Exploration détaillée des composantes de la glycorégulation chez des sportifs sujets aux hypoglycémies d’effort. Intérêt de l’oral minimal model
J.-F. Brun   Science & Sports Volume 26, Issue 5, November 2011, Pages 286-291

Les hypoglycémies à l’exercice (HE) sont une situation très fréquente mais peu étudiée. Elles surviennent chez des sujets présentant des valeurs élevées d’insulino-sensibilité (SI) et d’efficience glucidique (SG). SI et SG peuvent être calculées à partir de repas-tests par une modélisation mathématique qui permet aussi une étude approfondie des composantes de la sécrétion d’insuline.

Méthodes et résultats
Nous avons étudié les résultats fournis par cette méthode chez 19 sportifs se plaignant d’HE comparés à 58 sportifs appariés ne présentant pas ce problème. On observe des valeurs plus élevées de SI (p < 0,05) et SG (p

Conclusion
Ainsi, ces sujets ont une assimilation glucidique massive, leur sécrétion d’insuline se réduisant de façon compensatoire mais cette réduction a des limites et peut s’avérer insuffisante, notamment en ce qui concerne la sensibilité β-pancréatique au glucose.

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Muscle fatigue induced by two different resistances: Elastic tubing versus weight machines
Journal of Electromyography and Kinesiology Volume 21, Issue 6, December 2011, Pages 954-959   G. Melchiorri

Elastic tubes are devices relatively inexpensive, easy to use, portable and safe, which are claimed to provide advantages with respect to training with free weights or weight machine. The aim of this work was to assess neuromuscular modification induced by the use of two different muscle contraction modalities (elastic versus weight resistances) until exhaustion. Fourteen healthy physically active male students (age: 28 ± 6 years; body mass 72.1 ± 11.0 kg; height: 173.5 ± 6.9 cm) were recruited. They were requested to reach exhaustion with dynamic contraction at 70% of their own One Repetition Maximal (1RM) using, in two different days and in random order, Thera Band® tubes or traditional weight plates on an arm machine designed and built for those tasks. Before and after such contractions a standardized fatiguing isometric test (3 Maximal Voluntary Contractions, MVC plus 60 s at 60% MVC) was requested to assess differences induced by the exhaustion sessions. During fatiguing tests surface EMG signals were recorded from biceps brachii muscle with linear arrays of eight electrodes (silver bars 10 mm apart, 5 mm long, and 1 mm diameter) in single differential configuration. Initial values and rates of change of Average Rectified Value (ARV), MeaN power Frequency (MNF) and muscle fiber Conduction Velocity (CV) were calculated to compare the effects of the two contraction modalities. No differences were found between “elastic session” and “weight session” PRE MVCs (31.9 ± 8.8 and 29.9 ± 8.3 nm, respectively) and endurance times (28 ± 6 and 26 ± 7 s, respectively). The same was observed for POST values. During the post-contraction isometric fatigue test, the only parameters influenced by the contraction modality were the initial CV and the rate of change in CV which were 12% and 37% greater (p

These findings confirm others for which contractions done with the use of elastic band seem to require greater muscle activation; moreover, they highlight a sort of “muscle conditioning” after that specific contraction modality which requires the use of faster motor units. It is thus possible to consider the practical use of such elastic devices to increase the neuromuscular activation, for instance in specific rehabilitation settings where slow movements with minimal risk of injury are requested (post surgery rehabilitation, physical activity with elderly people or children).

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Is there a morning-to-evening difference in the acute IL-6 and cortisol responses to resistance exercise?
David Pledge   Cytokine Volume 55, Issue 2, August 2011, Pages 318-323

Exercise training is known to induce a molecular adaptation process involving inflammatory responses. However any time-of-day effect of exercise on inflammatory responses remains unknown. The aim of the present study was to investigate whether acute bouts of intense exercise performed at different times of the day would affect the release Interleukin-6 (IL-6), one of the most abundant cytokines in mammalian endocrine response to exercise. Cortisol levels were measured as a confirmation of correct timing of exercise and to determine any impact it may have on the cytokine release. Twelve healthy male participants carried out 30 min of intense exercise (3 sets of 8–12 repetitions for 4 resistance exercises at 70% of 1RM) in morning (08:15–09:00 h), and evening (18:15–19:00 h) sessions. An 8 h fasting period was required before each exercise session. Blood samples were taken immediately pre and post each exercise sessions to determine IL-6 and cortisol levels.

Our data show that whilst the training group showed no post-exercise changes in serum_IL-6 levels (P > 0.05), the control group on the other hand showed significant time-of-day modifications in serum_IL-6 levels (P = 0.008). Moreover, a significant interaction between intervention phase (pre-post training, AM vs. PM) and group (Exercise vs. Control) is evidenced in terms of serum_IL-6 levels (P = 0.014). This interaction however was nullified when the between group differences at baseline were partialled out in a covariate analysis (P > 0.05).

