Short-Term Acute Exercise Preconditioning Reduces Neurovascular Injury After Stroke Through Induced eNOS Activation

Sherif Hafez, Mohammad Badruzzaman Khan, Mohamed E. Awad, Jesse D. Wagner, David C. Hess

Research output: Contribution to journalArticle

Abstract

Physical exercise is known to reduce cardiovascular risk but its role in ischemic stroke is not clear. It was previously shown that an acute single bout of exercise reduced increased eNOS activation in the heart and reduced myocardial infarction. However, the impact of a single bout or short-term exercise on eNOS-induced neuroprotection after stroke was not previously studied. Accordingly, this study was designed to test the hypothesis that short-term acute exercise can provide “immediate neuroprotection” and improve stroke outcomes through induced eNOS activation. Male Wistar rats (300 g) were subjected to HIIT treadmill exercise for 4 days (25 min/day), break for 2 days, and then one acute bout for 30 min. Exercised animals were subjected to thromboembolic stroke 1 h, 6 h, 24 h, or 72 h after the last exercise session. At 24 h after stroke, control (sedentary) and exercised rats were tested for neurological outcomes, infarct size, and edema. The expression of active eNOS (p-S1177-eNOS) and active AMPK (p-T172-AMPK) was measured in the brain, cerebral vessels, and aorta. In an additional cohort, animals were treated with the eNOS inhibitor, L-NIO (I.P, 20 mg/kg), and stroked 1 h after exercise and compared with non-exercise animals. Acute exercise significantly reduced infarct size, edema, and improved functional outcomes, and significantly increased the expression of peNOS and pAMPK in the brain, cerebral vessels, and aorta. eNOS inhibition abolished the exercise-induced improvement in outcomes. Short-term acute preconditioning exercise reduced the neurovascular injury and improved functional outcomes after stroke through eNOS activation.

Original languageEnglish (US)
JournalTranslational Stroke Research
DOIs
StateAccepted/In press - Jan 1 2019

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Stroke
Exercise
Wounds and Injuries
AMP-Activated Protein Kinases
Aorta
Edema
Brain
Wistar Rats
Myocardial Infarction
Neuroprotection

Keywords

  • Ischemic stroke
  • Nitric oxide synthase 3
  • Preconditioning exercise

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Short-Term Acute Exercise Preconditioning Reduces Neurovascular Injury After Stroke Through Induced eNOS Activation",
abstract = "Physical exercise is known to reduce cardiovascular risk but its role in ischemic stroke is not clear. It was previously shown that an acute single bout of exercise reduced increased eNOS activation in the heart and reduced myocardial infarction. However, the impact of a single bout or short-term exercise on eNOS-induced neuroprotection after stroke was not previously studied. Accordingly, this study was designed to test the hypothesis that short-term acute exercise can provide “immediate neuroprotection” and improve stroke outcomes through induced eNOS activation. Male Wistar rats (300 g) were subjected to HIIT treadmill exercise for 4 days (25 min/day), break for 2 days, and then one acute bout for 30 min. Exercised animals were subjected to thromboembolic stroke 1 h, 6 h, 24 h, or 72 h after the last exercise session. At 24 h after stroke, control (sedentary) and exercised rats were tested for neurological outcomes, infarct size, and edema. The expression of active eNOS (p-S1177-eNOS) and active AMPK (p-T172-AMPK) was measured in the brain, cerebral vessels, and aorta. In an additional cohort, animals were treated with the eNOS inhibitor, L-NIO (I.P, 20 mg/kg), and stroked 1 h after exercise and compared with non-exercise animals. Acute exercise significantly reduced infarct size, edema, and improved functional outcomes, and significantly increased the expression of peNOS and pAMPK in the brain, cerebral vessels, and aorta. eNOS inhibition abolished the exercise-induced improvement in outcomes. Short-term acute preconditioning exercise reduced the neurovascular injury and improved functional outcomes after stroke through eNOS activation.",
keywords = "Ischemic stroke, Nitric oxide synthase 3, Preconditioning exercise",
author = "Sherif Hafez and Khan, {Mohammad Badruzzaman} and Awad, {Mohamed E.} and Wagner, {Jesse D.} and Hess, {David C.}",
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AU - Hafez, Sherif

AU - Khan, Mohammad Badruzzaman

AU - Awad, Mohamed E.

AU - Wagner, Jesse D.

AU - Hess, David C.

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Physical exercise is known to reduce cardiovascular risk but its role in ischemic stroke is not clear. It was previously shown that an acute single bout of exercise reduced increased eNOS activation in the heart and reduced myocardial infarction. However, the impact of a single bout or short-term exercise on eNOS-induced neuroprotection after stroke was not previously studied. Accordingly, this study was designed to test the hypothesis that short-term acute exercise can provide “immediate neuroprotection” and improve stroke outcomes through induced eNOS activation. Male Wistar rats (300 g) were subjected to HIIT treadmill exercise for 4 days (25 min/day), break for 2 days, and then one acute bout for 30 min. Exercised animals were subjected to thromboembolic stroke 1 h, 6 h, 24 h, or 72 h after the last exercise session. At 24 h after stroke, control (sedentary) and exercised rats were tested for neurological outcomes, infarct size, and edema. The expression of active eNOS (p-S1177-eNOS) and active AMPK (p-T172-AMPK) was measured in the brain, cerebral vessels, and aorta. In an additional cohort, animals were treated with the eNOS inhibitor, L-NIO (I.P, 20 mg/kg), and stroked 1 h after exercise and compared with non-exercise animals. Acute exercise significantly reduced infarct size, edema, and improved functional outcomes, and significantly increased the expression of peNOS and pAMPK in the brain, cerebral vessels, and aorta. eNOS inhibition abolished the exercise-induced improvement in outcomes. Short-term acute preconditioning exercise reduced the neurovascular injury and improved functional outcomes after stroke through eNOS activation.

AB - Physical exercise is known to reduce cardiovascular risk but its role in ischemic stroke is not clear. It was previously shown that an acute single bout of exercise reduced increased eNOS activation in the heart and reduced myocardial infarction. However, the impact of a single bout or short-term exercise on eNOS-induced neuroprotection after stroke was not previously studied. Accordingly, this study was designed to test the hypothesis that short-term acute exercise can provide “immediate neuroprotection” and improve stroke outcomes through induced eNOS activation. Male Wistar rats (300 g) were subjected to HIIT treadmill exercise for 4 days (25 min/day), break for 2 days, and then one acute bout for 30 min. Exercised animals were subjected to thromboembolic stroke 1 h, 6 h, 24 h, or 72 h after the last exercise session. At 24 h after stroke, control (sedentary) and exercised rats were tested for neurological outcomes, infarct size, and edema. The expression of active eNOS (p-S1177-eNOS) and active AMPK (p-T172-AMPK) was measured in the brain, cerebral vessels, and aorta. In an additional cohort, animals were treated with the eNOS inhibitor, L-NIO (I.P, 20 mg/kg), and stroked 1 h after exercise and compared with non-exercise animals. Acute exercise significantly reduced infarct size, edema, and improved functional outcomes, and significantly increased the expression of peNOS and pAMPK in the brain, cerebral vessels, and aorta. eNOS inhibition abolished the exercise-induced improvement in outcomes. Short-term acute preconditioning exercise reduced the neurovascular injury and improved functional outcomes after stroke through eNOS activation.

KW - Ischemic stroke

KW - Nitric oxide synthase 3

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