Gnaiger 2015 Scand J Med Sci Sports

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Publications in the MiPMap
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 JAL, 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.

» PMID: 26589126 Open Access »O2k-brief

Gnaiger E, Boushel R, Soendergaard H, Munch-Andersen T, Damsgaard R, Hagen C, Diez-Sanchez C, Ara I, Wright-Paradis C, Schrauwen P, Hesselink M, Calbet JA, Christiansen M, Helge JW, Saltin B (2015) Scand J Med Sci Sports

Abstract: O2k-Publications: TopicsO2k-in brief

1OctM;2D;3G;4S;5Rot;6Omy;7U;7c;8Ama.png

During evolution, mtDNA haplogroups of arctic populations may have been selected for lower coupling of mitochondrial respiration to ATP production in favor of higher heat production. We show that mitochondrial coupling in skeletal muscle of traditional and westernized Inuit habituating northern Greenland is identical to Danes of western Europe haplogroups. Biochemical coupling efficiency was preserved across variations in diet, muscle fibre type and uncoupling protein-3 content. Mitochondrial phenotype displayed plasticity in relation to lifestyle and environment. Untrained Inuit and Danes had identical capacities to oxidize fat substrate in arm muscle, which increased in Danes during the 42 days of acclimation to exercise, approaching the higher level of the Inuit hunters. A common pattern emerges of mitochondrial acclimatization and evolutionary adaptation in humans at high latitude and high altitude where economy of locomotion may be optimized by preservation of biochemical coupling efficiency at modest mitochondrial density, when submaximum performance is uncoupled from VO2max and maximum capacities of oxidative phosphorylation.

Keywords: BMI, VO2max Bioblast editor: Gnaiger E O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros, CA Vancouver Boushel RC, NL Maastricht Schrauwen P, DK Copenhagen Christiansen M, ES CN Las Palmas Calbet JA

SUIT protocol

Science and adventure
Project of the Copenhagen Muscle Research Centre (CMRC), Rigshospitalet, Copenhagen, Denmark (Prof. Dr. Bengt Saltin). Logo of the CMRC Greenland 2004 Expedition, designed by Crownprince Frederik of Denmark.

Greenland expedition CMRC: science and adventure

» Greenland Expedition CMRC
» The Saltin Symposium: Exercise and Integrative Physiology (2015)


MitoEAGLE VO2max/BME database

  • Human vastus lateralis
  • 8 females & 8 males
  • 31 years
  • Active; Danes, baseline control in Copenhagen
  • H = 1.75 m
  • M = 74.5 kg
  • BME = 0.19
  • BMI = 24.3 kg·m-2
  • VO2max/M = 48.0 mL·min-1·kg-1
  • Permeabilized muscle fibres; 30 °C; GMSP; mw; conversions: Gnaiger 2009 Int J Biochem Cell Biol
  • JO2,P(NS) = 90.5 µmol·s-1·kg-1 wet muscle mass (37 °C)

Bengt Saltin - a Gentle Scientist

Saltin-Bengt 2015-June Salutation GnaigerE.jpg

Additional references

  • Marconi C, Marzorati M, Cerretelli P (2006) Work capacity of permanent residents of high altitude. High Alt Med Biol 7:105-115. - »Bioblast link«
  • Tam E, Bruseghini P, Calabria E, Sacco LD, Doria C, Grassi B, Pietrangelo T, Pogliaghi S, Reggiani C, Salvadego D, Schena F, Toniolo L, Verratti V, Vernillo G, Capelli C (2015) Gokyo Khumbu/Ama Dablam Trek 2012: effects of physical training and high-altitude exposure on oxidative metabolism, muscle composition, and metabolic cost of walking in women. Eur J Appl Physiol. - »Bioblast link«


O2k-brief.png

O2k-brief

» List of O2k-Publications presented as O2k-brief

MitoFit news 2015#18

  • 2015-11-25: Performance tests on skeletal muscle mitochondria of the Inuit haplogroup reveal fitness information beyond the uncoupling hypothesis for adaptations to the arctic climate. » MitoFit news - a contribution to K-Regio MitoFit.

