Etudes sur les hormones

Irisine: le lien entre la muscu et le renforcement osseux?

14/03/2018 | Etudes sur les hormones et Etudes Perte de poids et Etudes Anti-âge


Myokine—Irisin—and Its Effects Linking Bone and Muscle Function
Graziana Colaianni           Clinical Reviews in Bone and Mineral Metabolism March 2018, Volume 16, Issue 1, pp 16–21

Irisin is a myokine secreted by the skeletal muscle during physical activity both in mice and humans. Its first identified role was to activate the browning response in white adipocytes, subsequently triggering non-shivering thermogenesis; therefore, Irisin has raised great expectations as a potential target in the treatment of obesity. In 2015, we demonstrated that Irisin plays a central role in the control of bone mass, driving positive effects on cortical mineral density and bone mechanical properties. This effect on the bone was triggered using an Irisin dosage 70 times lower than the one needed to induce the browning response, suggesting that the skeleton is the primary target organ of this myokine. Moreover, our studies also highlighted the autocrine effect of Irisin on the skeletal muscle, overall suggesting that Irisin plays a fundamental role in the physiology of the musculoskeletal system. More recently, we demonstrated the efficacy of Irisin in preventing and restoring bone and muscle losses in a mouse model affected by disuse-induced osteoporosis and muscular atrophy. Hopefully, if future investigations will be confirmed in humans, it may lead to develop an Irisin-based therapy for physically disable or bedridden patients and it might also represent a countermeasure for astronauts subjected to microgravity.

Deca dick?

14/02/2018 | Etudes sur les hormones et Etudes Anti-âge


Nandrolone combined with strenuous resistance training reduces vascular nitric oxide bioavailability and impairs endothelium-dependent vasodilation
Steroids Volume 131, March 2018, Pages 7-13     ViniciusGuzzoni

• Nandrolone plus strenuous RT impairs acetylcholine-mediated aorta vasodilation.
• Nandrolone plus strenuous RT increased reactive species of oxygen levels.
• Nandrolone plus strenuous RT dramatically reduced vascular NO bioavailability.
• Nandrolone plus strenuous RT increased arterial wall thickness.
• Combination of nandrolone and strenuous RT might lead endothelial dysfunction.

Anabolic Androgenic Steroids (AASs) misuse has increased among adolescents and recreational athletes due to their potential effects on muscle hypertrophy. On the other hand, AAS might induce alterations on cardiovascular system, although some controversies regarding AAS on vascular properties remain unknown. To address this question, we aimed to investigate the effects of high doses of nandrolone combined with strenuous resistance training (RT) on function and structure of thoracic aorta. Rats were randomized into four groups: non-trained vehicle (NTV), trained vehicle (TV), non-trained nandrolone (NTN), and trained nandrolone (TN), and submitted to 6 weeks of treatment with nandrolone (5 mg/kg, twice a week) and/or resistance training. In vitro response of thoracic aorta to acetylcholine (ACh) was analyzed. Vascular nitric oxide (NO) and reactive oxygen species (ROS) synthesis were evaluated using 4,5-diaminofluorescein diacetate (DAF-2) and hydroethidine fluorescent techniques, respectively. Thoracic aorta was processed for microscopy analyses and tunica media thickness was measured. ACh-mediated relaxation response was impaired in endothelium intact aortic rings isolated from trained rats (TV and TN) as compared with their matched non-trained groups. TN rats showed reduced ACh-mediated vasodilatation than NTN rats. NO production and bioavailability decreased in thoracic aorta of nandrolone-treated rats in relation to their matched non-trained group (NTN vs. NTV; TN vs. TV). ROS production and tunica media thickness were increased in TN rats when compared with TV rats.

These findings indicate that high doses of nandrolone combined with strenuous RT affect NO bioavailability and might induce endothelial dysfunction and arterial morphological alterations.

