Bakkman 2007 ActaPhysiol: Difference between revisions
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{{Publication | {{Publication | ||
|title=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) 190:243β51. | |title=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) 190:243β51. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/17521315 PMID: 17521315] | |||
|authors=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M | |authors=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M | ||
|year=2007 | |year=2007 | ||
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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. | 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 | |keywords=altitude, apparent Km for oxygen, citrate synthase, cytochrome c oxidase, hypoxic exercise, mitochondrial function, oxidative capacity, respiration, latent mitochondrial dysfunction | ||
|editor=[[Gnaiger E]], | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, Exercise physiology;nutrition;life style | |area=Respiration, Exercise physiology;nutrition;life style | ||
|injuries=Oxidative stress;RONS | |||
|organism=Human | |organism=Human | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Isolated mitochondria | |preparations=Isolated mitochondria | ||
|topics=Oxygen kinetics | |topics=Oxygen kinetics | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|additional=latent mitochondrial dysfunction | |pathways=N | ||
|additional=latent mitochondrial dysfunction, MitoEAGLE BME, | |||
}} | }} | ||
== MitoEAGLE ''V''<sub>O2max</sub>/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 kgΒ·m<sup>-2</sup> | |||
:::* ''V''<sub>O2max/BM</sub> = 47.8 mLΒ·min<sup>-1</sup>Β·kg<sup>-1</sup> (= ''V''<sub>O2peak/BM</sub>/0.93) | |||
:::* Isolated mitochondria; 25 Β°C; PM<sub>''P''</sub>; conversions: [[Gnaiger 2009 Int J Biochem Cell Biol]] | |||
:::* ''J''<sub>O2,''P''</sub>(NS) = 97.7 Β΅molΒ·s<sup>-1</sup>Β·kg<sup>-1</sup> wet muscle mass (37 Β°C) | |||
::::* ''J''<sub>O2,''P''</sub>(PM) = 62.5 Β΅molΒ·s<sup>-1</sup>Β·kg<sup>-1</sup> wet muscle mass (37 Β°C) | |||
::::* ''J''<sub>O2,''P''</sub>(NS) = ''J''<sub>O2,''P''</sub>(PM)/0.64 | |||
::::* 8.3 Β΅M mt-protein/mg ''m''<sub>w</sub> | |||
---- |
Revision as of 00:34, 9 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) 190:243β51. |
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. β’ Keywords: altitude, apparent Km for oxygen, citrate synthase, cytochrome c oxidase, hypoxic exercise, mitochondrial function, oxidative capacity, respiration, latent mitochondrial dysfunction β’ 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 kgΒ·m-2
- VO2max/BM = 47.8 mLΒ·min-1Β·kg-1 (= VO2peak/BM/0.93)
- Isolated mitochondria; 25 Β°C; PMP; conversions: Gnaiger 2009 Int J Biochem Cell Biol
- JO2,P(NS) = 97.7 Β΅molΒ·s-1Β·kg-1 wet muscle mass (37 Β°C)
- JO2,P(PM) = 62.5 Β΅molΒ·s-1Β·kg-1 wet muscle mass (37 Β°C)
- JO2,P(NS) = JO2,P(PM)/0.64
- 8.3 Β΅M mt-protein/mg mw