References: BME and VO2max

» VO2max
 Reference
Bakkman 2007 ActaPhysiolBakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared with normoxic training at the same relative work rate. Acta Physiol (Oxford) 190:243–51.
Boushel 2007 DiabetologiaBoushel RC, Gnaiger E, Schjerling P, Skovbro M, Kraunsoee R, Dela F (2007) Patients with Type 2 diabetes have normal mitochondrial function in skeletal muscle. Diabetologia 50:790-6.
Chambers 2020 J Appl Physiol (1985)Chambers TL, Burnett TR, Raue U, Lee GA, Finch WH, Graham BM, Trappe TA, Trappe S (2020) Skeletal muscle size, function, and adiposity with lifelong aerobic exercise. J Appl Physiol (1985) 128:368–78.
Daussin 2008 Am J Physiol Regul Integr Comp PhysiolDaussin FN, Zoll J, Dufour SP, Ponsot E, Lonsdorfer-Wolf E, Doutreleau S, Mettauer B, Piquard F, Geny B, Richard R (2008) Effect of interval versus continuous training on cardiorespiratory and mitochondrial functions: relationship to aerobic performance improvements in sedentary subjects. Am J Physiol Regul Integr Comp Physiol 295:R264-72.
Garnier 2005 FASEB JGarnier A, Fortin D, Zoll J, N'Guessan B, Mettauer B, Lampert E, Veksler V, Ventura-Clapier R (2005) Coordinated changes in mitochondrial function and biogenesis in healthy and diseased human skeletal muscle. FASEB J 19:43-52.
Gnaiger 2015 Scand J Med Sci SportsGnaiger 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 JAL, 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.
Gnaiger 2019 MiP2019
Erich Gnaiger
OXPHOS capacity in human muscle tissue and body mass excess – the MitoEAGLE mission towards an integrative database (Version 6; 2020-01-12).
Loe 2013 PLOS ONELoe H, Rognmo Ø, Saltin B, Wisløff U (2013) Aerobic capacity reference data in 3816 healthy men and women 20-90 years. PLOS ONE 8:e64319.
Mettauer 2001 J Am Coll CardiolMettauer B, Zoll J, Sanchez H, Lampert E, Ribera F, Veksler V, Bigard X, Mateo P, Epailly E, Lonsdorfer J, Ventura-Clapier R (2001) Oxidative capacity of skeletal muscle in heart failure patients versus sedentary or active control subjects. J Am Coll Cardiol 38:947-54.
Mogensen 2006 J PhysiolMogensen M, Bagger M, Pedersen PK, Fernström M, Sahlin K (2006) Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency. J Physiol 571:669-81.
N'Guessan 2004 Mol Cell BiochemN'Guessan B, Zoll J, Ribera F, Ponsot E, Lampert E, Ventura-Clapier R, Veksler V, Mettauer B (2004) Evaluation of quantitative and qualitative aspects of mitochondrial function in human skeletal and cardiac muscles. Mol Cell Biochem 256-257:267-80.
Pesta 2011 Am J Physiol Regul Integr Comp PhysiolPesta 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.
Ponsot 2006 J Appl Physiol (1985)Ponsot E, Dufour SP, Zoll J, Doutrelau S, N'Guessan B, Geny B, Hoppeler H, Lampert E, Mettauer B, Ventura-Clapier R, Richard R (2006) Exercise training in normobaric hypoxia in endurance runners. II. Improvement of mitochondrial properties in skeletal muscle. J Appl Physiol (1985) 100:1249-57.
Pribis 2010 NutrientsPribis P, Burtnack CA, McKenzie SO, Thayer J (2010) Trends in body fat, body mass index and physical fitness among male and female college students. Nutrients 2:1075-85.
Raboel 2009 Diabetes Obes MetabRaboel R, Hojberg PM, Almdal T, Boushel RC, Haugaard SB, Madsbad S, Dela F (2009) Improved glycaemic control decreases inner mitochondrial membrane leak in type 2 diabetes. Diabetes Obes Metab 11:355-60.
Rasmussen 2001 Am J Physiol Endocrinol MetabRasmussen UF, Rasmussen HN, Krustrup P, Quistorff B, Saltin B, Bangsbo J (2001) Aerobic metabolism of human quadriceps muscle: in vivo data parallel measurements on isolated mitochondria. Am J Physiol Endocrinol Metab 280:E301-7.
Rasmussen 2003 Eur J PhysiolRasmussen UF, Krustrup P, Kjaer M, Rasmussen HN (2003) Human skeletal muscle mitochondrial metabolism in youth and senescence: no signs of functional changes in ATP formation and mitochondrial oxidative capacity. Pflugers Arch – Eur J Physiol 446:270-78.
Zoll 2002 J PhysiolZoll J, Sanchez H, N'Guessan B, Ribera F, Lampert E, Bigard X, Surrurier B, Fortin D, Geny B, Veksler V, Ventura-Clapier R, Mettauer B (2002) Physical activity changes the regulation of mitochondrial respiration in human skeletal muscle. J Physiol 543:191-200.

