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Purpose: To examine the effects of a 10-day exercise-training cessation on semantic memory functional activation in older distance runners. Methods: Ten master runners (62.6 ± 7.0 years) with a long-term endurance-training history (29.0 ± 6.0 years) underwent a 10-day training cessation. Before and immediately after the training cessation, semantic memory activation was measured during the famous name recognition task, using functional magnetic resonance imaging. Results: The 10-day training cessation resulted in greater semantic memory activation in three brain regions, including the left inferior frontal gyrus, parahippocampal gyrus, and inferior semilunar lobule. The 10-day training cessation did not significantly alter famous name recognition task performance. Conclusions: The findings demonstrate that even a relatively short period without exercise training alters the functional activation patterns of semantic memory–related neural networks. Increased semantic memory activation after training cessation may indicate reduced neural efficiency during successful memory retrieval. [ABSTRACT FROM AUTHOR]

We sought to delineate the effects of acute and chronic exercise on the regulation of intracellular nitric oxide (N[O.sub.i]) production in putative endothelial progenitor cells (EPCs). Putative EPC colony-forming units (CFU-EC) were cultured from blood drawn before and after 30 min of treadmill exercise at 75% of maximal oxygen uptake in active (n = 8) and inactive (n = 8) men. CFU-EC were similar between groups at baseline, but increased after exercise in active men only (P = 0.04). CFU-EC expressed Dower NADPH oxidase subunit [gp91.sup.phox] mRNA and elevated endothelial nitric oxide synthase mRNA in active relative to inactive men at baseline (P < 0.05). Acute exercise reduced [gp91.sup.phox] mRNA in CFU-EC of both groups (P < 0.05), whereas [p47.sup.phox] mRNA levels were reduced in the inactive group only (P = 0.02). There were no differences between groups or with acute exercise in xanthine oxidase, superoxide dismutase isoforms, or gluthathione peroxidase-1 mRNA levels. N[O.sub.i] was significantly greater in CFU-EC of active men at baseline (P = 0.004). N[O.sub.i] increased in CFU-EC of inactive men with acute exercise, and in vitro experiments with apocynin indicated the increased N[O.sub.i] production was caused by suppression of NADPH oxidase. However, the increases in N[O.sub.i] with the different treatments in the inactive group did not reach the baseline levels in the active group (P < 0.05). We conclude that acute exercise increases N[O.sub.i] in cells generated by the CFU-EC assay through an NADPH oxidase-inhibition mechanism in sedentary men. However, differences due to chronic exercise must involve additional factors. Our findings support exercise as a means to improve putative EPC function and suggest a novel mechanism that may explain this effect. physical activity; angiogenesis; oxidative stress doi: 10.1152/ajpheart.00347.2009.

In endothelial cells, [NF-[kappa]B is an important intracellular signaling molecule by which changes in wall shear stress are transduced into the nucleus to initiate downstream endothelial nitric oxide synthase (NOS3) gene expression. We investigated whether NF-[kappa] light-chain gene enhancer in B cells 1 (NFKB 1) promoter polymorphism ([sup.-94]NFKB1 I/D, where I is the insertion allele and D is the deletion allele) was associated with 1) NOS3 gene expression in endothelial cells under physiological levels of unidirectional laminar shear stress (LSS) and 2) endothelial function in prehypertensive and stage I hypertensive individuals before and after a 6-mo supervised endurance exercise intervention. Competitive EMSAs revealed that proteins present in the nuclei of endothelial cells preferentially bound to the I allele NFKB1 promoter compared with the D allele. Reporter gene assays showed that the I allele promoter had significantly higher activity than the D allele. In agreement with these observations, homozygous II genotype cells had higher p50 expression levels than homozygous DD genotype cells. Cells with the homozygous II genotype showed a greater increase in NOS3 protein expression than did homozygous DD genotype cells under LSS. Functional experiments on volunteers confirmed higher baseline reactive hyperemic forearm blood flow, and, furthermore, the subgroup analysis revealed that DD homozygotes were significantly less prevalent in the exercise responder group compared with II and ID genotypes. We conclude that the [sup.-94]NFKB1 I/D promoter variation contributes to the modulation of vascular function and adaptability to exercise-induced flow shear stress, most likely due to differences in NFKB1 gene transactivity. nuclear factor-[kappa] light-chain gene enhancer in B cells 1; nitric oxide synthase 3; shear stress

In its role as an endothelial cell proliferation and migration factor, vascular endothelial growth factor (VEGF) can affect peripheral circulation and therefore impact maximal oxygen consumption (V[O.sub.2 max]). Because of the role of VEGF, and because variation in the VEGF gene has the ability to alter VEGF gene expression and VEGF protein level, we hypothesized that VEGF gene polylnorphisms are related to VEGF gene expression in human myoblasts and V[O.sub.2 max] before and after aerobic exercise training. We analyzed the effects of the VEGF -2578/ -1154/-634 protnoter region haplotype on VEGF gene expression by using a luciferase reporter assay in cultured human myoblasts and found that the AAG and CGC haplotypes resulted m significantly higher hypoxia-stimulated VEGF gene expression than the AGG and CGG haplotypes. Consistent with these results, we found that individuals with at least one copy of the AAG or CGC haplotype had higher V[O.sub.2 max] before and after aerobic exercise training than did subjects with only the AGG and/or CGG haplotype. In conclusion, we found that VEGF-2578/-1154/-634 haplotype impacts VEGF gene expression in human myoblasts and is associated with V[O.sub.2 max]. These results have potential implications for aerobic exercise training and may prove relevant in the study of pathological conditions that can be affected by angiogenesis, such as coronary artery disease and peripheral artery disease. angiogenesis; exercise; genetics; polymorphism