Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury. Issue 6 (29th March 2013)
- Record Type:
- Journal Article
- Title:
- Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury. Issue 6 (29th March 2013)
- Main Title:
- Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury
- Authors:
- Dornbos, David
Zwagerman, Nathan
Guo, Miao
Ding, Jamie Y.
Peng, Changya
Esmail, Fatema
Sikharam, Chaitanya
Geng, Xiaokun
Guthikonda, Murali
Ding, Yuchuan - Abstract:
- <abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Physical exercise preconditioning is known to ameliorate stroke‐induced injury. In addition to several other mechanisms, the beneficial effect of preischemic exercise following stroke is due to an upregulated capacity to maintain energy supplies. Adult male Sprague‐Dawley rats were used in exercise and control groups. After 1–3 weeks of exercise, several enzymes were analyzed as a gauge of the direct effect of physical exercise on cerebral metabolism. As a measure of metabolic capacity, an ADP/ATP ratio was obtained. Glucose transporters (GLUT1 and GLUT3) were monitored to assess glucose influx, and phosphofructokinase (PFK) was measured to determine the rate of glycolysis. Hypoxia‐induced factor‐1α (HIF‐1α) and 5′AMP‐activated protein kinase (AMPK) levels were also determined. These same analyses were performed on preconditioned and control rats following an ischemic/reperfusion (I/R) insult. Our results show that GLUT1, GLUT3, PFK, AMPK, and HIF‐1α were all increased following 3 weeks of exercise training. In addition, the ADP/ATP ratio was chronically elevated during these 3 weeks. After I/R injury, HIF‐1α and AMPK were significantly higher in exercised rats. The ADP/ATP ratio was reduced in preconditioned rats in the acute phase after stroke, suggesting a lower level of metabolic disorder. GLUT1 and GLUT3 were also increased in the acute phase in exercise rats, indicating that these<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Physical exercise preconditioning is known to ameliorate stroke‐induced injury. In addition to several other mechanisms, the beneficial effect of preischemic exercise following stroke is due to an upregulated capacity to maintain energy supplies. Adult male Sprague‐Dawley rats were used in exercise and control groups. After 1–3 weeks of exercise, several enzymes were analyzed as a gauge of the direct effect of physical exercise on cerebral metabolism. As a measure of metabolic capacity, an ADP/ATP ratio was obtained. Glucose transporters (GLUT1 and GLUT3) were monitored to assess glucose influx, and phosphofructokinase (PFK) was measured to determine the rate of glycolysis. Hypoxia‐induced factor‐1α (HIF‐1α) and 5′AMP‐activated protein kinase (AMPK) levels were also determined. These same analyses were performed on preconditioned and control rats following an ischemic/reperfusion (I/R) insult. Our results show that GLUT1, GLUT3, PFK, AMPK, and HIF‐1α were all increased following 3 weeks of exercise training. In addition, the ADP/ATP ratio was chronically elevated during these 3 weeks. After I/R injury, HIF‐1α and AMPK were significantly higher in exercised rats. The ADP/ATP ratio was reduced in preconditioned rats in the acute phase after stroke, suggesting a lower level of metabolic disorder. GLUT1 and GLUT3 were also increased in the acute phase in exercise rats, indicating that these rats were better able to increase rates of metabolism immediately after ischemic injury. In addition, PFK expression was increased in exercise rats showing an enhanced glycolysis resulting from exercise preconditioning. Altogether, exercise preconditioning increased the rates of glucose metabolism, allowing a more rapid and more substantial increase in ATP production following stroke. © 2013 Wiley Periodicals, Inc.</p> </abstract> … (more)
- Is Part Of:
- Journal of neuroscience research. Volume 91:Issue 6(2013:Jun.)
- Journal:
- Journal of neuroscience research
- Issue:
- Volume 91:Issue 6(2013:Jun.)
- Issue Display:
- Volume 91, Issue 6 (2013)
- Year:
- 2013
- Volume:
- 91
- Issue:
- 6
- Issue Sort Value:
- 2013-0091-0006-0000
- Page Start:
- 818
- Page End:
- 827
- Publication Date:
- 2013-03-29
- Subjects:
- Neurobiology -- Periodicals
612 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4547 ↗
http://www3.interscience.wiley.com/cgi-bin/jhome/109668564 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jnr.23203 ↗
- Languages:
- English
- ISSNs:
- 0360-4012
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5022.090000
British Library DSC - BLDSS-3PM
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