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Both oxidative stress and telomere transcription are up-regulated by acute endurance exercise in human skeletal muscle. Whether and how life-long exercise training influences the antioxidant system response at transcriptional level and TERRA expression is unknown, especially during aging. Response to acute endurance exercise was investigated in muscle biopsies of 3 male subjects after 45 min of cycling. MCP-1 and SOD1 mRNA levels increased up to, 15-fold and 63%, respectively, after the cycling session while the mRNA levels of SOD2 were downregulated by 25%. The effects of chronic endurance exercise and aging were tested in the blood and muscle of 34 male subjects divided into four groups: young (YU) or old (OU) untrained, young (YT) or old (OT) trained cyclists. Long-term endurance training limited the age-dependent elevation in SOD1 (OT vs OU, −26%, P = 0.03) and the decline in SOD2 mRNA levels (OU vs YU, −41%, P = 0.04). A high endurance training status alleviated the age-related increase in the aging biological marker MCP-1 in plasma (OU vs YU, +48%, P = 0.005). Similar results were observed for telomeric transcription as the age-associated increase in 16p TERRA levels (OU vs YU, +39%, P = 0.001) was counteracted by a high endurance training status (OT vs OU, −63%, P = 0.0005). In conclusion, as MCP-1, we propose that the age-related TERRA accumulation might represent a novel biological marker of aging. Those aging-related increase expression might be alleviated by a high endurance training status. Whether those biological markers of aging are linked to an elevation of oxidative stress is still an open question. Therefore, whether the positive adaptations provided by endurance training indeed reduce oxidative stress, including at telomeres, and whether TERRA plays any role in this, need to be further investigated.

Activating transcription factor (ATF) 3 regulates chemokine expression in various cell types and tissues. Herein, we studied this regulation in contracting muscle cells in vitro , and in skeletal muscle after muscle-damaging exercise in vivo . C 2 C 12 myotubes with normal or low ATF3 levels (atf3_siRNA) were electrically stimulated (EPS). Also, ATF3-knockout (ATF3-KO) and control mice ran downhill until exhaustion, and muscles were analyzed post-exercise. EPS increased ATF3 levels in myotubes ( P ccl ) 2 mRNA increased post-EPS, but atf3_siRNA attenuated the response ( P ccl6 basal mRNA, and down-regulated ccl9 and chemokine C-X-C motif ligand ( cxcl ) 1 basal mRNAs. Post-exercise, ATF3-KO mice showed exacerbated mRNA levels of ccl6 and ccl9 in soleus ( P ccl2 and interleukin ( il ) 1β ( P il6 mRNA level increased only in ATF3-KO ( P cxcl1 mRNA showed a similar trend ( P = 0.082). Cluster of differentiation-68 ( cd68 ) mRNA, a macrophage marker, increased in quadriceps and soleus independently of genotype ( P in vitro and skeletal muscle in vivo , but the regulation differs in each model. Cells other than myofibers may thus participate in the response observed in skeletal muscle. Our results also indicate that ATF3-independent mechanisms would regulate macrophage infiltration upon muscle-damaging exercise. The implications of chemokine regulation in skeletal muscle remain to be determined.

BACKGROUND: Sarcopenia contributes to the decreased quality of life in the older person. While resistance exercise is an effective measure to increase muscle mass and strength, the hypertrophic response may be blunted in old age. OBJECTIVES: To determine 1) whether hypertrophy in the m. plantaris of old mice was blunted compared to adult and 2) whether this was related to a reduced satellite cell (SC) density and 3) how resveratrol affects hypertrophy in old mice. METHODS: In adult (7.5 months, n=11), old (23.5 months, n=10) and old-resveratrol-treated (n=10) male C57BL/6J mice, hypertrophy of the left m. plantaris was induced by denervation of its synergists. The contralateral leg served as control. RESULTS: After six weeks, overload-induced myofiber hypertrophy and IIB-IIA shift in myofiber type composition were less pronounced in old than adult mice (P=0.03), irrespective of resveratrol treatment. Muscles from old mice had a lower SC density than adult muscles (P=0.002). Overload-induced SC proliferation (P

Inulin-type fructans (ITF) are nondigestible/fermentable carbohydrates which are able - through the modification of the gut microbiota - to counteract high-fat (HF) diet-induced obesity, endotoxemia and related-metabolic alterations. However, their influence on adipose tissue metabolism has been poorly studied until now. The aim of this study was to assess the influence of ITF supplementation on adipose tissue metabolism, by focusing on a G protein-coupled receptor (GPR), GPR43, as a potential link between gut fermentation processes and white adipose tissue development. Male C57bl6/J mice were fed a standard diet or an HF diet without or with ITF (0.2 g/day per mouse) during 4 weeks. The HF diet induced an accumulation of large adipocytes, promoted peroxisome proliferator activated receptor gamma (PPARγ)-activated differentiation factors and led to a huge increase in GPR43 expression in the subcutaneous adipose tissue. All those effects were blunted by ITF treatment, which modulated the gut microbiota in favor of bifidobacteria at the expense of Roseburia spp. and of Clostridium cluster XIVa. The dietary modulation of GPR43 expression seems independent of endotoxemia, in view of data obtained in vivo (acute and chronic lipopolysaccharides treatment). In conclusion, ITF, which promote gut fermentation, paradoxically counteract GPR43 overexpression induced in the adipose tissue by an HF diet, a phenomenon that correlates with a beneficial effect on adiposity and with potential decrease in PPARγ-activated processes. ispartof: Journal of Nutritional Biochemistry vol:22 issue:8 pages:712-722 ispartof: location:United States status: published

