Topic 2. Nutrition and control of muscle mass under situation of metabolic challenge

Fiche du document

Date

11 janvier 2019

Discipline
Périmètre
Langue
Identifiants
Collection

OpenEdition Books

Organisation

OpenEdition

Licences

https://www.openedition.org/12554 , info:eu-repo/semantics/openAccess




Citer ce document

Xavier Bigard et al., « Topic 2. Nutrition and control of muscle mass under situation of metabolic challenge », INSEP-Éditions, ID : 10.4000/books.insep.1874


Métriques


Partage / Export

Résumé 0

The control of muscle mass results from the balance between the levels of contractile protein synthesis and breakdown. Physical exercise and nutrition both influence muscle mass through modifications of the net balance between protein synthesis and protein degradation rates.Several studies showed that the muscle protein acute synthesis was firstly regulated through the translation initiation of messenger RNA (mRNA) by activation of a variety of intracellular signalling proteins, especially those involved within the signalling cascade of the mammalian target of rapamycin (mTOR). In humans, the stimulation of muscle protein synthesis after a meal or physical exercise is accompanied by increased activity of the mTOR signalling pathway, after phosphorylation of 70 kDa ribosomal protein S6 kinase (p70S6K or S6K1) and its target, the S6 ribosomal protein (rpS6). There are now a lot of scientific evidences that demonstrate the major role played by the mTORC1 complex in the regulation of muscle mass in response to a large variety of stimulus, including nutrients, growth factors and insulin.More recently, the major impact of the 5’AMP-activated protein kinase (AMPK), an intracellular energy sensor, on the control of muscle cells’size has been updated. AMPK, that plays a key role on the control of the cell energy homeostasis is activated during physical exercise in skeletal muscles. This AMPK activation is vital for restoring intracellular energy balance via inhibition of energy-consuming biosynthetic processes and concomitant activation of pathways that increase ATP production. AMPK activation reduces protein synthesis by 45% in homogenates of muscles, and decreases the activation of both mTOR and rpS6 kinases. Decreased protein synthesis as a result of mTORC1 signaling inhibition could explain a number of muscle adaptations specific to the physical training, including the fact that in general, training in endurance is not associated to increased muscle mass. Many other targets downstream from mTOR could also play a major role in skeletal muscle physiology, such as the FoxO (Forkhead box O) family of transcription factors which stimulate muscle proteins breakdown through upregulation of atrogenes.Prolonged, high-intensity sport events, such as ironman Triathlons, raids or ultra-endurance races, are always performed in negative energy balance. This type of metabolic stress leads to AMPK activation and makes energy intake of particular importance during the event. The role played by nutrition to prevent the effects of prolonged high-intensity exercise on negative energy balance, and then muscle atrophy, has to be considered in order to reach two main objectives. First, to prevent glycogen depletion and provide enough carbohydrate to working skeletal muscles during the race (and then minimize AMPK activation), second to favor the muscle protein status recovery early after the end of exhaustive exercise.

document thumbnail

Par les mêmes auteurs

Sur les mêmes sujets

Sur les mêmes disciplines

Exporter en