We also found that the main effect of experimental phase on Cortisol was present in both the trained (P = 0.004) and control groups (p

0.05).

Based on the current data, we would propose that exercise and/or time-of-day would not interfere with clinical endocrine profiling of IL-6 in a population.

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Melatonin: The smart killer: The human trophoblast as a model
Dave Lanoix         Molecular and Cellular Endocrinology Volume 348, Issue 1, 2 January 2012, Pages 1-11

Melatonin has both the ability to induce intrinsic apoptosis in tumor cells while it inhibits it in non-tumor cells. Melatonin kills tumor cells through induction of reactive oxygen species generation and activation of pro-apoptotic pathways. In contrast, melatonin promotes the survival of non-tumor cells due to its antioxidant properties and the inhibition of pro-apoptotic pathways. In primary human villous trophoblast, a known pseudo-tumorigenic tissue, melatonin promotes the survival through inhibition of the Bax/Bcl-2 pathway while in BeWo choriocarcinoma cell line melatonin induces permeabilization of the mitochondrial membrane leading to cellular death. These findings suggest that the trophoblast is a good model to study the differential effects of melatonin on the intrinsic apoptosis pathway. This review describes the differential effects of melatonin on the intrinsic apoptosis pathway in tumor and non-tumor cells and presents the trophoblast as a novel model system in which to study these effects of melatonin.

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Myostatin Induces Degradation of Sarcomeric Proteins through a Smad3 Signaling Mechanism During Skeletal Muscle Wasting
Sudarsanareddy Lokireddy, Craig McFarlane, Xiaojia Ge, Huoming Zhang, Siu Kwan Sze, Mridula Sharma and Ravi Kambadur
Molecular Endocrinology November 1, 2011 vol. 25 no. 11 1936-1949

Ubiquitination-mediated proteolysis is a hallmark of skeletal muscle wasting manifested in response to negative growth factors, including myostatin. Thus, the characterization of signaling mechanisms that induce the ubiquitination of intracellular and sarcomeric proteins during skeletal muscle wasting is of great importance. We have recently characterized myostatin as a potent negative regulator of myogenesis and further demonstrated that elevated levels of myostatin in circulation results in the up-regulation of the muscle-specific E3 ligases, Atrogin-1 and muscle ring finger protein 1 (MuRF1). However, the exact signaling mechanisms by which myostatin regulates the expression of Atrogin-1 and MuRF1, as well as the proteins targeted for degradation in response to excess myostatin, remain to be elucidated. In this report, we have demonstrated that myostatin signals through Smad3 (mothers against decapentaplegic homolog 3) to activate forkhead box O1 and Atrogin-1 expression, which further promotes the ubiquitination and subsequent proteasome-mediated degradation of critical sarcomeric proteins. Smad3 signaling was dispensable for myostatin-dependent overexpression of MuRF1. Although down-regulation of Atrogin-1 expression rescued approximately 80% of sarcomeric protein loss induced by myostatin, only about 20% rescue was seen when MuRF1 was silenced, implicating that Atrogin-1 is the predominant E3 ligase through which myostatin manifests skeletal muscle wasting. Furthermore, we have highlighted that Atrogin-1 not only associates with myosin heavy and light chain, but it also ubiquitinates these sarcomeric proteins. Based on presented data we propose a model whereby myostatin induces skeletal muscle wasting through targeting sarcomeric proteins via Smad3-mediated up-regulation of Atrogin-1 and forkhead box O1.

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Neural conduction and excitability following a simple warm up
Journal of Science and Medicine in Sport   Alan J. Pearce

Objective: This study examined the effect of a generic, active warm up on neural and muscular conduction time. Design: Single group, pre-post design. Method: Central and peripheral neuromuscular conduction time was quantified in the abductor pollicis brevis (APB) and gastrocnemius muscles of 18 healthy participants (mean age 25.9 ± 5.8 years, 12 males) using transcranial magnetic stimulation (TMS) and M-wave techniques, prior to and immediately following an active warm up consisting of 5 min running at 65% of maximum heart rate. Neural conduction time, for both TMS and M-wave, was quantified as the time between stimulus artefact and deflection of the wave form, whilst muscle conduction time for TMS and M-wave, was quantified from the stimulus artefact to the absolute peak twitch response. Results: Following the warm up protocol, a significant reduction in muscle conduction time was found in both TMS and M-wave of 0.43 ms (P = 0.02) and 0.30 ms (P = 0.001) for the APB; and 0.29 ms (P < 0.001) and 0.87 ms (P = 0.003) for the gastrocnemius, respectively. No change was found in neural conduction using either TMS or M-wave techniques. Conclusions: These findings support previous data which demonstrate an improvement in muscular conduction time and subsequent improvement in athletic performance post warm up. The data also make evident that changes in muscular conduction time are a global response to warm up and are not directly related to muscular activity. In contrast, neural conduction time did not change and should not be confused with changes in muscular conduction time in the literature.

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