Abstract
Food restriction has a great impact on skeletal muscle mass by inducing muscle protein
breakdown to provide substrates for energy production through gluconeogenesis. Genetic
models of hyper-muscularity interfere with the normal balance between protein synthesis
and breakdown which eventually results in extreme muscle growth. Mutations or deletions
in the myostatin gene result in extreme muscle mass. Here we evaluated the impact
of food restriction for a period of 5 weeks on skeletal muscle size (i. e., fibre
cross-sectional area), fibre type composition and contractile properties (i. e., tetanic
and specific force) in myostatin null mice. We found that this hyper-muscular model
was more susceptible to catabolic processes than wild type mice. The mechanism of
skeletal muscle mass loss was examined and our data shows that the myostatin null
mice placed on a low calorie diet maintained the activity of molecules involved in
protein synthesis and did not up-regulate the expression of genes pivotal in ubiquitin-mediated
protein degradation. However, we did find an increase in the expression of genes associated
with autophagy. Surprisingly, the reduction on muscle size was followed by improved
tetanic and specific force in the null mice compared to wild type mice. These data
provide evidence that food restriction may revert the hyper-muscular phenotype of
the myostatin null mouse restoring muscle function.
Key words
myostatin - muscle mass - muscle strength - nutritional intervention
