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Les muscles sont des réservoirs à nitrate

24/05/2015 | Etudes sur les hormones et Etudes Compléments alimentaires

 

Skeletal muscle as an endogenous nitrate reservoir
Barbora Piknova       Nitric Oxide Volume 47, 1 May 2015, Pages 10–16

Highlights
• Skeletal muscle is the major endogenous nitrate source and reservoir in mammals.
• Blood serve as a transporter for nitrate from muscle into internal organs.
• Internal organs have active nitrate reductases and are source of body nitrite.

The nitric oxide synthase (NOS) family of enzymes form nitric oxide (NO) from arginine in the presence of oxygen. At reduced oxygen availability NO is also generated from nitrate in a two step process by bacterial and mammalian molybdopterin proteins, and also directly from nitrite by a variety of five-coordinated ferrous hemoproteins. The mammalian NO cycle also involves direct oxidation of NO to nitrite, and both NO and nitrite to nitrate by oxy-ferrous hemoproteins. The liver and blood are considered the sites of active mammalian NO metabolism and nitrite and nitrate concentrations in the liver and blood of several mammalian species, including human, have been determined. However, the large tissue mass of skeletal muscle had not been generally considered in the analysis of the NO cycle, in spite of its long-known presence of significant levels of active neuronal NOS (nNOS or NOS1).

We hypothesized that skeletal muscle participates in the NO cycle and, due to its NO oxidizing heme protein, oxymyoglobin has high concentrations of nitrate ions. We measured nitrite and nitrate concentrations in rat and mouse leg skeletal muscle and found unusually high concentrations of nitrate but similar levels of nitrite, when compared to the liver. The nitrate reservoir in muscle is easily accessible via the bloodstream and therefore nitrate is available for transport to internal organs where it can be reduced to nitrite and NO. Nitrate levels in skeletal muscle and blood in nNOS−/− mice were dramatically lower when compared with controls, which support further our hypothesis. Although the nitrate reductase activity of xanthine oxidoreductase in muscle is less than that of liver, the residual activity in muscle could be very important in view of its total mass and the high basal level of nitrate.

We suggest that skeletal muscle participates in overall NO metabolism, serving as a nitrate reservoir, for direct formation of nitrite and NO, and for determining levels of nitrate in other organs.

Les muscles sont des réservoirs à nitrate

24/05/2015 | Etudes sur les hormones et Etudes Compléments alimentaires

 

Skeletal muscle as an endogenous nitrate reservoir
Barbora Piknova       Nitric Oxide Volume 47, 1 May 2015, Pages 10–16

Highlights
• Skeletal muscle is the major endogenous nitrate source and reservoir in mammals.
• Blood serve as a transporter for nitrate from muscle into internal organs.
• Internal organs have active nitrate reductases and are source of body nitrite.

The nitric oxide synthase (NOS) family of enzymes form nitric oxide (NO) from arginine in the presence of oxygen. At reduced oxygen availability NO is also generated from nitrate in a two step process by bacterial and mammalian molybdopterin proteins, and also directly from nitrite by a variety of five-coordinated ferrous hemoproteins. The mammalian NO cycle also involves direct oxidation of NO to nitrite, and both NO and nitrite to nitrate by oxy-ferrous hemoproteins. The liver and blood are considered the sites of active mammalian NO metabolism and nitrite and nitrate concentrations in the liver and blood of several mammalian species, including human, have been determined. However, the large tissue mass of skeletal muscle had not been generally considered in the analysis of the NO cycle, in spite of its long-known presence of significant levels of active neuronal NOS (nNOS or NOS1).

We hypothesized that skeletal muscle participates in the NO cycle and, due to its NO oxidizing heme protein, oxymyoglobin has high concentrations of nitrate ions. We measured nitrite and nitrate concentrations in rat and mouse leg skeletal muscle and found unusually high concentrations of nitrate but similar levels of nitrite, when compared to the liver. The nitrate reservoir in muscle is easily accessible via the bloodstream and therefore nitrate is available for transport to internal organs where it can be reduced to nitrite and NO. Nitrate levels in skeletal muscle and blood in nNOS−/− mice were dramatically lower when compared with controls, which support further our hypothesis. Although the nitrate reductase activity of xanthine oxidoreductase in muscle is less than that of liver, the residual activity in muscle could be very important in view of its total mass and the high basal level of nitrate.

We suggest that skeletal muscle participates in overall NO metabolism, serving as a nitrate reservoir, for direct formation of nitrite and NO, and for determining levels of nitrate in other organs.

La tension, plus que le temps sous tension déclenche l’anabolisme

23/05/2015 | Etudes Musculation

 

High force development augments skeletal muscle signalling in resistance exercise modes equalized for time under tension
Sebastian Gehlert     Pflügers Archiv - European Journal of Physiology June 2015, Volume 467, Issue 6, pp 1343-1356

How force development and time under tension (TUT) during resistance exercise (RE) influence anabolic signalling of skeletal muscle is incompletely understood. We hypothesized that high force development during RE is more important for post-exercise-induced signalling than submaximal and fatiguing RE with lower force development but similar TUT.