Resume Objectif. – Il s'agit ici d'etudier, sur modele animal, les effets d'une supplementation prolongee avec de la creatine sur la cinetique de recuperation d'un muscle lent et oxydatif, le soleaire, apres induction d'une degenerescence etendue (par infiltration de notexine). Resultats et Discussion. – Que les animaux aient ete ou non supplementes en creatine, les resultats suivants ont ete obtenus : 1) La masse du muscle soleaire est recuperee 35 jours apres la lesion. 2) Le profil d'expression des isoformes de MHC est similaire a celui d'un muscle soleaire intact 28 jours apres la lesion. 3) L'activite de la CS est recuperee 14 jours apres la lesion, tandis que l'activite specifique H-LDH reste legerement inferieure a celle du muscle intact. 4) La myogenine a un pic d'expression a trois jours. Conclusion. – Contrairement a l'hypothese initiale, proposee apres des etudes in vitro, la supplementation en creatine n'a pas d'effet benefique sur la cinetique de recuperation du muscle squelettique evaluee in vivo apres lesion par un myotoxique.

Resume Objectifs. – Mise en evidence d'un mecanisme d'action de la creatine sur l'anabolisme musculaire. Synthese des faits. – L'addition de creatine au milieu de differenciation de cellules C2C12 provoque l'hypertrophie des myotubes et accroit la quantite d'ARNm d'IGF. Sur cette base, nous avons emis l'hypothese qu'une complementation en creatine favoriserait l'anabolisme musculaire en augmentant l'expression d'IGF. Au cours d'un protocole croise en double insu, des biopsies ont ete prelevees au niveau du vaste externe au repos et apres un exercice chez des sujets qui avaient ingere de la creatine ou un placebo durant cinq jours (21 g/jour). Apres la complementation en creatine, le muscle au repos exprimait plus d'ARNm d'IGF. L'exercice augmentait l'ARNm d'IGF, mais cet effet n'etait pas potentialise par la creatine. Conclusion. – L'accroissement de masse corporelle souvent rapporte apres une complementation en creatine pourrait etre induit par une ou des voie(s) de signalisation impliquant IGF.

Introduction Les acides gras polyinsatures (AGPI) n-3 jouent un role important sur le metabolisme lipidique de part leur capacite a stimuler la β-oxydation et a diminuer la lipogenese. Une augmentation du ratio n-6/n-3 est observee dans les phospholipides du foie de patientes atteintes de steatose hepatique non alcoolique. L’implication d’une diminution en AGPI n-3 dans l’accumulation de lipides au niveau du foie a ete peu etudie jusqu’a ce jour. Cette etude a pour but d’explorer le mecanisme implique dans l’accumulation des triglycerides dans le foie chez la souris carencee en AGPI n-3. Materiels et Methodes 24 souris mâles C57Bl6J ont ete nourries avec une diete controle (n-6/n-3 = 6,9) ou une diete carencee en AGPI n-3 (n-6/n-3 = 120) durant 3 mois. Resultats La carence en n-3 induit une accumulation de lipides dans le foie (triglyceride et cholesterol). L’incubation de tranches de foie en presence de 14 C-acetate et de 14 C-palmitate a revele une augmentation de la synthese et de l’esterification des acides gras dans le foie des souris carencees. La secretion hepatique de triglycerides, evaluee par inhibition de la lipoproteine lipase, est egalement augmentee chez les souris carencees. Les analyses microarrays demontrent, dans le foie des souris carencees, une augmentation de l’expression de toutes les enzymes impliquees dans la lipogenese et de SREBP-1c, un facteur de transcription cle dans le controle de leur expression. L’augmentation de l’expression de SREBP-1c ne peut pas etre expliquee par une augmentation de l’insulinemie, mais pourrait etre tributaire de l’activation de LXR (augmentation de l’expression d’ABCA1) et/ou du stress du reticulum (augmentation de la proteine d’IRE1α). Conclusion La carence en AGPI n-3 provoque une accumulation de lipides dans le foie suite a une stimulation de la lipogenese. SREBP-1c semble etre un facteur cle dans cette activation de la voie lipogenique et l’augmentation de son expression pourrait dependre de la stimulation de l’activite de LXR ou d’un stress du reticulum.