Abstract

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-1α PPAR-γ coactivator-1α) 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 (Murf1) and muscle atrophy F-box, ou Atrogin-1 (MAFbx) which are required for ubiquitin–ligase activity. Interleukin-6 (IL-6) plays a special and specific physiological-role on the training-induced muscle responses. Prolonged exercise is associated with an increase in plasma IL-6, which results from an enhanced production by skeletal muscle. Production of IL-6 in contracting skeletal muscles can account for the exercise-induced increase in plasma IL-6. An inverse relationship was shown between muscle cytokine production and muscle glycogen availability; muscle-derived IL-6 is released into the circulation during exercise and is likely to exert an effect on the liver and adipose tissue, thereby contributing to the maintenance of glucose homeostasis during exercise and mediating exercise-induced lipolysis. These results indicate that IL-6 may represent an important link between contracting skeletal muscles and exercise-related metabolic changes, and should be viewed as an important biochemical factor to account for the exercise-related metabolic and immune changes, and recovery. Future prospects. – Taken together, these results clearly have a major impact in exercise physiology and muscle biology. They contribute to improve our knowledge on the acute and adaptive muscle responses to changes in workload, and on muscle recovery. Moreover, these researches have a potential impact in the medium term to develop pharmacological treatments and strategies devoted to avoid muscle inactivity.

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