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OP-MB02 Molecular Biology 2<br />

ship are lacking (3). One primary aim <strong>of</strong> the present study was to test this hypothesis and whether there is a further interaction <strong>of</strong> oxidative<br />

stress (OS) and antioxidant (AO) responses following an Ironman (IM) triathlon.<br />

Methods: Blood samples were taken from 42 male triathletes (mean±SD: age: 35.3±7.0 yr, cycling VO2 peak: 56.6±6.2 ml kg-1 min-1) 2<br />

days (d) before an IM, then immediately, 1, 5, and 19 d post-race. Blood was analysed for inflammatory, immune-endocrine responses,<br />

muscle damage, OS markers, endogenous and exogenous AOs and plasma AO capacity (1, 2). 20 and 28 subjects were randomly<br />

selected for the assessment <strong>of</strong> DNA and chromosomal stability in lymphocytes measured via the cytokinesis block micronucleus cytome<br />

(CBMN Cyt) (4) and the single cell gel electrophoresis (SCGE) assays (including lesion specific enzymes), respectively. Correlation, onefactorial<br />

ANOVA and post hoc analyses were applied to assess potential associations.<br />

Results: The IM induced a pronounced initial systemic inflammatory response (2). Concomitantly with a transient increase in most OS<br />

markers there were strong AO responses (1). Increased DNA instability was detected by the SCGE technique, but these changes were<br />

temporarily. Endpoints within the CBMN Cyt assay actually decreased post-race (4). No associations were found between endpoints <strong>of</strong><br />

DNA stability and inflammation or muscle damage (3). Endonuclease III-sensitive sites correlated negatively with the oxygen radical<br />

absorbance capacity immediately (r= -0.54; P 0.05) were recorded in blood insulin or total or phosphorylated Akt<br />

at any time point or between genders. While there were no sex differences in total 4E-BP1, the phosphor <strong>of</strong> 4E-BP1 was significantly higher<br />

at rest in males compared to females (P < 0.05). Following exercise, there was a significant reduction in phosphorylation <strong>of</strong> 4E-BP1 in the<br />

males but not the females. By 2 h post-exercise phosphorylation <strong>of</strong> 4E-BP1 had returned to resting levels for both males and females.<br />

While there were no differences in the resting or post-exercise muscle Akt or other physiological measures such as HR, blood lactate or<br />

blood insulin, the females had a reduced phosphorylation <strong>of</strong> 4E-BP1 at rest compared to the males. Additionally there was no significant<br />

change in phosphorylation <strong>of</strong> 4E-BP1 in the females following exercise. However, similar to studies using males and performing resistance<br />

exercise, the males in the present study had a reduction in phosphorylation <strong>of</strong> 4E-BP1 post exercise, which returned to basal levels<br />

by 2 h. These results indicate there may be small sex differences in the translational machinery regulating muscle mass. The lack <strong>of</strong><br />

change in phosphorylation <strong>of</strong> 4E-BP1 following exercise in females may be due to sex differences in activation <strong>of</strong> AMPKinase, previously<br />

reported following intense exercise.<br />

THE AKT-DEPENDENT ENDOTHELIAL NITRIC OXIDE SYNTHASE (ENOS) PHOSPHORYLATION IS NOT THE PRIMARY MO-<br />

LECULAR MECHANISM UNDERLYING THE BENEFICIAL EFFECT OF LONG-TERM EXERCISE ON ATHEROSCLEROSIS<br />

PELLEGRIN, M., MIGUET-ALFONSI, C., BOUZOURENE, K., AUBERT, J.F., BERTHELOT, A., MAZZOLAI, L., LAURANT, P.<br />

SERVICE OF VASCULAR MEDICINE AND EXERCISE PREVENTION INNOVATION AND TECHNICO-SPORTING WATCHING DEPARTMENT<br />

Introduction: Exercise reduces atherosclerosis extension in humans and animal models (Niebauer et al., 1997; Pellegrin et al., 2007).<br />

However, the precise anti-atherosclerotic molecular mechanisms <strong>of</strong> exercise are still unclear. Exercise-induced increase <strong>of</strong> vascular<br />

eNOS phosphorylation through the protein kinase Akt has been regarded as a vasculoprotective mechanism in patients with coronary<br />

artery disease (Hambrecht et al., 2003). Therefore, the aim <strong>of</strong> this study was to assess whether this regulatory pathway underlie the<br />

beneficial effect <strong>of</strong> exercise in experimental atherosclerosis using Apolipoprotein E-deficient mice (ApoE-/-) mice.<br />

Methods: Hypercholesterolemic ApoE-/- mice were subjected to 24-week swimming exercise (50 min/day; 5 days/week). A group <strong>of</strong><br />

sedentary animals were used as controls. Morphometry and characteristics <strong>of</strong> plaque stability were assessed in plaques from aortic<br />

sinus by immunohistochemistry. Expression <strong>of</strong> eNOS, eNOS phosphorylation at Ser1177, Akt, and Akt phosphorylation at Ser473 were<br />

measured in aortas by western blot.<br />

522 14 TH<br />

ANNUAL CONGRESS OF THE EUROPEAN COLLEGE OF SPORT SCIENCE

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