Etudes Musculation

Retour de la théorie de l’hyperplasie comme mode de croissance

18/08/2017 | Etudes Musculation

 

Differential requirement for satellite cells during overload-induced muscle hypertrophy in growing versus mature mice
Kevin A. Murach   Skelet Muscle. 2017; 7: 14.

Pax7+ satellite cells are required for skeletal muscle fiber growth during post-natal development in mice. Satellite cell-mediated myonuclear accretion also appears to persist into early adulthood. Given the important role of satellite cells during muscle development, we hypothesized that the necessity of satellite cells for adaptation to an imposed hypertrophic stimulus depends on maturational age.

Methods

Pax7CreER-R26RDTA mice were treated for 5 days with vehicle (satellite cell-replete, SC+) or tamoxifen (satellite cell-depleted, SC-) at 2 months (young) and 4 months (mature) of age. Following a 2-week washout, mice were subjected to sham surgery or 10 day synergist ablation overload of the plantaris (n = 6–9 per group). The surgical approach minimized regeneration, de novo fiber formation, and fiber splitting while promoting muscle fiber growth. Satellite cell density (Pax7+ cells/fiber), embryonic myosin heavy chain expression (eMyHC), and muscle fiber cross sectional area (CSA) were evaluated via immunohistochemistry. Myonuclei (myonuclei/100 mm) were counted on isolated single muscle fibers.

Results

Tamoxifen treatment depleted satellite cells by ≥90% and prevented myonuclear accretion with overload in young and mature mice (p < 0.05). Satellite cells did not recover in SC- mice after overload. Average muscle fiber CSA increased ~20% in young SC+ (p = 0.07), mature SC+ (p < 0.05), and mature SC- mice (p < 0.05). In contrast, muscle fiber hypertrophy was prevented in young SC- mice. Muscle fiber number increased only in mature mice after overload (p < 0.05), and eMyHC expression was variable, specifically in mature SC+ mice.

Conclusions

Reliance on satellite cells for overload-induced hypertrophy is dependent on maturational age, and global responses to overload differ in young versus mature mice.

Rôle de la sirtuine 1 dans l’hypertrophie

02/03/2017 | Etudes sur les hormones et Etudes Musculation et Etudes Anti-âge

 

SIRT1 may play a crucial role in overload induced hypertrophy of skeletal muscle
Erika Koltai J physiol 2017

Significant skeletal muscle mass guarantees functional wellbeing and is important for high level performance in many sports. Although the molecular mechanism for skeletal muscle hypertrophy has been well-studied, it still is not completely understood. In the present study, we used a functional overload model to induce plantaris muscle hypertrophy by surgically removing the soleus, and gastrocnemius muscles in rats. Two weeks of muscle ablation resulted in a 40% increase in muscle mass, which was associated with a significant increase in SIRT1 content and activity (P

< 0.001). SIRT1-regulated Akt, eNOS, GLUT4 levels were also induced in hypertrophied muscles, and SIRT1 levels correlated with muscle mass, paired box protein 7 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinamide phosphoribosyltransferase (Nampt) levels. Alternatively, decreased FOXO1 and increased K48 polyubiquitination also suggest that SIRT1 could also be involved in the catabolic process of hypertrophy. Furthermore, increased levels of K63 and muscle RING finger 2 (MuRF2) protein could also be important enhancers of muscle mass. We report here that the levels of miR1 and miR133a decrease in hypertrophy and negatively correlate with muscle mass, SIRT1, and Nampt levels. Our results reveal a strong agreement between SIRT1 levels and activity, SIRT1 regulated pathways, and overload-induced hypertrophy.

These findings, along with the well-known regulatory

roles that SIRT1 plays in modulating both anabolic and catabolic pathways, allow us to propose the hypothesis that SIRT1 may actually play a crucial causal role in overload induced hypertrophy of skeletal muscle. This hypothesis will now require rigorous direct and functional testing.

Effets de l’exercice sur les concentrations de l’irisine

21/10/2016 | Etudes cardio et Etudes Musculation et Etudes Perte de poids et Etudes Anti-âge

 

Effets de l’exercice sur les concentrations de l’irisine circulatoire chez les adultes sains : revue générale
Science & Sports Volume 31, Issue 5, October 2016, Pages 251–260       A.C. Rodrigues

Objectifs

L’irisine est une myokine induite par l’exercice, responsable de la régulation de la protéine découplante 1 (UCP-1) dans le tissu adipeux beige. Cette étude vise à faire le point sur les effets d’exercice aigus et chroniques sur les concentrations circulantes d’irisine chez les adultes sains.

