Cerebral metabolism after forced or voluntary physical exercise

Kinni, Harish; Guo, Miao; Ding, Jamie Y.; Konakondla, Sanjay; Dornbos, David; Tran, Raymond; Guthikonda, Murali; Ding, Yuchuan

doi:10.1016/j.brainres.2011.02.076

Cited by 78 publications

(69 citation statements)

References 34 publications

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“…The increased need for energy production following hypoxia requires more glucose to be available within neurons, and these two glucose transporters work together to shuttle glucose from the circulation into neurons. GLUT1 and GLUT3 are known to have increased expression following exercise preconditioning (Kinni et al, 2011). Following ischemia/reperfusion injury, GLUT1 and GLUT3 levels are elevated in the first 4 hours after reperfusion is established in exercise preconditioned rats, but expression is equal to control at 24 hours after injury (unpublished data).…”

Section: Atp Productionmentioning

confidence: 91%

“…PFK expression is known to be upregulated following increased metabolism and glycolysis and is has been shown to be neuroprotective in hypoglycemic conditions (Minchenko et al, 2003). Another study has revealed PFK is increased following exercise preconditioning (Kinni et al, 2011), and this enzyme is increased following ischemia/reperfusion injury, leading to increased neuronal metabolism and decreased neurologic deficits (unpublished data). The elevated ability of neurons to process glucose through glycolysis in exercise preconditioned animals underlies another key component of exercise-induced neuroprotection.…”

Section: Atp Productionmentioning

confidence: 93%

“…Previous studies have shown that forced exercise on a treadmill is slower but more constant than voluntary exercise occurs in shorter spurts with faster speed, although the total distance is equal in the two groups (Noble et al, 1999). This neuroprotection in forced exercise subjects led to decreased stroke volume, lessened neurologic deficit, upregulation of heat shock proteins, increased neurogenesis and cerebral metabolism (Hayes et al, 2008;Kinni et al, 2011;Leasure and Jones, 2008). These findings show that moderate exercise over a longer time period conveys more efficient and greater neuroprotection than more vigorous exercise over shorter time periods.…”

Section: Preconditioning Modalitiesmentioning

confidence: 96%

“…In addition to the aforementioned mechanisms, chronic exercise training also affects cerebral metabolism and energy production, allowing neurons to re-establish homeostasis more rapidly following acute ischemic stroke. A recent study revealed that forced exercise resulted in enhanced cerebral glycolysis and cerebral metabolism (Kinni et al, 2011). In addition to increasing glycolysis, exercise preconditioning is also well known to increase cerebral blood flow (CBF) and adenosine triphosphate (ATP) production (Ide and Secher, 2000;McCloskey et al, 2001;Ogoh and Ainslie, 2009).…”

Section: Metabolic Enhancementmentioning

confidence: 99%

“…When ATP concentrations drop, AMPK activates glycolysis in order to restore the cell's energy balance, allowing it to serve as an excellent marker of metabolic demand (Kahn et al, 2005). Following exercise training, levels of the active phosphorylated form of AMPK are increased in response to the elevated metabolic demand (Aschenbach et al, 2004;Kinni et al, 2011). Following ischemia/reperfusion injury, the active phosphorylated form of AMPK has been shown to be upregulated in preconditioned rats, suggesting an increased metabolic response to hypoxia in these exercised animals (unpublished data).…”

Section: Atp Productionmentioning

confidence: 99%

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Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Dornbos¹,

Ding²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia -Reperfusion Injury 301 neuroprotection after exercise has stopped.Another study revealed that the neuroprotective effects of exercise preconditioning appear to be long-lasting, showing that 3 weeks after cessation of exercise, rats still maintained lower levels of neurologic deficit and decreased stroke volume when compared to non-exercise rats (Ding et al., 2004b). Future human studies ought to determine the exact duration needed for maximal endogenous neuroprotection. Preconditioning modalitiesWhile various modalities, such as treadmill running, voluntary running, simple and complex exercise, have been shown to provide variable amounts of neuroprotection. When comparing forced exercise on a treadmill to voluntary running on a running wheel, rats forced to exercise on a treadmill tend to have better neurologic outcomes after stroke (Hayes et al., 2008). Previous studies have shown that forced exercise on a treadmill is slower but more constant than voluntary exercise occurs in shorter spurts with faster speed, although the total distance is equal in the two groups (Noble et al., 1999). This neuroprotection in forced exercise subjects led to decreased stroke volume, lessened neurologic deficit, upregulation of heat shock proteins, increased neurogenesis and cerebral metabolism (Hayes et al., 2008;Kinni et al., 2011;Leasure and Jones, 2008). These findings show that moderate exercise over a longer time period conveys more efficient and greater neuroprotection than more vigorous exercise over shorter time periods. In addition to the studies assessing forced and voluntary exercise, differences have also been established when comparing simple and complex exercise. This study analyzed simple exercise as the repetitive movements of treadmill running, whereas complex exercise constituted enriched activities which required both balance and coordination (Ding et al., 2003). Following ischemia/reperfusion injury, rats preconditioned with complex exercise demonstrated increased synaptogenesis and improved neurologic outcomes when compared to simple treadmill exercise (Ding et al., 2003;Jones et al., 1999). Simple exercise training also alleviates much of the injury following ischemia/reperfusion, but its benefit is less pronounced than what is observed with complex exercise training. Although no human studies have definitively shown the most effective means of exercise for enhanced neuroprotection, these animal studies provide a solid framework for the development of appropriate exercise regimens. Moderate exercise intensity, including components of balance, coordination and stress, taking place over a sustained duration seem to be the most neuroprotective when compared to other exercise modalities and intensities.

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Section: Atp Productionmentioning

confidence: 91%

Section: Atp Productionmentioning

confidence: 93%

Section: Preconditioning Modalitiesmentioning

confidence: 96%

Section: Metabolic Enhancementmentioning

confidence: 99%

Section: Atp Productionmentioning

confidence: 99%

See 3 more Smart Citations

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Dornbos¹,

Ding²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Exercise‐Induced Protection Against Aging and Neurodegenerative Diseases

Marques‐Aleixo

Santos‐Alves

Moreira

et al. 2015

Diet and Exercise in Cognitive Function and Neurological Diseases

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Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury

Dornbos

Zwagerman²,

Guo³

et al. 2013

J of Neuroscience Research

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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.

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Cerebral metabolism after forced or voluntary physical exercise

Cited by 78 publications

References 34 publications

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Exercise‐Induced Protection Against Aging and Neurodegenerative Diseases

Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury

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