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Efficacité de l’Actovegin chez le sportif?

06/02/2016 | Etudes cardio et Etudes Compléments alimentaires


Actovegin, a non-prohibited drug increases oxidative capacity in human skeletal muscle
European Journal of Sport Science         Published online: 08 Jan 2016       Stine D. Søndergård

Actovegin, a deproteinized haemodialysate of calf blood, is suggested to have ergogenic properties, but this potential effect has never been investigated in human skeletal muscle. To investigate this purported ergogenic effect, we measured the mitochondrial respiratory capacity in permeabilized human skeletal muscle fibres acutely exposed to Actovegin in a low and in a high dose. We found that Actovegin, in the presence of complex I-linked substrates increased the oxidative phosphorylation (OXPHOS) capacity significantly in a concentration-dependent manner (19 ± 3, 31 ± 4 and 45 ± 4 pmol/mg/s). Maximal OXPHOS capacity with complex I and II-linked substrate was increased when the fibres were exposed to the high dose of Actovegin (62 ± 6 and 77 ± 6 pmol/mg/s) (p < .05). The respiratory capacity of the electron transfer system as well as Vmax and Km were also increased in a concentration-dependent manner after Actovegin exposure (70 ± 6, 79 ± 6 and 88 ± 7 pmol/mg/s; 13 ± 2, 25 ± 3 and 37 ± 4 pmol/mg/s; 0.08 ± 0.02, 0.21 ± 0.03 and 0.36 ± 0.03 mM, respectively) (p < .05).

In summary, we report for the first time that Actovegin has a marked effect on mitochondrial oxidative function in human skeletal muscle. Mitochondrial adaptations like this are also seen after a training program in human subjects. Whether this improvement translates into an ergogenic effect in athletes and thus reiterates the need to include Actovegin on the World Anti-Doping Agency’s active list remains to be investigated.

L’acide docosapentaénoïque: le nouvel oméga 3?

05/02/2016 | Etudes Compléments alimentaires et Etudes Perte de poids et Etudes Anti-âge


Short update on docosapentaenoic acid: a bioactive long-chain n-3 fatty acid
Current Opinion in Clinical Nutrition & Metabolic Care: March 2016 - Volume 19 - Issue 2 - p 88–91     Kaur, Gunveen

Purpose of review: Docosapentaenoic acid (DPA) is a long-chain n-3 polyunsaturated fatty acid that is intermediary between eicosapentaenoic acid and docosahexaenoic acid in the n-3 synthesis pathway. DPA is part of our normal diet through fish and lean red meat. In recent years, DPA has received increasing attention as an important bioactive fatty acid in light of its potential beneficial health effects, which include anti-inflammatory actions, antiplatelet aggregation, and improved plasma lipid prolife. This review provides a short summary of the most recent research on DPA.

Recent findings: In this review, we report on the latest association data as well as data generated from in-vitro and in-vivo studies on DPA and cardiovascular health, mental health, inflammation, and cancer. We also report on the newly identified DPA metabolites and their effects on exacerbation of inflammation in animal models.

Summary: Although there is a growing body of evidence supporting DPA’s role as an important bioactive fatty acid, there is a need for more ‘cause and effect studies’, clinical trials and studies which can reveal whether DPA plays separate roles to those identified for eicosapentaenoic acid and docosahexaenoic acid.

Le foie produit de la follistatine

04/02/2016 | Etudes sur les hormones


Circulating Follistatin Is Liver-Derived and Regulated by the Glucagon-to-Insulin Ratio
Jakob S. Hansen         The Journal of Clinical Endocrinology & Metabolism   2016 Volume 101, Issue 2

Follistatin is a plasma protein recently reported to increase under conditions with negative energy balance, such as exercise and fasting in humans. Currently, the perception is that circulating follistatin is a result of para/autocrine actions from various tissues. The large and acute increase in circulating follistatin in response to exercise suggests that it may function as an endocrine signal.

Objective: We assessed origin and regulation of circulating follistatin in humans.

Design/Interventions: First, we assessed arterial-to-venous difference of follistatin over the splanchnic bed at rest and during exercise in healthy humans. To evaluate the regulation of plasma follistatin we manipulated glucagon-to-insulin ratio in humans at rest as well as in cultured hepatocytes. Finally, the impact of follistatin on human islets of Langerhans was assessed.