MitoPedia: BME and mitObesity

» Body mass excess and mitObesity | BME and mitObesity news | Summary |

TermAbbreviationDescription
BME cutoff pointsBME cutoffObesity is defined as a disease associated with an excess of body fat with respect to a healthy reference condition. Cutoff points for body mass excess, BME cutoff points, define the critical values for underweight (-0.1 and -0.2), overweight (0.2), and various degrees of obesity (0.4, 0.6, 0.8, and above). BME cutoffs are calibrated by crossover-points of BME with established BMI cutoffs.
Body fat excessBFEIn the healthy reference population (HRP), there is zero body fat excess, BFE, and the fraction of excess body fat in the HRP is expressed - by definition - relative to the reference body mass, M°, at any given height. Importantly, body fat excess, BFE, and body mass excess, BME, are linearly related, which is not the case for the body mass index, BMI.
Body massm [kg]; M [kg·x-1]The body mass, M, is the mass (kilogram [kg]) of an individual (object) [x] and is expressed in units [kg/x]. Whereas the body weight changes as a function of gravitational force (you are weightless at zero gravity; your floating weight in water is different from your weight in air), your mass is independent of gravitational force, and it is the same in air and water.
Body mass excessBMEThe body mass excess, BME, is an index of obesity and as such BME is a lifestyle metric. The BME is a measure of the extent to which your actual body mass, M [kg/x], deviates from M° [kg/x], which is the reference body mass [kg] per individual [x] without excess body fat in the healthy reference population, HRP. A balanced BME is BME° = 0.0 with a band width of -0.1 towards underweight and +0.2 towards overweight. The BME is linearly related to the body fat excess.
Body mass indexBMIThe body mass index, BMI, is the ratio of body mass to height squared (BMI=M·H-2), recommended by the WHO as a general indicator of underweight (BMI<18.5 kg·m-2), overweight (BMI>25 kg·m-2) and obesity (BMI>30 kg·m-2). Keys et al (1972; see 2014) emphasized that 'the prime criterion must be the relative independence of the index from height'. It is exactly the dependence of the BMI on height - from children to adults, women to men, Caucasians to Asians -, which requires adjustments of BMI-cutoff points. This deficiency is resolved by the body mass excess relative to the healthy reference population.
ComorbidityComorbidities are common in obesogenic lifestyle-induced early aging. These are preventable, non-communicable diseases with strong associations to obesity. In many studies, cause and effect in the sequence of onset of comorbidities remain elusive. Chronic degenerative diseases are commonly obesity-induced. The search for the link between obesity and the etiology of diverse preventable diseases lead to the hypothesis, that mitochondrial dysfunction is the common mechanism, summarized in the term 'mitObesity'.
Healthy reference populationHRPA healthy reference population, HRP, establishes the baseline for the relation between body mass and height in healthy people of zero underweight or overweight, providing a reference for evaluation of deviations towards underweight or overweight and obesity. The WHO Child Growth Standards (WHO-CGS) on height and body mass refer to healthy girls and boys from Brazil, Ghana, India, Norway, Oman and the USA. The Committee on Biological Handbooks compiled data on height and body mass of healthy males from infancy to old age (USA), published before emergence of the fast-food and soft-drink epidemic. Four allometric phases are distinguished with distinct allometric exponents. At heights above 1.26 m/x the allometric exponent is 2.9, equal in women and men, and significantly different from the exponent of 2.0 implicated in the body mass index, BMI [kg/m2].
Height of humansh [m]; H [m·x-1]The height of humans, h, is given in SI units in meters [m]. Humans are countable objects, and the symbol and unit of the number of objects is N [x]. The average height of N objects is, H = h/N [m/x], where h is the heights of all N objects measured on top of each other. Therefore, the height per human has the unit [m·x-1] (compare body mass [kg·x-1]). Without further identifyer, H is considered as the standing height of a human, measured without shoes, hair ornaments and heavy outer garments.
MitObesity drugsBioactive mitObesity compounds are drugs and nutraceuticals with more or less reproducible beneficial effects in the treatment of diverse preventable degenerative diseases implicated in comorbidities linked to obesity, characterized by common mechanisms of action targeting mitochondria.
ObesityObesity is a disease resulting from excessive accumulation of body fat. In common obesity (non-syndromic obesity) excessive body fat is due to an obesogenic lifestyle with lack of physical exercise ('couch') and caloric surplus of food consumption ('potato'), causing several comorbidities which are characterized as preventable non-communicable diseases. Persistent body fat excess associated with deficits of physical activity induces a weight-lifting effect on increasing muscle mass with decreasing mitochondrial capacity. Body fat excess, therefore, correlates with body mass excess up to a critical stage of obesogenic lifestyle-induced sarcopenia, when loss of muscle mass results in further deterioration of physical performance particularly at older age.
VO2maxVO2max; VO2max/MMaximum oxygen consumption, VO2max, is measured by spiroergometry on human and animal organisms capable of controlled physical exercise performance on a treadmill or cycle ergometer. VO2max is the maximum respiration of an organism, expressed as the volume of O2 at STPD consumed per unit of time per individual object [mL.min-1.x-1]. If normalized per body mass of the individual object, M [kg.x-1], mass specific maximum oxygen consumption, VO2max/M, is expressed in units [mL.min-1.kg-1].


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mtDNA;mt-genetics, Comparative MiP;environmental MiP, Gender, Exercise physiology;nutrition;life style 

Stress:Temperature  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Marker enzyme, TCA cycle and matrix dehydrogenases  Regulation: Coupling efficiency;uncoupling, Cyt c  Coupling state: LEAK, OXPHOS, ET  Pathway: F, N, S, ROX  HRR: Oxygraph-2k, O2k-Protocol 

MitoFitPublication, VO2max, BMI, BME, 1OctM;2D;3G;4S;5Rot;6Omy;7U-, SUIT-016, SUIT-016 O2 pfi D044, MitoEAGLE BME