Pesta 2011 Am J Physiol Regul Integr Comp Physiol: Difference between revisions
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{{Publication | {{Publication | ||
|title=Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans.. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2011 Jul 20. [Epub ahead of print] | |title=Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans.. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2011 Jul 20. [Epub ahead of print] | ||
|authors=Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E | |authors=Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E | ||
|year=2011 | |year=2011 | ||
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|abstract=Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training-"specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia (F(iO2)=21% or 13.5%). Biopsies were taken from the m. vastus lateralis and cycle-ergometric incremental V(O2max) exercise tests were performed under normoxia, before and after the 10-week training program. The main finding was a significant increase (P<0.05) of tissue-specific fatty acid oxidation capacity, after endurance and strength training under normoxia (2.6- and 2.4-fold for ET(N) and ST(N); N=8 and 3) and hypoxia (2.0-fold for ET(H) and ST(H); N=7 and 7), and higher coupling control of oxidative phosphorylation. The enhanced lipid OXPHOS capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P<0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in tissue-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, octanoylcarnitine). No significant increase was observed in mtDNA content. Physiological OXPHOS capacity increased significantly in ET(N) (P<0.01), with the same trend in ET(H) and ST(H) (P<0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active life style induced muscular changes of mitochondrial quality representative of mitochondrial health. | |abstract=Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training-"specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia (F(iO2)=21% or 13.5%). Biopsies were taken from the m. vastus lateralis and cycle-ergometric incremental V(O2max) exercise tests were performed under normoxia, before and after the 10-week training program. The main finding was a significant increase (P<0.05) of tissue-specific fatty acid oxidation capacity, after endurance and strength training under normoxia (2.6- and 2.4-fold for ET(N) and ST(N); N=8 and 3) and hypoxia (2.0-fold for ET(H) and ST(H); N=7 and 7), and higher coupling control of oxidative phosphorylation. The enhanced lipid OXPHOS capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P<0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in tissue-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, octanoylcarnitine). No significant increase was observed in mtDNA content. Physiological OXPHOS capacity increased significantly in ET(N) (P<0.01), with the same trend in ET(H) and ST(H) (P<0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active life style induced muscular changes of mitochondrial quality representative of mitochondrial health. | ||
|keywords=mitochondrial respiration, endurance training, strength training, human skeletal muscle, permeabilized fibers, OXPHOS capacity, coupling control, fatty acid oxidation | |keywords=mitochondrial respiration, endurance training, strength training, human skeletal muscle, permeabilized fibers, OXPHOS capacity, coupling control, fatty acid oxidation | ||
|mipnetlab= | |mipnetlab=AT_Innsbruck_Gnaiger E, AT_Innsbruck_OROBOROS | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 19:21, 10 August 2011
| [[Has title::Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans.. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2011 Jul 20. [Epub ahead of print]]] |
Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, Parson W, Burtscher M, Schocke M, Gnaiger E (2011) Am. J. Physiol. Regul. Integr. Comp. Physiol.
Abstract: Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training-"specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia (F(iO2)=21% or 13.5%). Biopsies were taken from the m. vastus lateralis and cycle-ergometric incremental V(O2max) exercise tests were performed under normoxia, before and after the 10-week training program. The main finding was a significant increase (P<0.05) of tissue-specific fatty acid oxidation capacity, after endurance and strength training under normoxia (2.6- and 2.4-fold for ET(N) and ST(N); N=8 and 3) and hypoxia (2.0-fold for ET(H) and ST(H); N=7 and 7), and higher coupling control of oxidative phosphorylation. The enhanced lipid OXPHOS capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P<0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in tissue-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, octanoylcarnitine). No significant increase was observed in mtDNA content. Physiological OXPHOS capacity increased significantly in ET(N) (P<0.01), with the same trend in ET(H) and ST(H) (P<0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active life style induced muscular changes of mitochondrial quality representative of mitochondrial health. • Keywords: mitochondrial respiration, endurance training, strength training, human skeletal muscle, permeabilized fibers, OXPHOS capacity, coupling control, fatty acid oxidation
• O2k-Network Lab: AT_Innsbruck_Gnaiger E, AT_Innsbruck_OROBOROS
Labels:
Stress:Hypoxia Organism: Human Tissue;cell: Skeletal Muscle Preparation: Permeabilized Cell or Tissue; Homogenate Enzyme: TCA Cycle and Matrix Dehydrogenases, Complex I, Complex II; Succinate Dehydrogenase, Complex III Regulation: Respiration; OXPHOS; ETS Capacity, Flux Control; Additivity; Threshold; Excess Capacity, Coupling; Membrane Potential, Mitochondrial Biogenesis; Mitochondrial Density, Substrate; Glucose; TCA Cycle, Fatty Acid, Amino Acid
HRR: Oxygraph-2k
ergometry