Twenty-two male subjects (24 ± 6 years, 181 ± 9 cm, 79 ± 2 kg) performed three distinct RE modes in the fed state with equal TUT but distinct force output:
(i) maximal eccentric RE (ECC, n = 7) three sets, eight reps, 100 % eccentric dynamic force;
(ii) standard RE (STD, n = 7), three sets, 10 reps, 75 % dynamic force; and
(iii) high fatiguing single-set RE (HIT, n = 8), 20 reps, 100 % eccentric-concentric force;

vastus lateralis biopsies were collected at baseline, 15, 30, 60, 240 min and 24 h after RE, and the signalling of mechanosensitive and mammalian target of rapamycin (mTOR)-related proteins was determined.

The phosphorylation levels of pFAKTyr397, pJNKThr183/Tyr185, pAKTThr308/Ser473, pmTORSer2448, p4E-BP1Thr37/46, p70s6kThr389/Ser421/Thr424 and pS6Ser235/236 were significantly higher in ECC than those in STD and HIT at several time points (P 

< 0.01). pJNKThr183/Tyr185 and pS6Ser235/236 levels were significantly higher in type II myofibres in ECC compared with STD and HIT.

HIT exerted throughout the weakest signalling response.

We conclude that high force development during acute RE is superior for anabolic skeletal muscle signalling than fatiguing RE with lower force output but similar TUT. Our results suggest that this response is substantially driven by the higher activation of type II myofibres during RE.

Un blocage des récepteurs cannabinoïdes augmente l’anabolisme musculaire

15/05/2015 | Etudes sur les hormones et Etudes Musculation

 

Cannabinoid receptor 1 and acute resistance exercise – In vivo and in vitro studies in human skeletal muscle
Satu Pekkala         Peptides Volume 67, May 2015, Pages 55–63

Highlights
• Resistance exercise down-regulates Cannabinoid receptor 1 expression in human skeletal muscle.
• Blockage of Cannabinoid receptor 1 in skeletal muscle cells increases signaling downstream of mammalian target of rapamycin.
• Blockage of Cannabinoid receptor 1 increases protein synthesis in skeletal muscle cells.

Aim
This study aimed to determine whether Cannabinoid receptor 1 (CB1) is involved in mammalian target of rapamycin (mTOR) signaling and skeletal muscle protein synthesis.

Methods
This study used human vastus lateralis skeletal muscle biopsies obtained before and after a resistance exercise (RE) bout in young men (n = 18). The signaling mechanisms were studied in vitro in human myotubes. Protein expression was determined by Western blot and confocal microscopy, and gene expression by quantitative PCR. Protein synthesis was measured in vitro using puromycin-based SuNSET technique.

Results
In human skeletal muscle, an anabolic stimulus in the form of RE down-regulated CB1 expression. The negative change in CB1 expression was associated with increased phosphorylation of mTOR signaling proteins. In vitro, CB1 antagonist AM251 induced phosphorylation of mTOR downstream targets, ribosomal protein S6 kinase (S6K1), S6 and eukaryotic initiation factor 4E binding protein (4E-BP1) in human myotubes. These effects were ERK1/2-dependent and insensitive to mTOR inhibitor, rapamycin. Compared to AM251 treatment alone, inhibition of ERK1/2 by UO126 in the presence of AM251 decreased phosphorylation of S6K1, S6 and and 4E-BP1 at Thr37/46. AM251 increased protein synthesis in cultured human myotubes, which was not rapamycin-sensitive but was ERK1/2-dependent.

Conclusions
Our results indicate that RE down-regulates CB1 expression. Inhibition of CB1 signaling increases skeletal muscle anabolic signaling down-stream of mTOR and protein synthesis through ERK1/2. Our study may provide base for the development of CB1-blocking drugs to treat or prevent muscle wasting.

Moins de Firmicutes avec la glutamine

01/05/2015 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge

 

Oral supplementation with l-glutamine alters gut microbiota of obese and overweight adults: A pilot study
Nutrition Volume 31, Issue 6, June 2015, Pages 884–889     Alessandra Zanin Zambom de Souza

• Oral supplementation with l-glutamine (GLN) promotes changes in the gut microbiota composition.
• The ratio of Firmicutes to Bacteroidetes decreased after GLN supplementation.
• Firmicutes and Actinobacteria reduced significantly after glutamine supplementation.
• The effects of oral supplementation with GLN on gut microbiota are similar to those seen in weight loss.

Objective

The aim of this study was to determine whether oral supplementation with l-glutamine (GLN) modifies the gut microbiota composition in overweight and obese adults.

Methods

Thirty-three overweight and obese adults, ages between 23 and 59 y and body mass index between 25.03 and 47.12 kg/m2, were randomly assigned to receive either oral supplementation with 30 g of l-alanine (ALA group control) or 30 g of GLN (GLN group) daily for 14 d. We analyzed the gut microbiota composition with new-generation sequencing techniques and bioinformatics analysis.