Rôle des recepteurs aux androgènes sur la masse grasse

02/02/2018 | Etudes sur les hormones et Etudes Perte de poids


The androgen receptor in bone marrow progenitor cells negatively regulates fat mass
Patricia K Russell J Endo 2018

It is well established that testosterone negatively regulates fat mass in humans and mice, however the mechanism by which testosterone exerts these effects is poorly understood. We and others have shown that deletion of the androgen receptor (AR) in male mice results in a phenotype that mimics the three key clinical aspects of hypogonadism in human males; increased fat mass, and decreased bone and muscle mass. We now show that replacement of the AR gene specifically in mesenchymal progenitor cells (PCs) residing in the bone marrow of Global-ARKO mice, in the absence of the AR in all other tissues (PC-AR Gene Replacements), completely attenuates their increased fat accumulation. Inguinal subcutaneous white adipose tissue and intra-abdominal retroperitoneal visceral adipose tissue depots in PC-AR Gene Replacement mice were 50-80% lower than wild type (WT) and 75-90% lower than Global-ARKO controls at 12 weeks of age. The marked decrease in subcutaneous and viceral fat mass in PC-AR Gene Replacements was associated with an increase in the number of small adipocytes and a healthier metabolic profile compared to WT controls, characterised by normal serum leptin and elevated serum adiponectin levels. Euglycaemic/hyperinsulinaemic clamp studies reveal that the PC-AR Gene replacement mice have improved whole-body insulin sensitivity with higher glucose infusion rates compared to WT mice and increased glucose uptake into subcutaneous and intra-abdominal fat.

In conclusion, these data provide the first evidence for an action of androgens via the AR in mesenchymal bone marrow PCs to negatively regulate fat mass and improve metabolic function.

Rôle de la Ghréline, post-exercice

23/01/2018 | Etudes cardio et Etudes sur les hormones


Ghrelin mediates exercise endurance and the feeding response post-exercise
Bharath K. Mani         Mol Met. 2018.01.006

•High intensity exercise transiently increases plasma ghrelin.
•Without ghrelin action on its receptors (growth hormone secretagogue receptors), exercise markedly reduces food intake.
•An intact ghrelin system enhances exercise endurance.

Exercise training has several well-established health benefits, including many related to body weight, appetite control, and blood glucose homeostasis. However, the molecular mechanisms and, in particular, the hormonal systems that mediate and integrate these beneficial effects are poorly understood. In the current study, we aimed to investigate the role of the hormone ghrelin and its receptor, the growth hormone secretagogue receptor (GHSR; ghrelin receptor), in mediating the effects of exercise on food intake and blood glucose following exercise as well as in regulating exercise endurance capacity.

We used two mouse models of treadmill running to characterize the changes in plasma ghrelin with exercise. We also assessed the role of the ghrelin system to influence food intake and blood glucose after exercise, exercise endurance, and parameters potentially linked to responses to exercise. Mice lacking GHSRs (GHSR-null mice) and wild-type littermates were studied.

An acute bout of exercise transiently elevated plasma acyl-ghrelin. Without the action of this increased ghrelin on GHSRs (as in GHSR-null mice), high intensity interval exercise markedly reduced food intake compared to control mice. The effect of exercise to acutely raise blood glucose remained unmodified in GHSR-null mice. Exercise-induced increases in plasma ghrelin positively correlated with endurance capacity, and time to exhaustion was reduced in GHSR-null mice as compared to wild-type littermates. In an effort to mechanistically explain their reduced exercise endurance, exercised GHSR-null mice exhibited an abrogated sympathoadrenal response, lower overall insulin-like growth factor-1 levels, and altered glycogen utilization.

Exercise transiently increases plasma ghrelin. GHSR-null mice exhibit decreased food intake following high intensity interval exercise and decreased endurance when submitted to an exercise endurance protocol. These data suggest that an intact ghrelin system limits the capacity of exercise to restrict food intake following exercise, although it enhances exercise endurance.

Effet de l’exercice physique sur les niveaux de GDF-15

23/01/2018 | Etudes sur les hormones et Etudes Musculation


Exercise increases circulating GDF15 in humans
Maximilian Kleinert         Mol Met 2017.12.016

•Circulating GDF15 increases during exercise and during recovery from exercise in humans.
•Skeletal muscle tissue appears not to be the source for this exercise-induced increase in GDF15 levels.

The growth differentiation factor 15 (GDF15) is a stress-sensitive circulating factor that regulates systemic energy balance. Since exercise is a transient physiological stress that has pleiotropic effects on whole-body energy metabolism, we herein explored the effect of exercise on a) circulating GDF15 levels and b) GDF15 release from skeletal muscle in humans.

Seven healthy males either rested or exercised at 67% of their VO2max for 1 h and blood was sampled from the femoral artery and femoral vein before, during, and after exercise. Plasma GDF15 concentrations were determined in these samples.