Informations

Nous avons réalisé, à partir des bases de données Medline et ScienceDirect, une revue de la littérature parue entre janvier 2012 et mars 2016, en utilisant les termes d’indexation suivants : irisine, exercice aigu, exercice chronique et entraînement. Pour les besoins de l’analyse, les études ont été divisés en exercice aigu et exercice chronique. Seize articles répondaient aux critères d’inclusion/exclusion, huit études portant sur l’exercice aigu, quatre avec l’exercice chronique et quatre avec les deux. Parmi les études portant sur l’exercice aigu, deux seulement n’ont pas observé d’augmentation des concentrations sériques et plasmatiques d’irisine après la séance d’exercice. L’exercice en résistance et l’exercice à haute intensité augmentaient davantage l’irisine que l’exercice aérobie et que l’exercice à faible d’intensité. Une seule étude a révélé une augmentation des concentrations circulantes d’irisine après plusieurs semaines d’entraînement en comparaison aux concentrations mesurées avant entraînement. Une autre étude a observé une augmentation des concentrations circulantes d’irisine dans le groupe entraîné par rapport au groupe témoin.

Conclusion

L’exercice aigu augmente les concentrations circulantes d’irisine. L’exercice en résistance et l’exercice à haute intensité augmentent davantage l’irisine. Par contre, un entraînement prolongé de plusieurs semaines ne semble pas modifier les concentrations circulantes d’irisine.

De nouvelles cellules souches découvertes dans les muscles

30/09/2016 | Echauffement et blessures et Etudes Musculation

 

The first characterization of a novel (non-satellite cell) stem cell population in human skeletal muscle
J.P. Nederveen     Appl. Physiol. Nutr. Metab. Vol. 41, 2016 S376

Skeletal muscle stem cells (satellite cells; SC) represent the primary
cell population responsible for muscle regeneration/repair. SC content
and activation has been show to increase in response to muscle
damaging exercise. However, non-satellite cell progenitors, under experimental
conditions in animals, have been identified to form skeletal
muscle
when the SC population is compromised. PW1+ interstitial
cells (PIC) have also been shown, experimentally, to contribute to
muscle repair in animals. This cell population, however, has never
been identified in humans. We sought to examine the changes in both
PIC and SC content following a single bout of eccentric exercise. Ten
sedentary males (24±3 years of age; mean±SEM) were recruited. Percutaneous
muscle biopsies from the vastus lateralis muscle were taken
prior to a bout of eccentric exercise (Pre), and 6h, 24h, and 72 h
post-exercise. Muscle fiber size, SC and PIC content were determined
via immunofluorescent microscopy. mRNA expression was assessed
by RT-PCR. The number of SC increased from Pre (10.3±0.8 Pax7+cells/
100 fibers) to 72h post-exercise (12.3±2.0 Pax7+cells/100 fibers, p<0.05).
Similarly, PW1+ cells increased from Pre (2.1±0.6 PW1+ cells/100 fibers)
to 72h post-exercise (6.8±2.5 PW1+ cells/100 fibers, p<0.05). PW1 mRNA
expression was significantly (p<0.05) increased 1.9-fold from Pre to
72h post-exercise. Here, for the first time in humans, we identify a
population of cells which are located in the interstitium that respond
to eccentrically-induced muscle damage in a similar fashion to SC.

 

Le sport élève ton niveau d’albumine…

30/06/2016 | Etudes cardio et Echauffement et blessures et Etudes Musculation et Etudes Anti-âge

 

Le sport élève ton niveau d’albumine…

Exercise-induced albuminuria is related to metabolic syndrome
Sharon Greenberg                 American Journal of Physiology - Renal Physiology Published 1 June 2016 Vol. 310 no. 11, F1192-F1196

