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Difference between revisions of "Jacobs 2012 Abstract Bioblast"

From Bioblast
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|event=[[Bioblast 2012]]
|event=[[Bioblast 2012]]
|abstract=[[File:P1050379.JPG‎|right|150px|Robert Jacobs]]
|abstract=[[File:P1050379.JPG‎|right|150px|Robert Jacobs]]
Differences in skeletal muscle respiratory capacity parallel that of aerobic fitness. It is unknown whether mitochondrial content, alone, can fully account for these differences in skeletal muscle respiratory capacity. The aim of the present study was to examine quantitative and qualitative mitochondrial characteristics across four different groups (n = 6 each), separated by cardiorespiratory fitness. [[High-resolution respirometry]] was performed on muscle samples to compare respiratory capacity and efficiency in active (AT), well-trained (WT), highly-trained (HT), and elite (ET) individuals. Maximal exercise capacity (ml O2 min-1 kg-1) differed across all groups with mean ± SD values of 51 ± 4, 64 ± 5, 71 ± 2, and 77 ± 3, respectively. Mitochondrial content assessed by citrate synthase activity was higher in ET compared to AT and WT (29 ± 7 versus 19 ± 4 and 16 ± 4 nmol min-1 mg ww-1, respectively). When normalizing mitochondrial respiration to content, the respiratory capacities during maximal fatty acid oxidation (p = 0.003), maximal state 3 respiration (p = 0.021), and total electron transport system capacity (p = 0.008) varied between groups. The coupling efficiency of β-oxidation, however, was not affected by level of fitness. These data demonstrate the quantitative and qualitative differences that exist in skeletal muscle mitochondrial respiratory capacity and efficiency across individuals that differ in aerobic capacity. Mitochondrial-specific respiration capacities during β-oxidation, maximal oxidative phosphorylation, and electron transport system capacity all improve in parallel with aerobic capacity, independent of mitochondrial content in human skeletal muscle.
Differences in skeletal muscle respiratory capacity parallel that of aerobic fitness. It is unknown whether mitochondrial content, alone, can fully account for these differences in skeletal muscle respiratory capacity. The aim of the present study was to examine quantitative and qualitative mitochondrial characteristics across four different groups (n = 6 each), separated by cardiorespiratory fitness. [[High-resolution respirometry]] was performed on muscle samples to compare respiratory capacity and efficiency in active (AT), well-trained (WT), highly-trained (HT), and elite (ET) individuals. Maximal exercise capacity (ml O<sub>2</sub> min<sup>-1</sup> kg<sup>-1</sup>) differed across all groups with mean ± SD values of 51 ± 4, 64 ± 5, 71 ± 2, and 77 ± 3, respectively. Mitochondrial content assessed by citrate synthase activity was higher in ET compared to AT and WT (29 ± 7 versus 19 ± 4 and 16 ± 4 nmol min<sup>-1</sup> mg ww<sup>-1</sup>, respectively). When normalizing mitochondrial respiration to content, the respiratory capacities during maximal fatty acid oxidation (p = 0.003), maximal state 3 respiration (p = 0.021), and total electron transport system capacity (p = 0.008) varied between groups. The coupling efficiency of β-oxidation, however, was not affected by level of fitness. These data demonstrate the quantitative and qualitative differences that exist in skeletal muscle mitochondrial respiratory capacity and efficiency across individuals that differ in aerobic capacity. Mitochondrial-specific respiration capacities during β-oxidation, maximal oxidative phosphorylation, and electron transport system capacity all improve in parallel with aerobic capacity, independent of mitochondrial content in human skeletal muscle.
|keywords=Mitochondria, Exercise, Skeletal muscle, Fat oxidation
|keywords=Mitochondria, Exercise, Skeletal muscle, Fat oxidation
|mipnetlab=CH Zurich Lundby C
|mipnetlab=CH Zurich Lundby C

Revision as of 10:04, 19 November 2012

Jacobs RA, Lundby C (2012) Mitochondria express enhanced quality as well as quantity in parallel with aerobic fitness across recreationally active individuals up to elite athletes.

Link: MiPNet17.12 Bioblast 2012 - Open Access

Jacobs RA, Lundby C (2012)

Event: Bioblast 2012

Robert Jacobs

Differences in skeletal muscle respiratory capacity parallel that of aerobic fitness. It is unknown whether mitochondrial content, alone, can fully account for these differences in skeletal muscle respiratory capacity. The aim of the present study was to examine quantitative and qualitative mitochondrial characteristics across four different groups (n = 6 each), separated by cardiorespiratory fitness. High-resolution respirometry was performed on muscle samples to compare respiratory capacity and efficiency in active (AT), well-trained (WT), highly-trained (HT), and elite (ET) individuals. Maximal exercise capacity (ml O2 min-1 kg-1) differed across all groups with mean ± SD values of 51 ± 4, 64 ± 5, 71 ± 2, and 77 ± 3, respectively. Mitochondrial content assessed by citrate synthase activity was higher in ET compared to AT and WT (29 ± 7 versus 19 ± 4 and 16 ± 4 nmol min-1 mg ww-1, respectively). When normalizing mitochondrial respiration to content, the respiratory capacities during maximal fatty acid oxidation (p = 0.003), maximal state 3 respiration (p = 0.021), and total electron transport system capacity (p = 0.008) varied between groups. The coupling efficiency of β-oxidation, however, was not affected by level of fitness. These data demonstrate the quantitative and qualitative differences that exist in skeletal muscle mitochondrial respiratory capacity and efficiency across individuals that differ in aerobic capacity. Mitochondrial-specific respiration capacities during β-oxidation, maximal oxidative phosphorylation, and electron transport system capacity all improve in parallel with aerobic capacity, independent of mitochondrial content in human skeletal muscle.

Keywords: Mitochondria, Exercise, Skeletal muscle, Fat oxidation

O2k-Network Lab: CH Zurich Lundby C


Labels:


Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized cells  Enzyme: TCA Cycle and Matrix Dehydrogenases"TCA Cycle and Matrix Dehydrogenases" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property.  Regulation: Flux Control; Threshold; Excess Capacity"Flux Control; Threshold; Excess Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Fatty Acid"Fatty Acid" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.  Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property. 

HRR: Oxygraph-2k 



Affiliations and author contributions

Zurich Center for Integrative Human Physiology (ZIHP), Zurich, Switzerland; Email: [email protected];

Institute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Switzerland;

Institute of Physiology, University of Zurich, Switzerland


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