Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Ponsot 2006 J Appl Physiol (1985)

From Bioblast
Revision as of 22:14, 8 December 2019 by Gnaiger Erich (talk | contribs)
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


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, MitoEAGLE BME 

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 = 1.04
  • BMI = 21.8 kg·m-2
  • VO2max/BM = 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)