scholarly journals Sex-Specific Skeletal Muscle Fatigability and Decreased Mitochondrial Oxidative Capacity in Adult Rats Exposed to Postnatal Hyperoxia

2018 ◽  
Vol 9 ◽  
Author(s):  
Laura H. Tetri ◽  
Gary M. Diffee ◽  
Gregory P. Barton ◽  
Rudolf K. Braun ◽  
Hannah E. Yoder ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Capacity ◽  
Adult Rats ◽  
Mitochondrial Oxidative Capacity

scholarly journals Effect of high-fat feeding on metabolic efficiency and mitochondrial oxidative capacity in adult rats

2003 ◽  
Vol 90 (5) ◽  
pp. 953-960 ◽  
Author(s):  
Susanna Iossa ◽  
Lillà Lionetti ◽  
Maria P. Mollica ◽  
Raffaella Crescenzo ◽  
Monica Botta ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Intake ◽  
High Fat Diet ◽  
Oxidative Capacity ◽  
Metabolic Efficiency ◽  
High Fat ◽  
Adult Rats ◽  
Serum Leptin ◽  
Mitochondrial Oxidative Capacity ◽  
Fat Feeding

The changes in metabolic efficiency, body composition, and nutrient partitioning induced by high-fat feeding were evaluated in adult rats (90d of age). The alterations in serum free triiodothyronine, insulin, and leptin levels, as well as in hepatic and skeletal muscle metabolism, were also assessed. Rats were fed either a low- or a high-fat diet for 2 weeks. Relative to the low-fat feeding, energy intake and expenditure, as well as body-energy gain, lipid gain, and energetic efficiency, were increased by the high-fat feeding. Increased serum leptin levels accompanied these variations. A positive correlation between serum leptin levels and percentage of body fat was found in the rats fed the low- or high-fat diet, with a significant divergence between the slope of the regression lines. Furthermore, a negative correlation between serum leptin level and energy intake was found in the rats fed the low-fat diet, while a positive correlation was found in the rats fed the high-fat diet. Finally, the high-fat feeding decreased the hepatic and skeletal muscle mitochondrial oxidative capacity. It is concluded that, in adult rats, a nutritional factor such as a high level of fat in the diet induces obesity, leptin resistance, and impairment of mitochondrial capacity, all phenomena typical of unrestrained aged rats.

Short term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes

2021 ◽  
Author(s):  
Daniele A. Cardinale ◽  
Kasper D. Gejl ◽  
Kristine Grøsfjeld Petersen ◽  
Joachim Nielsen ◽  
Niels Ørtenblad ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Quality Control ◽  
Oxidative Capacity ◽  
Endurance Athletes ◽  
Training Period ◽  
Moderate Intensity ◽  
Mitochondrial Quality Control ◽  
Quality Control Program ◽  
Mitochondrial Oxidative Capacity ◽  
Mitochondrial Respiratory

Aim: The maintenance of healthy and functional mitochondria is the result of a complex mitochondrial turnover and herein quality-control program which includes both mitochondrial biogenesis and autophagy of mitochondria. The aim of this study was to examine the effect of an intensified training load on skeletal muscle mitochondrial quality control in relation to changes in mitochondrial oxidative capacity, maximal oxygen consumption and performance in highly trained endurance athletes. Methods: 27 elite endurance athletes performed high intensity interval exercise followed by moderate intensity continuous exercise 3 days per week for 4 weeks in addition to their usual volume of training. Mitochondrial oxidative capacity, abundance of mitochondrial proteins, markers of autophagy and antioxidant capacity of skeletal muscle were assessed in skeletal muscle biopsies before and after the intensified training period. Results: The intensified training period increased several autophagy markers suggesting an increased turnover of mitochondrial and cytosolic proteins. In permeabilized muscle fibers, mitochondrial respiration was ~20 % lower after training although some markers of mitochondrial density increased by 5-50%, indicative of a reduced mitochondrial quality by the intensified training intervention. The antioxidative proteins UCP3, ANT1, and SOD2 were increased after training, whereas we found an inactivation of aconitase. In agreement with the lower aconitase activity, the amount of mitochondrial LON protease that selectively degrades oxidized aconitase, was doubled. Conclusion: Together, this suggests that mitochondrial respiratory function is impaired during the initial recovery from a period of intensified endurance training while mitochondrial quality control is slightly activated in highly trained skeletal muscle.

AMPK controls exercise endurance, mitochondrial oxidative capacity, and skeletal muscle integrity

2014 ◽  
Vol 28 (7) ◽  
pp. 3211-3224 ◽  
Author(s):  
Louise Lantier ◽  
Joachim Fentz ◽  
Rémi Mounier ◽  
Jocelyne Leclerc ◽  
Jonas T. Treebak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Capacity ◽  
Mitochondrial Oxidative Capacity ◽  
Exercise Endurance

scholarly journals Eicosapentaenoic acid but not docosahexaenoic acid restores skeletal muscle mitochondrial oxidative capacity in old mice

Aging Cell ◽  
2015 ◽  
Vol 14 (5) ◽  
pp. 734-743 ◽  
Author(s):  
Matthew L. Johnson ◽  
Antigoni Z. Lalia ◽  
Surendra Dasari ◽  
Maximilian Pallauf ◽  
Mark Fitch ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Docosahexaenoic Acid ◽  
Eicosapentaenoic Acid ◽  
Oxidative Capacity ◽  
Mitochondrial Oxidative Capacity ◽  
Old Mice

scholarly journals A Plasma Proteomic Signature of Skeletal Muscle Mitochondrial Function

2020 ◽  
Vol 21 (24) ◽  
pp. 9540
Author(s):  
Marta Zampino ◽  
Toshiko Tanaka ◽  
Ceereena Ubaida-Mohien ◽  
Giovanna Fantoni ◽  
Julián Candia ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Proteins ◽  
Recovery Time ◽  
Oxidative Capacity ◽  
Resonance Spectroscopy ◽  
Longitudinal Analyses ◽  
Post Exercise ◽  
Age Related ◽  
Mitochondrial Oxidative Capacity ◽  
Independent Cohort

Although mitochondrial dysfunction has been implicated in aging, physical function decline, and several age-related diseases, an accessible and affordable measure of mitochondrial health is still lacking. In this study we identified the proteomic signature of muscular mitochondrial oxidative capacity in plasma. In 165 adults, we analyzed the association between concentrations of plasma proteins, measured using the SOMAscan assay, and skeletal muscle maximal oxidative phosphorylation capacity assessed as post-exercise phosphocreatine recovery time constant (τPCr) by phosphorous magnetic resonance spectroscopy. Out of 1301 proteins analyzed, we identified 87 proteins significantly associated with τPCr, adjusting for age, sex, and phosphocreatine depletion. Sixty proteins were positively correlated with better oxidative capacity, while 27 proteins were correlated with poorer capacity. Specific clusters of plasma proteins were enriched in the following pathways: homeostasis of energy metabolism, proteostasis, response to oxidative stress, and inflammation. The generalizability of these findings would benefit from replication in an independent cohort and in longitudinal analyses.

scholarly journals Decreased mitochondrial oxidative capacity or reduced metabolic efficiency in skeletal muscle in congestive heart failure?

1996 ◽  
Vol 27 (2) ◽  
pp. 114
Author(s):  
Graham Kemp ◽  
Stamatis Adamopoulos ◽  
Campbell Thompson ◽  
John Stratton ◽  
Françoise Brunotte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Oxidative Capacity ◽  
Metabolic Efficiency ◽  
Mitochondrial Oxidative Capacity
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