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Authors AX Bigard
Title   Muscles responses to exercice and recovery
Full source     Science & Sports, 2004, Vol 19, Iss 5, pp 246-263

Objectives. - The aim of this symposium entitled ''Muscle plasticity and 
regeneration'' was devoted to put in touch several international scientists on 
issues that concern skeletal and cardiac muscle, their adaptive responses to 
physical training, and characteristics of their recovery. Topics. - Professor 
James Skinner is involved in an extensive study whose objective is to examine 
the role played by the genetic basis of responses to physical training and of 
concomitant changes in risk factors for cardiovascular and metabolic diseases 
(HERITAGE study). During this study, he showed that expected changes in the 
maximal oxygen uptake (a marker of the positive responses to training) depended 
neither on gender, race, age, nor on initial physical fitness. Therefore, all 
these results clearly suggest that the ''high-responder to training'' phenotype 
vary according to the interaction between many genes and between these genes 
and environment. The gene encoding for the angiotensin converting enzyme was 
one of the potential genes able to account for the high, early and complete 
response to physical training. Results of the Heritage Family Study were not in 
accordance with this hypothesis and nothing clearly suggests that the I variant 
of the human ACE gene was involved in the extent of adaptive responses to 
repeated exercise. Many studies have been published during these last years, 
with the purpose to examine the molecular mechanisms that explain, at least 
partly, the adaptive muscles responses to physical training. Marked and 
significant advances have been done to explain the molecular and cellular 
events involved in the training-induced increase in mitochondrial density 
within skeletal muscle; alteration in the balance of the intracellular energy 
status is one of the major events involved in the AMP-activated protein kinase 
(AMPkinase activation). AMPkinase activation increases the expression of a 
transcription factor (PGC-1alpha PPAR-gamma coactivator-1alpha) that 
coordinately controls the expression of both nuclear and mitochondrial genomes. 
Endurance training also induces an increase in the muscle capillary bed. This 
increase is mainly related to an enhanced vascular endothelial growth factor 
expression (VEGF). Exercise-induced intracellular hypoxia is one major event of 
VEGF gene expression during exercise. The effects of strength training on 
skeletal muscle result mainly on changes in muscle mass. Considerable advances 
have been done to understand the molecular mechanisms and interaction involved 
in the signalling pathways activated by insulin-like growth factor-1 (IGF-1). 
On the other hand, inhibition of the ubiquitin-proteasome pathway could be 
important to increase muscle size during strength training; a particular 
attention has been paid on the activation of two enzymes, namely muscle ring 
finger 1 (Murf 1) and muscle atrophy F-box, on Atrogin-1 (MAFbx) which are 
required for ubiquitin-ligase activity. Interleukin-6 (IL-6) plays a special 
and specific physiological-role on the


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