Studies on mitochondrial and microsomal phospholipids and phospholipase A2 in heart from rats subjected to prolonged exercise.

Abstract

Alterations in phospholipids and phospholipase A2 activity produced in cardiac mitochondria and microsomes by prolonged exercise and the effect of quinacrine on these changes have been studied in two types of experiment done on rats subjected to prolonged swimming exercise. In Experiment I, rats swam for 0.5, 1.5 or 3 h carrying a weight representing 3% of body weight. At the end of exercise or after varying recovery periods, the hearts were removed, mitochondria and microsomes were isolated and phospholipid constituents, cholesterol and phospholipase A2 (PLA2) determined. The phosphatidylethanolamine (PE) and phosphatidylcholine (PC) levels in mitochondria were progressively reduced by exercise for 0.5, 1.5, and 3 h as compared with control rats (the rats which trained to swim with loading for 4 days and took rest for 1 night). After recovery periods of 6 and 12 h, levels were partially restored, but after 24 and 48 h they decreased slightly below the control values. By 120-240 h, PE and PC levels recovered to slightly higher values than control. In microsomes, PE and PC levels were also decreased at the end of exercise for 0.5, 1.5, or 3 h, but over recovery periods of 6 to 48 h, they gradually increased and stabilized. In Experiment II designed to study the cause of the exercise-induced decrease in PE and PC, intravenous quinacrine was used to inhibit PLA2. PE and PC in exercised rats injected with saline (ES group) were markedly decreased after prolonged exercise when compared with control rats injected with saline (CS group). In exercise rats injected with quinacrine (EQ group), PC was significantly decreased when compared with the CS group while PE was slightly decreased but was not significantly different. Total activity (TA) and specific activity (SA) of PLA2 in mitochondria did not differ significantly in the three groups. In microsomes, TA in the ES group was significantly increased compared with the CS group while that in EQ group was slightly increased but was not significantly different. SA was unchanged in three groups. These results suggest that quinacrine can partially prevent the decrease of phospholipid and partially inhibit the activity of PLA2 after prolonged exercise. RCR in ES group increased significantly after prolonged exercise while RCR in EQ group tended to increase. ADP/O ratio was not significantly different in all groups.