scholarly journals Differential effects of endurance training and creatine depletion on regional mitochondrial adaptations in rat skeletal muscle

2000 ◽  
Vol 350 (2) ◽  
pp. 547-553 ◽  
Author(s):  
Damien ROUSSEL ◽  
Florence LHENRY ◽  
Laurent ECOCHARD ◽  
Brigitte SEMPORE ◽  
Jean-Louis ROUANET ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Endurance Training ◽  
Oxidative Capacity ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Sedentary Control ◽  
Muscle Mitochondria ◽  
F1 Atpase ◽  
Skeletal Muscle Mitochondria ◽  
Subsarcolemmal Mitochondria

To examine the combined effects of 2-week endurance training and 3-week feeding with β-guanidinopropionic acid (GPA) on regional adaptability of skeletal muscle mitochondria, intermyofibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM) were isolated from quadriceps muscles of sedentary control, trained control, sedentary GPA-fed and trained GPA-fed rats. Mitochondrial oxidative phosphorylation was assessed polarographically by using pyruvate plus malate, succinate (plus rotenone), and ascorbate plus N,N,N´,N´-tetramethyl-p-phenylenediamine (TMPD) (plus antimycin) as respiratory substrates. Assays of cytochrome c oxidase and F1-ATPase activities were also performed. In sedentary control rats, IFM exhibited a higher oxidative capacity than SSM, whereas F1-ATPase activities were similar. Training increased the oxidative phosphorylation capacity of mitochondria with both pyruvate plus malate and ascorbate plus TMPD as substrates, with no differences between IFM and SSM. In contrast, the GPA diet mainly improved the overall SSM oxidative phosphorylation capacity, irrespective of the substrate used. Finally, the superimposition of training to feeding with GPA strongly increased both oxidase and enzymic activities in SSM, whereas no cumulative effects were found in IFM mitochondria. It therefore seems that endurance training and feeding with GPA, which are both known to alter the energetic status of the muscle cell, might mediate distinct biochemical adaptations in regional skeletal muscle mitochondria.

65 Fatty acid oxidation in human skeletal muscle mitochondria determined by oxidative phosphorylation as a function of age

Mitochondrion ◽  
2007 ◽  
Vol 7 (6) ◽  
pp. 422-423
Author(s):  
George Kypriotakis ◽  
Bruce H. Cohen ◽  
Sumit Parikh ◽  
Douglas S. Kerr ◽  
Charles L. Hoppel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Oxidative Phosphorylation ◽  
Fatty Acid Oxidation ◽  
Human Skeletal Muscle ◽  
Acid Oxidation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

scholarly journals Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3

2019 ◽  
Vol 127 (4) ◽  
pp. 1117-1127
Author(s):  
Jessica R. Dent ◽  
Byron Hetrick ◽  
Shahriar Tahvilian ◽  
Abha Sathe ◽  
Keenan Greyslak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electron Transport ◽  
Complex I ◽  
Physiological Function ◽  
Oxidative Capacity ◽  
Signal Transducer ◽  
Muscle Mitochondria ◽  
Complex Ii ◽  
Skeletal Muscle Mitochondria ◽  
Transcription 3

Signal transducer and activator of transcription 3 (STAT3) was recently found to be localized to mitochondria in a number of tissues and cell types, where it modulates oxidative phosphorylation via interactions with the electron transport proteins, complex I and complex II. Skeletal muscle is densely populated with mitochondria although whether STAT3 contributes to skeletal muscle oxidative capacity is unknown. In the present study, we sought to elucidate the contribution of STAT3 to mitochondrial and skeletal muscle function by studying mice with muscle-specific knockout of STAT3 (mKO). First, we developed a novel flow cytometry-based approach to confirm that STAT3 is present in skeletal muscle mitochondria. However, contrary to findings in other tissue types, complex I and complex II activity and maximal mitochondrial respiratory capacity in skeletal muscle were comparable between mKO mice and floxed/wild-type littermates. Moreover, there were no genotype differences in endurance exercise performance, skeletal muscle force-generating capacity, or the adaptive response of skeletal muscle to voluntary wheel running. Collectively, although we confirm the presence of STAT3 in skeletal muscle mitochondria, our data establish that STAT3 is dispensable for mitochondrial and physiological function in skeletal muscle. NEW & NOTEWORTHY Whether signal transducer and activator of transcription 3 (STAT3) can regulate the activity of complex I and II of the electron transport chain and mitochondrial oxidative capacity in skeletal muscle, as it can in other tissues, is unknown. By using a mouse model lacking STAT3 in muscle, we demonstrate that skeletal muscle mitochondrial and physiological function, both in vivo and ex vivo, is not impacted by the loss of STAT3.

A magnesium-responsive defect of respiration and oxidative phosphorylation in skeletal muscle mitochondria of dystrophic hamsters

1970 ◽  
Vol 48 (12) ◽  
pp. 1332-1338 ◽  
Author(s):  
K. Wrogemann ◽  
M. C. Blanchaer ◽  
B. E. Jacobson
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Respiratory Rate ◽  
Test System ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Muscle Necrosis ◽  
Presence And Absence ◽  
Stimulation Of

Skeletal muscle mitochondria were isolated in the presence and absence of the proteinase Nagarse from dystrophic hamsters of the BIO 14.6 strain, aged 45–196 days, and from normal hamsters. Mitochondria from the dystrophic animals prepared by glass-on-glass homogenization without Nagarse in 0.25 M sucrose – 1 mM EDTA, pH 7.4, did not differ from normal in their respiratory rate or capacity for oxidative phosphorylation. However, these functions were subnormal in mitochondria isolated with Nagarse from the same animals, both in the presence and absence of albumin. Respiration measured with an O2 electrode was reduced by 50–70% and the stimulation of O2 uptake normally seen after ADP addition was minimal or absent. This was most marked in mitochondria from young hamsters about 65 days old with muscle necrosis. The defect was ameliorated by addition to the Polarographie test system of an ATP trap or of Mg2+, one of the trap constituents. This ion, when added to the defective mitochondria prior to ADP and substrate, restored respiration and oxidative phosphorylation to values that did not differ significantly from those found with skeletal muscle mitochondria of normal hamsters.

scholarly journals Endurance training increases the efficiency of rat skeletal muscle mitochondria

2016 ◽  
Vol 468 (10) ◽  
pp. 1709-1724 ◽  
Author(s):  
Jerzy A. Zoladz ◽  
Agnieszka Koziel ◽  
Andrzej Woyda-Ploszczyca ◽  
Jan Celichowski ◽  
Wieslawa Jarmuszkiewicz
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Rat Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

scholarly journals Effect of Calcium on the Oxidative Phosphorylation Cascade in Skeletal Muscle Mitochondria

Biochemistry ◽  
2013 ◽  
Vol 52 (16) ◽  
pp. 2793-2809 ◽  
Author(s):  
Brian Glancy ◽  
Wayne T. Willis ◽  
David J. Chess ◽  
Robert S. Balaban
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Phosphorylation Cascade
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