Etudes cardio

Une supplémentation en corps cétoniques booste la récupération énergétique

17/08/2017 | Etudes cardio et Etudes Compléments alimentaires et Etudes Perte de poids

 

A Ketone Ester Drink Increases Postexercise Muscle Glycogen Synthesis in Humans
HOLDSWORTH, DAVID A         Medicine & Science in Sports & Exercise: September 2017 - Volume 49 - Issue 9 - p 1789–1795

Introduction: Physical endurance can be limited by muscle glycogen stores, in that glycogen depletion markedly reduces external work. During carbohydrate restriction, the liver synthesizes the ketone bodies, D-β-hydroxybutyrate, and acetoacetate from fatty acids. In animals and in the presence of glucose, D-β-hydroxybutyrate promotes insulin secretion and increases glycogen synthesis. Here we determined whether a dietary ketone ester, combined with plentiful glucose, can increase postexercise glycogen synthesis in human skeletal muscle.

Methods: After an interval-based glycogen depletion exercise protocol, 12 well-trained male athletes completed a randomized, three-arm, blinded crossover recovery study that consisted of consumption of either a taste-matched, zero-calorie control or a ketone monoester drink, followed by a 10-mM glucose clamp or saline infusion for 2 h. The three postexercise conditions were control drink then saline infusion, control drink then hyperglycemic clamp, or ketone ester drink then hyperglycemic clamp. Skeletal muscle glycogen content was determined in muscle biopsies of vastus lateralis taken before and after the 2-h clamps.

Results: The ketone ester drink increased blood D-β-hydroxybutyrate concentrations to a maximum of 5.3 versus 0.7 mM for the control drink (P < 0.0001). During the 2-h glucose clamps, insulin levels were twofold higher (31 vs 16 mU·L−1, P < 0.01) and glucose uptake 32% faster (1.66 vs 1.26 g·kg−1, P < 0.001). The ketone drink increased by 61 g, the total glucose infused for 2 h, from 197 to 258 g, and muscle glycogen was 50% higher (246 vs 164 mmol glycosyl units per kilogram dry weight, P < 0.05) than after the control drink.

Conclusion: In the presence of constant high glucose concentrations, a ketone ester drink increased endogenous insulin levels, glucose uptake, and muscle glycogen synthesis.

Rôle de l’entraînement sur la densité mitochondriale

09/06/2017 | Etudes cardio et Etudes Perte de poids

 

Exercise training increases skeletal muscle mitochondrial volume density by enlargement of existing mitochondria and not de novo biogenesis
Anne-Kristine Meinild Lundby       Acta physiol 2017

Aims

1) determine whether exercise induced increases in muscle mitochondrial volume density (MitoVD) is related to enlargement of existing mitochondria or de novo biogenesis, 2) establish if measures of mitochondrial-specific enzymatic activities are valid biomarkers for exercise induced increases in MitoVD.
Method

Skeletal muscle samples were collected from twenty-one healthy males prior to and following 6 weeks of endurance training. Transmission electron microscopy was used for estimation of mitochondrial densities and profiles. Biochemical assays, western blotting and high resolution respirometry were applied to detect changes in specific mitochondrial functions.
Result

MitoVD increased with 55 ± 9% (P

< 0.001), whereas the number of mitochondrial profiles per area of skeletal muscle remained unchanged following training

. Citrate synthase activity (CS) increased (44 ± 12%, P < 0.001) however, there were no functional changes in oxidative phosphorylation capacity (OXPHOS, CI+IIP) or cytochrome c oxidase (COX) activity. Correlations were found between MitoVD and CS (P=0.01; r=0.58), OXPHOS, CI+CIIP (P=0.01; R=0.58) and COX (P=0.02; R=0.52) before training, after training a correlation was found between MitoVD and CS activity only (P=0.04; R=0.49). Intrinsic respiratory capacities decreased (P < 0.05) with training when respiration was normalized to MitoVD. This was not the case when normalized to CS activity although the percentage change was comparable.
Conclusions

MitoVD was increased by inducing mitochondrial enlargement rather than de novo biogenesis. CS activity may be appropriate to track training induced changes in MitoVD.

Rôles des peptides mitochondriaux dans la perte de graisse

09/06/2017 | Etudes cardio et Etudes Perte de poids

 

Mitochondrial derived peptides as novel regulators of metabolism
Su-Jeong Kim             J Physiol 2017
         
Mitochondrial derived peptides represent a new class of circulating signalling molecules. Humanin, the first member of this class, has been shown to have several metabolic effects such as reducing weight gain and visceral fat and increasing glucose stimulated insulin release. The discovery of several other new members such as MOTS-c and SHLP1-6, have further added to this group. These new peptides have also been found to affect metabolism with MOTS-c potently decreasing weight gain in mice on a high fat diet. In this review, we will cover the basic biology of this class of peptides and discuss the relevance to organismal metabolism.

