scholarly journals THE RELATIONSHIP BETWEEN CYTOCHONDRIA AND MYOFIBRILS IN PIGEON SKELETAL MUSCLE

1953 ◽  
Vol 98 (1) ◽  
pp. 81-98 ◽  
Author(s):  
John W. Harman ◽  
Ursula H. Osborne
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Oxidative Metabolism ◽  
Krebs Cycle ◽  
Oxidative Capacity ◽  
Breast Muscle ◽  
Oxidative Enzymes ◽  
Mitochondrial Oxidative Capacity ◽  
The Relationship ◽  
Oxidative Rate

In pigeon breast muscle the mitochondria are the principal site of oxidative metabolism, whereas the myofibrils are incapable of oxidizing intermediates of the Krebs cycle. The mitochondria contain the oxidative enzymes, and the sarcosomes are associated with a factor which accelerates the mitochondrial oxidative rate. The maintenance of myofibrillar contractility and structure is closely correlated with preservation of mitochondrial oxidative capacity and structure. By use of fluoride and dinitrophenol the connection between mitochondrial metabolism and myofibrillar behavior is shown to occur through the process of oxidative phosphorylation.

Skeletal muscle phosphocreatine recovery in exercise-trained humans is dependent on O2availability

1999 ◽  
Vol 86 (6) ◽  
pp. 2013-2018 ◽  
Author(s):  
Luke J. Haseler ◽  
Michael C. Hogan ◽  
Russell S. Richardson
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Metabolism ◽  
Gastrocnemius Muscle ◽  
Plantar Flexion ◽  
Oxidative Capacity ◽  
Submaximal Exercise ◽  
Resonance Spectroscopy ◽  
The Relationship ◽  
Male Subjects ◽  
Plantar Flexion Exercise

In skeletal muscle, phosphocreatine (PCr) recovery from submaximal exercise has become a reliable and accepted measure of muscle oxidative capacity. During exercise, O2 availability plays a role in determining maximal oxidative metabolism, but the relationship between O2 availability and oxidative metabolism measured by31P-magnetic resonance spectroscopy (MRS) during recovery from exercise has never been studied. We used 31P-MRS to study exercising human gastrocnemius muscle under conditions of varied fractions of inspired O2 [Formula: see text]) to test the hypothesis that varied O2availability modulates PCr recovery from submaximal exercise. Six male subjects performed three bouts of 5-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery in a 1.5-T magnet while breathing three different[Formula: see text] concentrations (0.10, 0.21, and 1.00). Under each[Formula: see text] treatment, the PCr recovery time constants were significantly different, being longer in hypoxia [33.5 ± 4.1 s (SE)] and shorter in hyperoxia (20.0 ± 1.8 s) than in normoxia (25.0 ± 2.7 s) ( P ≤ 0.05). End-exercise pH was not significantly different among the three treatments (7.08 ± 0.01 for 0.10, 7.04 ± 0.01 for 0.21, and 7.04 ± 0.02 for 1.00). These results demonstrate that PCr recovery is significantly altered by[Formula: see text] and suggest that, after submaximal exercise, PCr recovery, under normoxic conditions, is limited by O2 availability.

HIF-1α in endurance training: suppression of oxidative metabolism

2007 ◽  
Vol 293 (5) ◽  
pp. R2059-R2069 ◽  
Author(s):  
Steven D. Mason ◽  
Helene Rundqvist ◽  
Ioanna Papandreou ◽  
Roger Duh ◽  
Wayne J. McNulty ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Oxidative Metabolism ◽  
Hypoxia Inducible Factor ◽  
Transcriptional Response ◽  
Oxidative Capacity ◽  
Pyruvate Dehydrogenase Kinase ◽  
Amp Activated Protein Kinase ◽  
Training Protocol

During endurance training, exercising skeletal muscle experiences severe and repetitive oxygen stress. The primary transcriptional response factor for acclimation to hypoxic stress is hypoxia-inducible factor-1α (HIF-1α), which upregulates glycolysis and angiogenesis in response to low levels of tissue oxygenation. To examine the role of HIF-1α in endurance training, we have created mice specifically lacking skeletal muscle HIF-1α and subjected them to an endurance training protocol. We found that only wild-type mice improve their oxidative capacity, as measured by the respiratory exchange ratio; surprisingly, we found that HIF-1α null mice have already upregulated this parameter without training. Furthermore, untrained HIF-1α null mice have an increased capillary to fiber ratio and elevated oxidative enzyme activities. These changes correlate with constitutively activated AMP-activated protein kinase in the HIF-1α null muscles. Additionally, HIF-1α null muscles have decreased expression of pyruvate dehydrogenase kinase I, a HIF-1α target that inhibits oxidative metabolism. These data demonstrate that removal of HIF-1α causes an adaptive response in skeletal muscle akin to endurance training and provides evidence for the suppression of mitochondrial biogenesis by HIF-1α in normal tissue.

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.

Physiological and biochemical correlates of increased work in trained iron-deficient rats

1988 ◽  
Vol 65 (1) ◽  
pp. 256-263 ◽  
Author(s):  
W. T. Willis ◽  
P. R. Dallman ◽  
G. A. Brooks
Keyword(s):  
Skeletal Muscle ◽  
Nadh Oxidase ◽  
Tca Cycle ◽  
Work Capacity ◽  
Oxidative Capacity ◽  
Oxidative Enzymes ◽  
Tca Cycle Enzymes ◽  
Iron Deficient ◽  
Old Rats ◽  
Physiological And Biochemical

We investigated physiological and biochemical factors associated with the improved work capacity of trained iron-deficient rats. Female 21-day-old rats were assigned to one of four groups, two dietary groups (50 and 6 ppm dietary iron) subdivided into two levels of activity (sedentary and treadmill trained). Iron deficiency decreased hemoglobin (61%), maximal O2 uptake. (VO2max) (40%), skeletal muscle mitochondrial oxidase activities (59-90%), and running endurance (94%). In contrast, activities of tricarboxylic acid (TCA) cycle enzymes in skeletal muscle were largely unaffected. Four weeks of mild training in iron-deficient rats resulted in improved blood lactate homeostasis during exercise and increased VO2max (15%), TCA cycle enzymes of skeletal muscle (27-58%) and heart (29%), and liver NADH oxidase (34%) but did not affect any of these parameters in the iron-sufficient animals. In iron-deficient rats training affected neither the blood hemoglobin level nor any measured iron-dependent enzyme pathway of skeletal muscle but substantially increased endurance (230%). We conclude that the training-induced increase in endurance in iron-deficient rats may be related to cardiovascular improvements, elevations in liver oxidative capacity, and increases in the activities of oxidative enzymes that do not contain iron in skeletal and cardiac 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.

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