Results: We demonstrate that in humans the liver is a major contributor to circulating follistatin both at rest and during exercise. Glucagon increases and insulin inhibits follistatin secretion both in vivo and in vitro, mediated via the secondary messenger cAMP in the hepatocyte. Short-term follistatin treatment reduced glucagon secretion from islets of Langerhans, whereas long-term follistatin treatment prevented apoptosis and induced proliferation of rat β cells.

Conclusions: In conclusion, in humans, the liver secretes follistatin at rest and during exercise, and the glucagon-to-insulin ratio is a key determinant of circulating follistatin levels. Circulating follistatin may be a marker of the glucagon-to-insulin tone on the liver.

Les galactosyl Oligosaccharides: le prochain supplément anti-inflammatoire?

04/02/2016 | Etudes Compléments alimentaires et Etudes Anti-âge


Human Milk Oligosaccharides and Synthetic Galactosyloligosaccharides Contain 3’-, 4-, and 6’-Galactosyllactose and Attenuate Inflammation in Human T84, NCM-460, and H4 Cells and Intestinal Tissue Ex Vivo.
Newburg DS           J Nutr. 2016 Feb;146(2):358-67.

The immature intestinal mucosa responds excessively to inflammatory insult, but human milk protects infants from intestinal inflammation. The ability of galactosyllactoses [galactosyloligosaccharides (GOS)], newly found in human milk oligosaccharides (HMOS), to suppress inflammation was not known.

OBJECTIVE: The objective was to test whether GOS can directly attenuate inflammation and to explore the components of immune signaling modulated by GOS.
METHODS: Galactosyllactose composition was measured in sequential human milk samples from days 1 through 21 of lactation and in random colostrum samples from 38 mothers. Immature [human normal fetal intestinal epithelial cell (H4)] and mature [human metastatic colonic epithelial cell (T84) and human normal colon mucosal epithelial cell (NCM-460)] enterocyte cell lines were treated with the pro-inflammatory molecules tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β) or infected with Salmonella or Listeria. The inflammatory response was measured as induction of IL-8, monocyte chemoattractant protein 1 (MCP-1), or macrophage inflammatory protein-3α (MIP-3α) protein by ELISA and mRNA by quantitative reverse transcriptase-polymerase chain reaction. The ability of HMOS or synthetic GOS to attenuate this inflammation was tested in vitro and in immature human intestinal tissue ex vivo.

RESULTS: The 3 galactosyllactoses (3’-GL, 4-GL, and 6’-GL) expressed in colostrum rapidly declined over early lactation (P < 0.05). In H4 cells, HMOS attenuated TNF-α- and IL-1β-induced expression of IL-8, MIP-3α, and MCP-1 to 48-51% and pathogen-induced IL-8 and MCP-1 to 26-30% of positive controls (P < 0.001). GOS reduced TNF-α- and IL-1β-induced inflammatory responses to 25-26% and pathogen-induced IL-8 and MCP-1 to 36-39% of positive controls (P < 0.001). GOS and HMOS mitigated nuclear translocation of nuclear transcription factor κB (NF-κB) p65. HMOS quenched the inflammatory response to Salmonella infection by immature human intestinal tissue ex vivo to 26% and by GOS to 50% of infected controls (P < 0.01).

CONCLUSION: Galactosyllactose attenuated NF-κB inflammatory signaling in human intestinal epithelial cells and in human immature intestine. Thus, galactosyllactoses are strong physiologic anti-inflammatory agents in human colostrum and early milk, contributing to innate immune modulation. The potential clinical utility of galactosyllactose warrants investigation.

Peut-on prévenir les blessure d’usure grâce au rythme cardiaque?

29/01/2016 | Echauffement et blessures


Musculoskeletal overuse injuries and heart rate variability: Is there a link?
Medical Hypotheses Volume 87, February 2016, Pages 1–7           Angela Spontelli Gisselman

Accurate detection and prevention of overuse musculoskeletal injuries is limited by the nature of somatic tissue injury. In the pathogenesis of overuse injuries, it is well recognized that an abnormal inflammatory response occurs within somatic tissue before pain is perceived which can disrupt the normal remodeling process and lead to subsequent degeneration. Current overuse injury prevention methods focused on biomechanical faults or performance standards lack the sensitivity needed to identify the status of tissue injury or repair.

