Striated muscle overload.

In response to increasing demand, cardiac muscle develops several adaptational mechanisms. Gene expression is modified: the heart hypertrophies and its structure changes in order to improve the efficiency of the contraction. The sarcomere modifications are both species and tissue specific. An isoenzymic shift of myosin from the high ATPase activity form V1 to the slow activity form V3 occurs in all conditions where V1 is initially predominant, i.e. rat (and also rabbit) ventricles and the atria of other species, including humans. The isoenzymic shift was not observed in conditions where V3 is predominant, as in human (and also cat and pig) ventricles. Similar changes are observed in skeletal muscle suggesting that the primary determinant of these modifications is not dependent on the innervation but only on the mechanical activity.