31P-MR Spectroscopy for the evaluation of energy metabolism in intact residual myocardium after acute myocardial infarction in humans

2001 ◽  
Vol 13 (2) ◽  
pp. 70-75 ◽  
Author(s):  
M. Beer ◽  
S. Buchner ◽  
J. Sandstede ◽  
M. Viehrig ◽  
C. Lipke ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Energy Metabolism ◽  
Mr Spectroscopy ◽  
31P Mr Spectroscopy

Abstract 332: Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Lichan Tao ◽  
Yihua Bei ◽  
Haifeng Zhang ◽  
Yanli Zhou ◽  
Jingfa Jiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Myocardial Infarct Size ◽  
Myocardial Energy Metabolism

Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury. However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. MI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.

Photic stimulation-induced alteration of brain energy metabolism measured by 31P-MR spectroscopy in patients with MELAS

1998 ◽  
Vol 155 (2) ◽  
pp. 182-185 ◽  
Author(s):  
Tadafumi Kato ◽  
Jun Murashita ◽  
Toshiki Shioiri ◽  
Masahiko Terada ◽  
Toshiro Inubushi ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Mr Spectroscopy ◽  
Photic Stimulation ◽  
Brain Energy Metabolism ◽  
Brain Energy ◽  
31P Mr Spectroscopy

scholarly journals Cerebral Energy Metabolism in Phenylketonuria: Findings by Quantitative In Vivo 31P MR Spectroscopy

2003 ◽  
Vol 53 (4) ◽  
pp. 654-662 ◽  
Author(s):  
Joachim Pietz ◽  
André Rupp ◽  
Friedrich Ebinger ◽  
Dietz Rating ◽  
Ertan Mayatepek ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Mr Spectroscopy ◽  
Cerebral Energy Metabolism ◽  
31P Mr Spectroscopy

scholarly journals Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

2015 ◽  
Vol 37 (1) ◽  
pp. 162-175 ◽  
Author(s):  
Lichan Tao ◽  
Yihua Bei ◽  
Shenghui Lin ◽  
Haifeng Zhang ◽  
Yanli Zhou ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Energy Metabolism ◽  
Exercise Training ◽  
Infarct Size ◽  
Mitochondrial Biogenesis ◽  
Myocardial Infarct ◽  
Immunofluorescent Staining ◽  
Myocardial Infarct Size ◽  
Myocardial Energy Metabolism

Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetrazolium chloride staining. Cardiac apoptosis was determined by TUNEL staining. Mitochondria density was checked by Mito-Tracker immunofluorescent staining. Quantitative reverse transcription polymerase chain reactions and Western blotting were used to determine genes related to apoptosis, autophagy and myocardial energy metabolism. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. AMI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.

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