Article

Effect of treadmill exercise on cell damage in rat hippocampal slices submitted to oxygen and glucose deprivation.

Programa de Pós Graduação em Ciências Biológicas-Neurociências, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite, 500, 90050-170, Porto Alegre, RS, Brazil.
Brain Research (impact factor: 2.73). 08/2007; 1157:121-5. DOI:10.1016/j.brainres.2007.04.045
Source: PubMed

ABSTRACT We have recently demonstrated that high intensity training exercise exacerbates brain damage, while a moderate intensity (2 weeks of 20 min/day of treadmill training) reduces the injury caused by in vitro ischemia, oxygen and glucose deprivation (OGD), to hippocampal slices from Wistar rats. In the present paper, the effect of different running programs on severity of ischemic OGD lesion was examined, by the evaluation of three protocols designed to simulate exercise conditions common to humans: one or three 20-min sessions per week, during 12 weeks (moderate intensity), and two 20-min daily sessions for 3 weeks. OGD caused an increase of lactate dehydrogenase (LDH) release into the incubation media, a marker of tissue necrosis, and a decline of cell viability, as assessed by the decrease of mitochondrial dehydrogenase activity (MTT method). Moderate exercise, three times a week during 12-week treadmill training, decreased LDH release after OGD, while one weekly session and 3 weeks of two daily sessions did not affect OGD-induced LDH released. No exercise protocol evaluated altered MTT reduction. Our data support the hypothesis that moderate intensity exercise reduces hippocampal susceptibility to in vitro ischemia.

0 0
 · 
0 Bookmarks
 · 
31 Views
  • Source
    Article: Forced, not voluntary, exercise effectively induces neuroprotection in stroke.
    Katherine Hayes, Shane Sprague, Miao Guo, William Davis, Asher Friedman, Ashwini Kumar, David F Jimenez, Yuchuan Ding
    [show abstract] [hide abstract]
    ABSTRACT: Previous treadmill exercise studies showing neuroprotective effects have raised questions as to whether exercise or the stress related to it may be key etiologic factors. In this study, we examined different exercise regimens (forced and voluntary exercise) and compared them with the effect of stress-only on stroke protection. Adult male Sprague-Dawley rats (n = 65) were randomly assigned to treatment groups for 3 weeks. These groups included control, treadmill exercise, voluntary running wheel exercise, restraint, and electric shock. Levels of the stress hormone, corticosterone, were measured in the different groups using ELISA. Animals from each group were then subjected to stroke induced by a 2-h middle cerebral artery (MCA) occlusion followed by 48-h reperfusion. Infarct volume was determined in each group, while changes in gene expression of stress-induced heat shock proteins (Hsp) 27 and 70 were compared using real-time PCR between voluntary and treadmill exercise groups. The level of corticosterone was significantly higher in both stress (P < 0.05) and treadmill exercise (P < 0.05) groups, but not in the voluntary exercise group. Infarct volume was significantly reduced (P < 0.01) following stroke in rats exercised on a treadmill. However, the amelioration of damage was not duplicated in voluntary exercise, even though running distance in the voluntary exercise group was significantly (P < 0.01) longer than that of the forced exercise group (4,828 vs. 900 m). Furthermore, rats in the electric shock group displayed a significantly increased (P < 0.01) infarct volume. Expression of both Hsp 27 and Hsp 70 mRNA was significantly increased (P < 0.01) in the treadmill exercise group as compared with that in the voluntary exercise group. These results suggest that exercise with a stressful component, rather than either voluntary exercise or stress alone, is better able to reduce infarct volume. This exercise-induced neuroprotection may be attributable to up-regulation of stress-induced heat shock proteins 27 and 70.
    Acta Neuropathologica 04/2008; 115(3):289-96. · 9.32 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

12-week treadmill training
 
2 weeks
 
20-min sessions
 
brain damage
 
cell viability
 
data support
 
hippocampal susceptibility
 
incubation media
 
intensity training exercise
 
ischemic OGD lesion
 
lactate dehydrogenase
 
mitochondrial dehydrogenase activity
 
Moderate exercise
 
moderate intensity
 
moderate intensity exercise
 
MTT reduction
 
OGD-induced LDH
 
simulate exercise conditions common
 
tissue necrosis
 
weekly session