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pubmed:abstractText |
Several proteins of the sarcomere differ from one muscle to the other, but it is also becoming evident that cardiac myosin, tropomyosin and troponin are species specific. Moreover, several properties of cardiac myosin could be modified under the influence of thyroxine, exercise, or overloading. These changes are closely related to the speed of shortening of the muscle and to the degree of stimulation of protein synthesis, but nobody is presently able to say if, in heart overloading, the modifications of myosin are a primary defect which is the origin of the failure or if they are only expressing a better adaptation of myocardial efficiency to the decrease of work.
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