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Decreased level of cardiac antioxidants in endurance-trained rats
M Kihlström1, J Ojala, A Salminen
1Department of Cell Biology, University of Jyväskylä, Finland.
Insights
Endurance swimming training in rats significantly reduced cardiac antioxidants, including catalase and vitamin E. This decrease in antioxidant levels may result from increased oxygen metabolism and free radical formation during prolonged exercise.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
- Exercise Science
Background:
- Endurance training impacts cardiac function and metabolism.
- Cardiac antioxidant systems are crucial for protecting against oxidative stress.
- The effects of prolonged swimming on cardiac antioxidants are not fully understood.
Purpose of the Study:
- To investigate the effects of a 194-200 hour swimming protocol on cardiac antioxidant levels in Han-Wistar rats.
- To examine regional differences in antioxidant activity within the rat myocardium following endurance training.
Main Methods:
- Han-Wistar rats underwent a prolonged swimming protocol (194-200 hours).
- Cardiac weight was measured.
- Activities of various antioxidant enzymes (catalase, Cu,Zn-superoxide dismutase, thioredoxin reductase, glutathione reductase, glucose-6-phosphate dehydrogenase, glutathione peroxidase) and concentrations of antioxidants (vitamin E, carnosine, anserine, sulphydryl groups) were assayed in the right and left ventricles (subendocardium and subepicardium).
Main Results:
- Endurance training increased cardiac weight.
- Activities of catalase, Cu,Zn-superoxide dismutase, thioredoxin reductase, and glutathione reductase decreased in specific cardiac regions.
- Vitamin E concentration decreased in the right ventricle and subendocardium.
- Glucose-6-phosphate dehydrogenase activity increased in the right ventricle and subepicardium.
- Glutathione peroxidase activity and levels of carnosine, anserine, and sulphydryl groups remained unchanged.
- Key findings included the equalization of catalase activity between ventricles and increased glucose-6-phosphate dehydrogenase activity in the right ventricle compared to the left.
Conclusions:
- Prolonged endurance swimming training leads to a decrease in cardiac antioxidant levels in rats.
- This reduction in antioxidants may be attributed to increased oxygen metabolism and subsequent free radical production.
- Endurance exercise alters the antioxidant profile of the heart, potentially impacting its susceptibility to oxidative damage.
Abstract:
Han-Wistar rats were exposed to a 194-200 h swimming protocol which caused a significant increase in the cardiac weight. The levels of various tissue antioxidants were assayed from the myocardium of the right ventricle and from the left ventricle (subendo- and subepimyocardium). This endurance training decreased the activities of catalase in the right ventricle and in the subendo- and subepimyocardium and Cu,Zn-superoxide dismutase in the subendomyocardium as well as the concentration of vitamin E in the right ventricle and in the subendomyocardium. Also, the activity of thioredoxin reductase decreased in each part of myocardium and that of glutathione reductase in the right ventricle and in the subepimyocardium. The activity of glucose-6-phosphate dehydrogenase increased in the right ventricle and in the subepimyocardium. The activity of glutathione peroxidase and the total tissue contents of carnosine and anserine and tissue sulphydryl groups remained unchanged as compared to the control group. The endurance training caused only minor changes in the regional distribution of antioxidants. The major findings were the disappearance of the difference in the activity of catalase between the right and the left ventricle and the increase in the activity of glucose-6-phosphate dehydrogenase as compared to that of the left ventricle. The results show that endurance training by swimming decreases the level of cardiac antioxidants. This decrease may be due to the increased oxygen metabolism and the subsequent increase in the formation of oxygen free radicals, which could deplete the antioxidant pool.