Microalbuminuria (MA) is a known marker for endothelial dysfunction and future cardiovascular events. Exercise-induced albuminuria (EiA) may precede the appearance of MA. Associations between EiA and metabolic syndrome (MS) have not been assessed so far. Our aim was to investigate this association in a large sample of apparently healthy individuals with no baseline albuminuria. This was a cross-sectional study of 2,027 adults with no overt cardiovascular diseases who took part in a health survey program and had no baseline MA. Diagnosis of MS was based on harmonized criteria. All patients underwent an exercise test (Bruce protocol), and urinary albumin was measured before and after the examination. Urinary albumin-to-creatinine ratio (ACR) values before and after exercise were 0.40 (0.21–0.89) and 1.06 (0.43–2.69) mg/g for median (interquartile range) respectively. A total of 394 (20%) subjects had EiA; ACR rose from normal rest values (0.79 mg/g) to 52.28 mg/g after exercise (P < 0.001); this effect was not shown for the rest of the study population. EiA was related to higher prevalence of MS (13.8% vs. 27.1%, P < 0.001), higher metabolic equivalents (P < 0.001), higher baseline blood pressure (P < 0.001), and higher levels of fasting plasma glucose, triglycerides, and body mass index (P < 0.001). Multivariate binary logistic regression model showed that subjects with MS were 98% more likely to have EiA (95% confidence interval: 1.13–3.46, P = 0.016).

In conclusion, EiA in the absence of baseline MA is independently related to MS.

Deux lignes plus loin, on te montre le contraire

29/06/2016 | Etudes cardio et Etudes Musculation

 

pour le coup, j’ai nettement moins de mal à croire cette étude

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle
Jackson J. Fyfe           American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 June 2016 Vol. 310 no. 11, R1297-R1311

We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mechanistic target of rapamycin complex 1 (mTORC1) signaling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean ± SD: age, 27 ± 4 yr; V̇o2 peak, 45.7 ± 9 ml·kg−1·min−1) performed three experimental trials in a randomized order: 1) RE (8 × 5 leg press repetitions at 80% 1-repetition maximum) performed alone and RE preceded by either 2) HIT cycling [10 × 2 min at 120% lactate threshold (LT); HIT + RE] or 3) work-matched MICT cycling (30 min at 80% LT; MICT + RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise and +1 h (RE + 1 h) and +3 h (RE + 3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACCSer79 and p70S6KThr389 phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTORSer2448 and rps6Ser235/236 phosphorylation at POST. RE-induced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE + 1 h for MICT + RE vs. both HIT + RE and RE. Expression of miR-133a, miR-378, and miR-486 was reduced at RE + 1 h for HIT + RE vs. both MICT + RE and RE.

Postexercise mTORC1 signaling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces postexercise expression of miRNAs implicated in skeletal muscle adaptation to RE.

Ca serait bien si c’était vrai

29/06/2016 | Etudes cardio et Etudes Musculation

 

c’est le gros problème de la “science”

Aerobic exercise augments muscle transcriptome profile of resistance exercise

Tommy R. Lundberg           American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 June 2016 Vol. 310 no. 11, R1279-R1287

Recent reports suggest that aerobic exercise may boost the hypertrophic response to short-term resistance training. This study explored the effects of an acute aerobic exercise bout on the transcriptional response to subsequent resistance exercise. Ten moderately trained men performed ∼45 min cycling on one leg followed by 4 × 7 maximal knee extensions for each leg, 15 min later. Thus, one limb performed aerobic and resistance exercise (AE + RE) while the opposing leg did resistance exercise only (RE). Biopsies were obtained from the vastus lateralis muscle of each leg 3 h after the resistance exercise bout. Using DNA microarray, we analyzed differences [≥1.5-fold, false discovery rate (FDR) ≤10%] in gene expression profiles for the two modes of exercise. There were 176 genes up (127)- or downregulated (49) by AE + RE compared with RE. Among the most significant differentially expressed genes were established markers for muscle growth and oxidative capacity, novel cytokines, transcription factors, and micro-RNAs (miRNAs). The most enriched functional categories were those linked to carbohydrate metabolism and transcriptional regulation. Upstream analysis revealed that vascular endothelial growth factor, cAMP-response element-binding protein, Tet methylcytosine dioxygenase, and mammalian target of rapamycin were regulators highly activated by AE + RE, whereas JnK, NF-κβ, MAPK, and several miRNAs were inhibited. Thus, aerobic exercise alters the skeletal muscle transcriptional signature of resistance exercise to initiate important gene programs promoting both myofiber growth and improved oxidative capacity.

These results provide novel insight into human muscle adaptations to diverse exercise modes and offer the very first genomic basis explaining how aerobic exercise may augment, rather than compromise, muscle growth induced by resistance exercise.

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