Recent evidence has revealed an apparent increase in the prevalence and impact of overuse musculoskeletal injuries in athletics. When compared to acute injuries, overuse injuries have a potentially greater negative impact on athletes’ overall health burden. Further, return to sport rehabilitation following overuse injury is complicated by the fact that the absence of pain does not equate to complete physiological healing of the injured tissue. Together, this highlights the need for exercise monitoring and injury prevention methods which incorporate assessment of somatic tissue response to loading.

One system primarily involved in the activation of pathways and neuromediators responsible for somatic tissue repair is the autonomic nervous system (ANS). Although not completely understood, emerging research supports the critical importance of peripheral ANS activity in the health and repair of somatic tissue injury. Due to its significant contributions to cardiac function, ANS activity can be measured indirectly with heart rate monitoring. Heart rate variability (HRV) is one index of ANS activity that has been used to investigate the relationship between athletes’ physiological response to accumulating training load.

Research findings indicated that HRV may provide a reflection of ANS homeostasis, or the body’s stress-recovery status. This noninvasive marker of the body’s primary driver of recovery has the potential to incorporate important and as yet unmonitored physiological mechanisms involved in overuse injury development.

We hypothesize that abnormal somatic tissue response to accumulating microtrauma may modulate ANS activity at the level of HRV. Exploring the link between HRV modulation and somatic tissue injury has the potential to reveal the putative role of ANS homeostasis on overuse musculoskeletal injury development.

Connectivité intermusculaire

19/01/2016 | Echauffement et blessures et Etudes Musculation


Altered mechanical interaction between rat plantar flexors due to changes in intermuscular connectivity
M. Bernabei               Scandinavian Journal of Medicine & Science in Sports   2016   Early View (Online Version of Record published before inclusion in an issue)

Connective tissue formation following muscle injury and remedial surgery may involve changes in the stiffness and configuration of the connective tissues linking adjacent muscles. We investigated changes in mechanical interaction of muscles by implanting either a tissue-integrating mesh (n = 8) or an adhesion barrier (n = 8) to respectively increase or decrease the intermuscular connectivity between soleus muscle (SO) and the lateral gastrocnemius and plantaris complex (LG+PL) of the rat. As a measure of mechanical interaction, changes in SO tendon forces and proximal–distal LG+PL force differences in response to lengthening LG+PL proximally were assessed 1 and 2 weeks post-surgery. The extent of mechanical interaction was doubled 1 week post-implantation of the tissue-integrating mesh compared to an unaffected compartment (n = 8), and was more than four times higher 2 weeks post-surgery. This was found only for maximally activated muscles, but not when passive. Implanting the adhesion barrier did not result in a reduction of the mechanical interaction between these muscles.

Our findings indicate that the ratio of force transmitted via myofascial, rather than myotendinous pathways, can increase substantially when the connectivity between muscles is enhanced. This improves our understanding of the consequences of connective tissue formation at the muscle boundary on skeletal muscle function.

Remodelage nerveux après le sport

19/01/2016 | Etudes cardio


Ultrasound visualization of nerve remodeling after strenuous exercise
Antonios Kerasnoudis     Muscle & Nerve Volume 53, Issue 2,  pages 320–324, February 2016

The aim of this case study is to describe the use of nerve ultrasound to visualize the morphological changes that occur during conduction velocity alterations after strenuous exercise.
Methods: A 32-year-old, healthy runner underwent clinical, electrophysiological, and ultrasound evaluation 24 hours before, 30 minutes after, and 24 hours after a marathon.

Results: An increase in motor conduction velocity of the median, ulnar, radial, and tibial nerves and sensory conduction velocity of the median and ulnar nerves was found between pre- and post-marathon studies.

An increase in the cross-sectional area of the median (carpal tunnel), ulnar (Guyon canal and elbow), fibular (fibular head), and tibial (ankle) nerves was documented. No changes in the MRC sum scale score of the various peripheral nerves were detected. Conclusion: The case described shows the morphological changes that occur in healthy peripheral nerves during conduction velocity alterations.

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