Mechanical load as stimulus for apoptosis and necrosis could be responsible for the loss of cardiomyocytes. Ventricular myocytes from young (3 months) and old (14-24 months) rats were cyclically stretched (cms; 5% elongation, 1 Hz) for 24 hrs. Spontaneous apoptosis was in myocytes from young rats 0.33±0.12% and from old rats 1.05±0.35% (Tunel assay); associated with a decrease of bcl-2. Cms increased the apoptosis to 0.58±0.18% in myocytes from young rats. Western blots showed that cms reduced bcl-2 and increased p53 (young rats). Bax was not changed by cms. These was confirmed by cytochrome c release (31±13%) and by the enrichment of cytosolic nucleosomes (11±8%). Cms did not influence the apoptosis in myocytes from old rats (Tunel-assay, bcl-2, bax or p53). Cms did not cause necrosis in myocytes from young rats. Cms increased the number of necrotic cells by showing the cell membrane rupture in myocytes from old rats (50±13% HEDAF-positive and 38±6% PI-positive cells) as well as by measuring the LDH release. The results suggest that cms induced apoptosis in myocytes of young rats but necrosis in myocytes from old rats which could be attributed to more stress sensitivity of cells from old rats.