Difference between revisions of "Bakkman 2007 ActaPhysiol"
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:::* [[BME]] = 1.19 | :::* [[BME]] = 1.19 | ||
:::* BMI = 24.5 kg·m<sup>-2</sup> | :::* BMI = 24.5 kg·m<sup>-2</sup> | ||
:::* ''V''<sub>O2max/BM</sub> = | :::* ''V''<sub>O2max/BM</sub> = 44.5 mL·min<sup>-1</sup>·kg<sup>-1</sup> | ||
:::* Isolated mitochondria; 25 °C; PM<sub>''P''</sub>; conversions: [[Gnaiger 2009 Int J Biochem Cell Biol]] | :::* Isolated mitochondria; 25 °C; PM<sub>''P''</sub>; conversions: [[Gnaiger 2009 Int J Biochem Cell Biol]] | ||
:::* ''J''<sub>O2,''P''</sub>(NS) = 97.7 µmol·s<sup>-1</sup>·kg<sup>-1</sup> wet muscle mass (37 °C) | :::* ''J''<sub>O2,''P''</sub>(NS) = 97.7 µmol·s<sup>-1</sup>·kg<sup>-1</sup> wet muscle mass (37 °C) |
Revision as of 09:30, 12 December 2019
Bakkman 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. |
Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Acta Physiol (Oxford)
Abstract: Aim: To investigate if training during hypoxia (H) improves the adaptation of muscle oxidative function compared with normoxic (N) training performed at the same relative intensity.
Method: Eight untrained volunteers performed one-legged cycle training during 4 weeks in a low-pressure chamber. One leg was trained under N conditions and the other leg under hypobaric hypoxia (526 mmHg) at the same relative intensity as during N (65% of maximal power output, Wmax). Muscle biopsies were taken from vastus lateralis before and after the training period. Muscle samples were analysed for the activities of oxidative enzymes [citrate synthase (CS) and cytochrome c oxidase (COX)] and mitochondrial respiratory function.
Results: Wmax increased with more than 30% over the training period during both N and H. CS activity increased significantly after training during N conditions (+20.8%, P < 0.05) but remained unchanged after H training (+4.5%, ns) with a significant difference between conditions (P < 0.05 H vs. N). COX activity was not significantly changed by training and was not different between exercise conditions [+14.6 (N) vs. -2.3% (H), ns]. Maximal ADP stimulated respiration (state 3) expressed per weight of muscle tended to increase after N (+31.2%, P < 0.08) but not after H training (+3.2%, ns). No changes were found in state four respiration, respiratory control index, P/O ratio, mitochondrial Ca2+ resistance and apparent Km for oxygen.
Conclusion: The training-induced increase in muscle oxidative function observed during N was abolished during H. Altitude training may thus be disadvantageous for adaptation of muscle oxidative function. • Keywords: altitude, apparent Km for oxygen, citrate synthase, cytochrome c oxidase, hypoxic exercise, mitochondrial function, oxidative capacity, respiration, latent mitochondrial dysfunction • Bioblast editor: Gnaiger E
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Stress:Oxidative stress;RONS Organism: Human Tissue;cell: Skeletal muscle Preparation: Isolated mitochondria
Regulation: Oxygen kinetics Coupling state: OXPHOS Pathway: N
latent mitochondrial dysfunction, MitoEAGLE BME
MitoEAGLE VO2max/BME data base
- Human vastus lateralis
- 3 females & 5 males
- 27.4 years
- Untrained
- h = 1.75 m
- m = 74.9 kg
- BME = 1.19
- BMI = 24.5 kg·m-2
- VO2max/BM = 44.5 mL·min-1·kg-1
- Isolated mitochondria; 25 °C; PMP; conversions: Gnaiger 2009 Int J Biochem Cell Biol
- JO2,P(NS) = 97.7 µmol·s-1·kg-1 wet muscle mass (37 °C)
- JO2,P(PM) = 62.5 µmol·s-1·kg-1 wet muscle mass (37 °C)
- JO2,P(NS) = JO2,P(PM)/0.64
- 8.3 µM mt-protein/mg mw