ABSTRACT
During prolonged motor restraint rearrangement of the lipid bilayer of membranes in the aortic ventricle of the heart progresses in parallel to atrophy of its contractile system. This rearrangement is characterised by a decrease in cholesterol and an increase in relative content of unsaturated phospholipids, initially contributing to activation of the lipid-dependent enzymatic systems, and more effective electromechanical conjugation. However, subsequent accumulation of toxic products of lipids peroxidation indicative of disturbed adaptation mechanisms involved in stress-reaction resulted in damage to the myocardial membranes, variations in the bioelectrical properties and deteriorated contractility, and diastolic relaxation of the cardiac muscle. Consequently, heart adaptability to load was reduced in the period of readaptation after hypokinesia. On the background of energy deficiency with subdued synthesis of contractile muscle proteins, levels of cholesterol, triglycerides and especially free fatty acids went up. Along with lipid peroxides these agents disrupt functioning of subcellular organelles and limit adaptation potentials of deconditioned heart.
