EUROMEDICA  Hanover 3-4  Juni 2010	Advanced methods of diagnosis, treatment and prophylactics
	European Academy of Natural Sciences, Hanover European Scientific Society, Hanover Berliner Medizinischen Gesellschaft, Berlin

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Aim of the study. The estimation of ultrastructural response and energy metabolism (NAD⁺ depending and electron transport systems) under chronic exercise in different age groups of albino rats: 1) 22-50 days old, 2) 5-10 month old, 3)11-18 month old, 4) 24-30 month old were into control and exercise groups until exhaustions (5 hours swimming per day during 14 days).

Cardiomyocites from left ventricule were collected both sedentary and post-severe exercise conditions. Simples for electron microscopical histostereometrical and biochemical analysis were carried out using a statistical analysis for revealed most informative morphological sings of exhaustions.

Among the morphological phenomena most common were destructive changes in cardiomyocytes mitochondria, appearance of mitochondria with the several additional compartment and different electrondensity matrix, also unusual atypical mitochondria wich corresponds criteria of chronic exhaustion in young animals .

Inhibition of NAD depending reactions, NAD/NAD⁺ 0,19 B and low level of oxidative phosphorilation have seen as results of physical load.

In the old-aged animals the decrease of the myofibrillar and vascular components volume and the diminish of the correlation between myofibrils and mitochondria were revealed, which caused the defective contractive function on cardiomyocytes. Apoptotic degeneration of myocytes was seen in old-animal cardiomyocytes, induced its metabolic changes and ischemization wich latter manifested with angio- and cardiosclerosis. Quantitative evalution of the density of the capillaries and their diameters in on young animals myocardium was made.

We also observed that exercise in young animals were ineffective and may serve a cause of exhaution and sudden deth. The development of mega-mitochondria having different morphology is demonstrated. Exercise alterations of myofibrils, dysrupture of intercalated disks with detectable decrease of reduction potential (' g⁰) are seen.

As a result we conclude that longterm exersice in young and old animals are not adequated and provoqe myocardial dysfunction. The estimate of the quantitative and qualitative data of the ultrastructure shows that under the chronic load by swimming in old aged animals group may provoqes the disturbance of the compensative processes.