A M Breger | PubMed Health

PubMed1977

[Mathematical model of transient long-term adaptation processes of the heart].

A mathematical model of the heart's long-term adaptation to changing load is described. The model is based on the long-term adaptation concept which assumes the phosphorylation potential changing in the heart muscle cells with the load to control the genetic apparatus activity and thus determine structural alterations ensuring adaptation. The computerized model reproduces the transient process in four major types of the heart's long-term adaptation, i.e. in a compensatory hypertrophy development and hypertrophy regression, as well as in the training and detraining states formation. The simulation results are in agreement with the available data and predict the phenomena that are not as yet substantiated by experiments.

Adaptation, Physiological↗

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The common mechanism of the heart's adaptation and deadaptation: hypertrophy and atrophy of the heart muscle.

The short-term adaptation of the heart cells to changing demands is controlled by the phosphorylation potential. By influencing protein synthesis, the same parameter also determines the long-term adaptation. Alterations in protein synthesis are not only of great significance for heart weight, but result in altered structural and enzymatic properties of cardiac cells which are decisive for mechanical performance. These alterations of myocardial tissue depend on the turnover rate of individual proteins. In the stage of adaptation, the proportion of short-living proteins increases whereas it decreases in the overadapted or deadapted (atrophic) organ. Thus, the variations in the ratio of cell structures in heart adaptation, overadaptation, and deadaptation can be explained by the quantitative difference in the control characteristics of transcriptiones encoding of short-living and long-living proteins.

Adaptation, Physiological↗