LIPID-PEROXIDATION CAPACITIES IN THE MYOCARDIUM OF ENDURANCE-TRAINED RATS AND MICE INVITRO

The endurance-training programme in Experiment 1 (Exp. 1) consisted of a total swimming time of 149 159 h per male Han Wistar rat and in Experiment 2 (Exp. 2) the male NMRI-mice run on a treadmill at a speed of 25 in min-1 1 h per day, 5 days a week for 3 weeks. One group of the rat hearts was perfused with 0.3 mm cumene hydroperoxide (CumOOH) while the others were fractioned (mitochondria, sarcolemma and sarcoplasmic reticulum) and these cell fractions and homogenates were used to determine the total concentration of peroxidative lipids and the susceptibility to lipid peroxidation. The perfusion with CumOOH caused the release of thiobarbituric acid reactive substances (TBARS) into the perfusate. The release of TBARS from the trained hearts was smaller than that of the control hearts (P < 0.01). The concentration of TBARS was also smaller in the myocardium of the right ventricle of the trained rats (P < 0.01). The concentration of reduced GSH remained at a higher level after the CumOOH perfusion suggesting a better redox state in the hearts of trained animals. The concentration of the lipids susceptible to lipid peroxidation was lower in the homogenates of the trained rat hearts (P < 0.05). However, this decrease could not be explained by any of the tissue fractions used when studied in rat hearts. In Exp. 2 the total concentration of lipids susceptible to peroxidation remained unchanged in the mice hearts. However, endurance training by running decreased (P < 0.01) the lipid peroxidation rate in mouse hearts and also decreased (P < 0.05) the sensitivity of myocardium to in vitro stimulated lipid peroxidation. The results suggest that endurance training by swimming or by running reduces the susceptibility of myocardium of rats and mice to chemically induced lipid peroxidation injuries in vitro.