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Ponsot 2006 J Appl Physiol (1985)

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Publications in the MiPMap
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.

» PMID: 16339351 Open Access

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) J Appl Physiol (1985)

Abstract: This study investigates whether adaptations of mitochondrial function accompany the improvement of endurance performance capacity observed in well-trained athletes after an intermittent hypoxic training program. Fifteen endurance-trained athletes performed two weekly training sessions on treadmill at the velocity associated with the second ventilatory threshold (VT2) with inspired O2 fraction = 14.5 % [hypoxic group (Hyp), N = 8] or with inspired O2 fraction = 21 % [normoxic group (Nor), N = 7], integrated into their usual training, for 6 wk. Before and after training, oxygen uptake (VO2) and speed at VT2, maximal VO2 (VO2max), and time to exhaustion at velocity of VO2max (minimal speed associated with VO2max) were measured, and muscle biopsies of vastus lateralis were harvested. Muscle oxidative capacities and sensitivity of mitochondrial respiration to ADP (Km) were evaluated on permeabilized muscle fibers. Time to exhaustion, VO2 at VT2, and VO2max were significantly improved in Hyp (+42, +8, and +5 %, respectively) but not in Nor. No increase in muscle oxidative capacity was obtained with either training protocol. However, mitochondrial regulation shifted to a more oxidative profile in Hyp only as shown by the increased Km for ADP (Nor: before 476 +/- 63, after 524 +/- 62 microM, not significant; Hyp: before 441 +/- 59, after 694 +/- 51 microM, P < 0.05). Thus including hypoxia sessions into the usual training of athletes qualitatively ameliorates mitochondrial function by increasing the respiratory control by creatine, providing a tighter integration between ATP demand and supply.

Bioblast editor: Gnaiger E

MitoEAGLE VO2max/BME data base

  • Human vastus lateralis
  • 15 (8+7) males
  • 30.6 years
  • Athletic, highly trained distance runners; control groups combined
  • H = 1.81 m
  • M = 71.1 kg
  • BME = 0.04
  • BMI = 21.8 kg·m-2
  • VO2max/M = 62.9 mL·min-1·kg-1
  • Permeabilized muscle fibres; 22 °C; GMP; md; conversions: Gnaiger 2009 Int J Biochem Cell Biol
  • JO2,P(NS) = 181 µmol·s-1·kg-1 wet muscle mass (37 °C)
  • JO2,P(GM) = 132 µmol·s-1·kg-1 wet muscle mass (37 °C)
  • JO2,P(NS) = JO2,P(GM)/0.73
  • Fiber wet mass to dry mass ratio = 3.5 (N'Guessan 2004 Mol Cell Biochem)

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. https://doi.org/10.1111/sms.12612
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.
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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.
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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.
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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.
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Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Hypoxia  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Intact organism 

Regulation: ADP  Coupling state: OXPHOS  Pathway:


VO2max, BMI, BME, MitoEAGLE BME