Difference between revisions of "Kadaja 2010 Exp Clin Cardiol"
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|authors=Kadaja L, Eimre M, Paju K, Roosimaa M, Podramaegi T, Kaasik P, Pehme A, Orlova E, Mudist M, Peet N, Piirsoo A, Seene T, Gellerich FN, Seppet EK | |authors=Kadaja L, Eimre M, Paju K, Roosimaa M, Podramaegi T, Kaasik P, Pehme A, Orlova E, Mudist M, Peet N, Piirsoo A, Seene T, Gellerich FN, Seppet EK | ||
|year=2010 | |year=2010 | ||
|journal=Exp | |journal=Exp Clin Cardiol | ||
|abstract=The present study was undertaken to characterize and review the changes in energy metabolism in rat myocardium in response to chronic exhaustive exercise. It was shown that a treadmill exercise program applied for six weeks led the rats into a state characterized by decreased performance, loss of body weight and enhanced muscle catabolism, indicating development of overtraining syndrome. Electron microscopy revealed disintegration of the cardiomyocyte structure, cellular swelling and appearance of peroxisomes. Respirometric assessment of mitochondria in saponin-permeabilized cells in situ revealed a decreased rate of oxidative phosphorylation (OXPHOS) due to diminished control over it by ADP and impaired functional coupling of adenylate kinase to OXPHOS. In parallel, reduced tissue content of cytochrome c was observed, which could limit the maximal rate of OXPHOS. The results are discussed with respect to relationships between the volume of work and corresponding energy metabolism. It is concluded that overtraining syndrome is not restricted to skeletal muscle but can affect cardiac muscle as well. | |abstract=The present study was undertaken to characterize and review the changes in energy metabolism in rat myocardium in response to chronic exhaustive exercise. It was shown that a treadmill exercise program applied for six weeks led the rats into a state characterized by decreased performance, loss of body weight and enhanced muscle catabolism, indicating development of overtraining syndrome. Electron microscopy revealed disintegration of the cardiomyocyte structure, cellular swelling and appearance of peroxisomes. Respirometric assessment of mitochondria in saponin-permeabilized cells in situ revealed a decreased rate of oxidative phosphorylation (OXPHOS) due to diminished control over it by ADP and impaired functional coupling of adenylate kinase to OXPHOS. In parallel, reduced tissue content of cytochrome c was observed, which could limit the maximal rate of OXPHOS. The results are discussed with respect to relationships between the volume of work and corresponding energy metabolism. It is concluded that overtraining syndrome is not restricted to skeletal muscle but can affect cardiac muscle as well. | ||
|keywords=Mitochondria; Overtraining; Oxidative phosphorylation; Rat Myocardium | |keywords=Mitochondria; Overtraining; Oxidative phosphorylation; Rat Myocardium | ||
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|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|organism=Rat | |organism=Rat | ||
|tissues=Cardiac | |tissues=Cardiac muscle | ||
|preparations=Permeabilized | |preparations=Permeabilized tissue | ||
|topics=Respiration; OXPHOS; ETS Capacity | |topics=Respiration; OXPHOS; ETS Capacity | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
Revision as of 01:48, 5 April 2012
| Kadaja L, Eimre M, Paju K, Roosimaa M, Podramaegi T, Kaasik P, Pehme A, Orlova E, Mudist M, Peet N, Piirsoo A, Seene T, Gellerich FN, Seppet EK (2010) Impaired oxidative phosphorylation in overtrained rat myocardium. Exp Clin Cardiol 15: 116-127. |
Kadaja L, Eimre M, Paju K, Roosimaa M, Podramaegi T, Kaasik P, Pehme A, Orlova E, Mudist M, Peet N, Piirsoo A, Seene T, Gellerich FN, Seppet EK (2010) Exp Clin Cardiol
Abstract: The present study was undertaken to characterize and review the changes in energy metabolism in rat myocardium in response to chronic exhaustive exercise. It was shown that a treadmill exercise program applied for six weeks led the rats into a state characterized by decreased performance, loss of body weight and enhanced muscle catabolism, indicating development of overtraining syndrome. Electron microscopy revealed disintegration of the cardiomyocyte structure, cellular swelling and appearance of peroxisomes. Respirometric assessment of mitochondria in saponin-permeabilized cells in situ revealed a decreased rate of oxidative phosphorylation (OXPHOS) due to diminished control over it by ADP and impaired functional coupling of adenylate kinase to OXPHOS. In parallel, reduced tissue content of cytochrome c was observed, which could limit the maximal rate of OXPHOS. The results are discussed with respect to relationships between the volume of work and corresponding energy metabolism. It is concluded that overtraining syndrome is not restricted to skeletal muscle but can affect cardiac muscle as well. • Keywords: Mitochondria; Overtraining; Oxidative phosphorylation; Rat Myocardium
• O2k-Network Lab: EE_Tartu_Seppet EK
Labels:
Organism: Rat
Tissue;cell: Cardiac muscle"Cardiac muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Preparation: Permeabilized tissue
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS 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.
HRR: Oxygraph-2k
