Previous findings have provided strong evidence that myostatin functions as
a negative regulator of muscle mass during development and growth. In the
present study , we test the hypothesis that myostatin may serve a similar f
unction in fully differentiated muscle experiencing modified loading. Our f
indings show that the myostatin expression can be modulated in fully differ
entiated, non-pathologicalskeletal muscle in a manner that is inversely rel
ated to changes in muscle mass. Atrophy of rat hind limb muscles induce by
10 days of unloading resulted in in a 165 decrease in plantaris mass, a 110
% increase in myostatin mRNA, and a 37% increase in myostatin protein. Immu
nohistochemical observations showed that a detectable increase in myostatin
concentration at myotendinous junctions during muscle unloading. The conce
ntration of myostatin mRNA and protein returned to values not significantly
different from ambulatory controls after 4 days of reloading, during which
time plantaris mass also returned to control values. However the results a
lso show that of 30min of daily muscle loading during the unloading period
were sufficient to prevent significant losses of muscle mass caused by musc
le unloading, although muscle mass loos during unloading is accompanied by
increases in myostatin.