Results

After 14 d of supplementation, adults in the GLN group exhibited statistically significant differences in the Firmicutes and Actinobacteria phyla compared with those in the ALA group. The ratio of Firmicutes to Bacteroidetes, a good biomarker for obesity, decreased in the GLN group from 0.85 to 0.57, whereas it increased from 0.91 to 1.12 in the ALA group. At the genus level, Dialister, Dorea, Pseudobutyrivibrio, and Veillonella, belonging to the Firmicutes phylum, had statistically significant reduction.

Conclusion

Oral supplementation with GLN, for a short time, altered the composition of the gut microbiota in overweight and obese humans reducing the Firmicutes to Bacteroidetes ratio, which resembled weight loss programs already seen in the literature.

Combien de leptin dans le tissu adipeux comparé aux muscles?

30/04/2015 | Etudes sur les hormones et Etudes Perte de poids

 

Estimation of human leptin concentration in the subcutaneous adipose and skeletal muscle tissues
Gerald Sendlhofer         European Journal of Clinical Investigation Volume 45, Issue 5,  pages 445–451, May 2015

Interstitial leptin concentrations in subcutaneous adipose and skeletal muscle tissues were determined by open-flow microperfusion.

Method
In 12 lean male subjects (age: 25·6 ± 1·1 years), a zero flow rate experiment using different flow rates was applied. Recovery was determined by urea as an internal reference. In the no-net-flux experiments, catheters were perfused with five solutions containing different concentrations of leptin. Concentrations of interstitial leptin were calculated by applying linear regression analysis to perfusate as opposed to sampled leptin concentrations.

Results
The zero flow rate protocol showed significantly higher concentrations of leptin in the interstitial fluid of subcutaneous adipose compared to skeletal muscle tissue [36·8 ± 10·32 vs. 7·1 ± 2·5% of the corresponding plasma level (P = 0·018)]. The recovery of urea in the samples was comparable for all catheters [79·4 ± 6·8 vs. 83·0 ± 5·8 of the corresponding plasma level, flow rate of 0·3 μL/min; (P = ns)] and was higher when compared to leptin. In the no-net-flux protocol, the concentration of leptin in subcutaneous adipose tissue was almost identical to plasma [90. 5 ± 7·0%] and the skeletal muscle tissue concentration of leptin was 23·7 ± 2·5% of the corresponding plasma level.

Conclusion
Open-flow microperfusion enables the estimation of leptin concentrations in subcutaneous adipose and skeletal muscle tissues in humans in vivo. This is the first documentation on the use of open-flow microperfusion to demonstrate that relevant amounts of leptin are also found in skeletal muscle tissue.

L’acide aspartique augmente t’il ou diminue t’il la sécrétion de testostérone?

08/04/2015 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge et Etudes sur les boosters sexuels et la sexualité

 

Three and six grams supplementation of d-aspartic acid in resistance trained men
Geoffrey W Melville       Journal of the International Society of Sports Nutrition 2015, 12:15

Although abundant research has investigated the hormonal effects of d-aspartic acid in rat models, to date there is limited research on humans. Previous research has demonstrated increased total testosterone levels in sedentary men and no significant changes in hormonal levels in resistance trained men. It was hypothesised that a higher dosage may be required for experienced lifters, thus this study investigated the effects of two different dosages of d-aspartic acid on basal hormonal levels in resistance trained men and explored responsiveness to d-aspartic acid based on initial testosterone levels.

Methods

Twenty-four males, with a minimum of two years’ experience in resistance training, (age, 24.5 ± 3.2 y; training experience, 3.4 ± 1.4 y; height, 178.5 ± 6.5 cm; weight, 84.7 ± 7.2 kg; bench press 1-RM, 105.3 ± 15.2 kg) were randomised into one of three groups: 6 g.d−1 plain flour (D0); 3 g.d−1 of d-aspartic acid (D3); and 6 g.d−1 of d-aspartic acid (D6). Participants performed a two-week washout period, training four days per week. This continued through the experimental period (14 days), with participants consuming the supplement in the morning. Serum was analysed for levels of testosterone, estradiol, sex hormone binding globulin, albumin and free testosterone was determined by calculation.

Results

D-aspartic acid supplementation revealed no main effect for group in: estradiol; sex-hormone-binding-globulin; and albumin. Total testosterone was significantly reduced in D6 (P = 0.03). Analysis of free testosterone showed that D6 was significantly reduced as compared to D0 (P = 0.005), but not significantly different to D3. Analysis did not reveal any significant differences between D3 and D0. No significant correlation between initial total testosterone levels and responsiveness to d-aspartic acid was observed (r = 0.10, P = 0.70).

Conclusions

The present study demonstrated that a daily dose of six grams of d-aspartic acid decreased levels of total testosterone and free testosterone (D6), without any concurrent change in other hormones measured. Three grams of d-aspartic acid had no significant effect on either testosterone markers. It is currently unknown what effect this reduction in testosterone will have on strength and hypertrophy gains.

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