OXIDATIVE STRESS-INDUCED APOPTOSIS IN RAT SKELETAL MUSCLES DURING A SINGLE RUNNING EXERCISE UP TO EXHAUSTION

The aim of this study was to investigate whether the oxidative stress may he the reason or apoptosis in skeletal muscles in rats. Rats were divided into two groups controls and exposed to physical exercise. Rats were running on the treadmill at the speed of 1 km/h until exhaustion. After the exercise, the concentration of lipid peroxidation markers - malonylodialdehyde and 4-hydroxyalkenes (MDA+4-HDA), and the level of reduced glutathione (GSH) was determined in the homogenates of the extensor digitorum longus (EDL) muscle and slow-twitch (ST) fibres in 2, 6, and 96 h of restitution. Aconitase activity as a marker of oxidative protein modification was determined in ST fibres and EDL muscle. Additionally, apoptosis was detected by the TUNEL technique. A significant increase in MDA+4HDA concentrations in comparison to the control group was noticed in both ST fibres and EDL muscle alter 6 h. GSH concentration in 2 and 6 h after exercise was significantly decreased in ST fibres and in EDL muscle in all measurements, when compared to the control group, Aconitase activity in ST fibres and EDL muscle was also significantly decreased 2 h after the exercise when compared to the control group, but increased in 6 h of restitution. Apoptotically-changed nuclei were observed only in EDL fibres. On the basis of the results and the suggested mechanism, it can be thought that the oxidative stress triggers apoptosis in ST fibres and in EDL muscle after exercise and it starts in the mitochondria.