr Comp Physiol 301:R1078–87.
  2. Short KR, Bigelow ML, Kahl J, Singh R, Coenen-Schimke J, Raghavakaimal S, Nair KS (2005) Decline in skeletal muscle mitochondrial function with aging in humans. Proc Natl Acad Sci U S A 102:5618-23.
  3. Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C (2012) The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals. Aging Cell 11:801-9.
  4. Lanza IR, Short DK, Short KR, Raghavakaimal S, Basu R, Joyner MJ, McConnell JP, Nair KS (2008) Endurance exercise as a countermeasure for aging. Diabetes 57:2933-42.
  5. Larsen S, Hey-Mogensen M, Rabol R, Stride N, Helge JW, Dela F (2012) The influence of age and aerobic fitness: Effects on mitochondrial respiration in skeletal muscle. Acta Physiol (Oxf) 205:423-32.
  6. Gnaiger E (2009) Capacity of oxidative phosphorylation in human skeletal muscle. New perspectives of mitochondrial physiology. Int J Biochem Cell Biol 41:1837–45.
  7. Votion DM, Gnaiger E, Lemieux H, Mouithys-Mickalad A, Serteyn D (2012) Physical fitness and mitochondrial respiratory capacity in horse skeletal muscle. PLoS One 7:e34890.

O2k-Network Lab: AT Innsbruck Oroboros

Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style, mt-Medicine 

Organism: Human, Horse 

Enzyme: Marker enzyme 

Pathway: F, N, S, NS  HRR: Oxygraph-2k