Kadaja 2010 Exp Clin Cardiol

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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 15:116-27.

» PMID: 21264069 Open Access

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 Paju K, DE Magdeburg Gellerich FN


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Organism: Rat  Tissue;cell: Heart  Preparation: Permeabilized tissue 


Coupling state: OXPHOS 

HRR: Oxygraph-2k