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Difference between revisions of "Ponsot 2006 J Appl Physiol (1985)"

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(Created page with "{{Publication |title=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...")
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|year=2006
|year=2006
|journal=J Appl Physiol (1985)
|journal=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 (''V''O2) and speed at VT2, maximal ''V''O2 (''V''O2 max), and time to exhaustion at velocity of ''V''O2 max (minimal speed associated with ''V''O2 max) were measured, and muscle biopsies of vastus lateralis were harvested. Muscle oxidative capacities and sensitivity of mitochondrial respiration to ADP (''K''m) were evaluated on permeabilized muscle fibers. Time to exhaustion, ''V''O2 at VT2, and ''V''O2 max 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 ''K''m 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.
|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 O<sub>2</sub> fraction = 14.5 % [hypoxic group (Hyp), ''N'' = 8] or with inspired O<sup>2</sup> fraction = 21 % [normoxic group (Nor), ''N'' = 7], integrated into their usual training, for 6 wk. Before and after training, oxygen uptake (''V''<sub>O2</sub>) and speed at VT2, maximal ''V''<sub>O2</sub> (''V''<sub>O2max</sub>), and time to exhaustion at velocity of ''V''<sub>O2max</sub> (minimal speed associated with ''V''<sub>O2max</sub>) were measured, and muscle biopsies of vastus lateralis were harvested. Muscle oxidative capacities and sensitivity of mitochondrial respiration to ADP (''K''<sub>m</sub>) were evaluated on permeabilized muscle fibers. Time to exhaustion, ''V''<sub>O2</sub> at VT2, and ''V''<sub>O2max</sub> 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 ''K''<sub>m</sub> 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.
|editor=[[Gnaiger E]],
|editor=[[Gnaiger E]],
}}
}}
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|couplingstates=OXPHOS
|couplingstates=OXPHOS
|pathways=N
|pathways=N
|additional=VO2max, BMI, BME,
|additional=VO2max, BMI, BME, MitoEAGLE BME,
}}
}}

Revision as of 21:13, 8 December 2019

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.

Β» 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.

β€’ Bioblast editor: Gnaiger E


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Hypoxia  Organism: Human 

Preparation: Intact organism 

Regulation: ADP  Coupling state: OXPHOS  Pathway:


VO2max, BMI, BME, MitoEAGLE BME