Plasma GDF15 levels increased 34% with exercise (p < 0.001) and further increased to 64% above resting values at 120 min (p < 0.001) after the cessation of exercise. There was no difference between the arterial and venous GDF15 concentration before, during, and after exercise. During a resting control trial, GDF15 levels measured in the same subjects were unaltered.

Vigorous submaximal exercise increases circulating GDF15 levels in humans, but skeletal muscle tissue does not appear to be the source.

Rôle de l’ IL-15/IL dans la synthèse des protéines après la muscu

17/01/2018 | Etudes sur les hormones et Etudes Musculation


Skeletal muscle IL-15/IL-15Rα and myofibrillar protein synthesis after resistance exercise
Scandinavian Journal of Medicine & Science Sports 28, Issue 1 January 2018 Pages 116–125
A. Pérez-López

In vitro and in vivo studies described the myokine IL-15 and its receptor IL-15Rα as anabolic/anti-atrophy agents, however, the protein expression of IL-15Rα has not been measured in human skeletal muscle and data regarding IL-15 expression remain inconclusive. The purpose of the study was to determine serum and skeletal muscle IL-15 and IL-15Rα responses to resistance exercise session and to analyze their association with myofibrillar protein synthesis (MPS).

Fourteen participants performed a bilateral leg resistance exercise composed of four sets of leg press and four sets of knee extension at 75% 1RM to task failure. Muscle biopsies were obtained at rest, 0, 4 and 24 hours post-exercise and blood samples at rest, mid-exercise, 0, 0.3, 1, 2, 4 and 24 hours post-exercise. Serum IL-15 was increased by ~5.3-fold immediately post-exercise, while serum IL-15Rα decreased ~75% over 1 hour post-exercise (P

<.001). Skeletal muscle IL-15Rα mRNA and protein expression were increased at 4 hours post-exercise by ~2-fold (P<.001) and ~1.3-fold above rest (P=.020), respectively. At 24 hours post-exercise, IL-15 (P=.003) and IL-15Rα mRNAs increased by ~2-fold (P=.002). Myofibrillar fractional synthetic rate between 0-4 hours was associated with IL-15Rα mRNA at rest (r=.662, P=.019), 4 hours (r=.612, P=.029), and 24 hours post-exercise (r=.627, P=.029). Finally, the

muscle IL-15Rα protein up-regulation was related to Leg press 1RM (r=.688, P=.003) and total weight lifted (r=.628, P=.009). In conclusion, IL-15/IL-15Rα signaling pathway is activated in skeletal muscle in response to a session of resistance exercise.

Impact nerveux des corticoïdes?

28/12/2017 | Etudes sur les hormones


Neural Correlates to the Increase in Maximal Force after Dexamethasone Administration
Baudry, Stéphane             Medicine & Science in Sports & Exercise. ., Post Acceptance: September 19, 2017

Purpose This study investigated the effects of short-term glucocorticoid administration on voluntary activation and intracortical inhibitory and facilitatory circuits.

Methods Seventeen healthy men participated in a pseudo randomized double-blind study to receive either dexamethasone (8 mg·d-1, n = 9 subjects) or placebo (n = 8 subjects) for 7 days. The ankle dorsiflexion torque, corresponding electromyography (EMG) of the tibialis anterior, and voluntary activation assessed by the interpolated twitch method using transcranial magnetic stimulation (TMS) were measured during a maximal voluntary contraction (MVC). Short-latency intracortical inhibition (SICI) and intracortical facilitation (ICF) were assessed at rest and during submaximal contraction (50% MVC torque) by paired-pulse TMS with the conditioning stimulus set at 0.8x of motor threshold (0.8x MT) and delivered 2 ms (SICI) and 13 ms (ICF) prior to the test stimulus (1.2x MT).

Results The MVC torque (+14%), tibialis anterior EMG (+31%) and voluntary activation (+3%) increased after glucocorticoid treatment (p<0.05). The increase in voluntary activation was associated with the gain in MVC torque (r2 = 0.56; p = 0.032). The level of SICI and the duration of the EMG silent period that followed the test TMS decreased (-18.6% and -13.5%, respectively) during the 50% MVC after treatment (p<0.05) while no significant change was observed for ICF. Neither SICI nor ICF changed after treatment when assessed at rest.

Conclusion Short-term dexamethasone treatment induced specific decrease in the excitability of intracortical inhibitory circuits that likely contributed to the increase in the voluntary activation and associated MVC torque.

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