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.

L’ibuprofène contre la fatigue?

28/09/2016 | Etudes cardio et Etudes sur les hormones et Echauffement et blessures

 

Ibuprofen intake increases exercise time to exhaustion: A possible role for preventing exercise-induced fatigue
F. D. Lima     Scandinavian Journal of Medicine & Science in Sports   volume 26, Issue 10 October 2016
Pages 1160–1170

Although the intake of nonsteroidal anti-inflammatory drugs (NSAIDs) intake by athletes prevents soreness, little is known concerning their role in exercise performance. This study assessed the effects of ibuprofen intake on an exhaustive protocol test after 6 weeks of swimming training in rats. Animals were divided into sedentary and training groups. After training, animals were subdivided into two subsets: saline or ibuprofen. Afterwards, three repeated swimming bouts were performed by the groups. Ibuprofen (15 mg/kg) was administered once a day. Pain measurements were performed and inflammatory and oxidative stress parameters were assayed in cerebral cortex and gastrocnemius muscle. Training, ibuprofen administration, or both combined (P 

< 0.05; 211 ± 18s, 200 ± 31s, and 279 ± 23s) increased exercise time to exhaustion.

Training decreased the acetylcholinesterase (AChE) activity (P 

< 0.05; 149 ± 11) in cerebral cortex.

Ibuprofen intake decreased the AChE activity after exhaustive protocol test in trained and sedentary rats (P < 0.05; 270 ± 60; 171 ± 38; and 273 ± 29). It also prevented neuronal tumor necrosis factor-α (TNF-α) and interleukin (IL 1β) increase. Fatigue elicited by this exhaustive protocol may involve disturbances of the central nervous system. Additive anti-inflammatory effects of exercise and ibuprofen intake support the hypothesis that this combination may constitute a more effective approach. In addition, ergogenic aids may be a useful means to prevent exercise-induced fatigue.

Trop de leucine: néfaste pour le cœur des sportifs?

04/07/2016 | Etudes cardio et Echauffement et blessures et Etudes Compléments alimentaires et Etudes Anti-âge

 

Long-term leucine supplementation aggravates prolonged strenuous exercise-induced cardiovascular changes in trained rats
Gustavo Barbosa dos Santos 14 June 2016       Exp Physiol 2016 Volume 101, Issue 7 1 July   Pages 811–820

New Findings    

What is the central question of this study?

Can long-term leucine supplementation prevent prolonged strenuous endurance exercise induced cardiac injury?

What is the main finding and its importance?

Prolonged endurance exercise does not seem to exceed cardiac energetic capacity, hence it does not represent an energy threat to this organ, at least in trained subjects. However, it may induce, in susceptible individuals, a state of cardiac electrical instability, which has been associated with ventricular arrhythmias and sudden cardiac death. This situation might be worsened when combined with leucine supplementation, which leads to increased blood pressure and cardiac injury. Leucine supplementation failed to prevent cardiac fatigue symptoms and may aggravate prolonged strenuous exercise-induced cardiovascular disturbances in trained rats.

Observational studies have raised concerns that prolonged strenuous exercise training may be associated with increased risk of cardiac arrhythmia and even primary cardiac arrest or sudden death. It has been demonstrated that leucine can reduce prolonged exercise-induced muscle damage and accelerate the recovery process. The aim of this study was to investigate the effects of prolonged strenuous endurance exercise on cardiovascular parameters and biomarkers of cardiac injury in trained adult male rats and assess the use of leucine as an auxiliary substance to prevent the likely cardiac adverse effects caused by strenuous exercise. Twenty-four male Wistar rats were randomly allocated to receive a balanced control diet (18% protein) or a leucine-rich diet (15% protein plus 3% leucine) for 6 weeks. The rats were submitted to 1 h of exercise, 5 days per week for 6 weeks. Three days after the training period, the rats were submitted to swimming exercise until exhaustion, and cardiac parameters were assessed. Exercising until exhaustion significantly increased cardiac biomarker levels, cytokines and glycogen content inhibited protein synthesis signalling and led to cardiac electrical disturbances. When combined with exercise, leucine supplementation led to greater increases in the aforementioned parameters and also a significant increase in blood pressure and protein degradation signalling. We report, for the first time, that leucine supplementation not only fails to prevent cardiac fatigue symptoms, but may also aggravate prolonged strenuous exercise-induced cardiovascular disturbances in trained rats. Furthermore, we find that exercising until exhaustion can cause cardiac electrical disturbances and damage cardiac myocytes.

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.

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