Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury. J Neurosci Res 2013 Jun;91(6):818-27
Date
04/05/2013Pubmed ID
23553672DOI
10.1002/jnr.23203Scopus ID
2-s2.0-84876475988 (requires institutional sign-in at Scopus site) 34 CitationsAbstract
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.
Author List
Dornbos D 3rd, Zwagerman N, Guo M, Ding JY, Peng C, Esmail F, Sikharam C, Geng X, Guthikonda M, Ding YAuthor
Nathan Zwagerman MD Associate Professor in the Neurosurgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBrain
Disease Models, Animal
Male
Physical Conditioning, Animal
Rats
Rats, Sprague-Dawley
Real-Time Polymerase Chain Reaction
Reperfusion Injury
Stroke
