Impact of Exercise Training and Detraining on Some Hemodynamics and Inflammatory Mediators in Hypertensive Rats

Abstract
Background: Physical exercise is suggested as a life style modification to improve hypertension.
Aim of Study: The aim of the present study was to prove that exercise training ameliorates the pathophysiology in hypertensive rats, and to investigate whether this effect is reversible after detraining.
Patients and Methods: Forty-eight adult male albino rats of local strain were used. Rats were equally divided into two main groups, normotensive and hypertensive groups. Each main group was equally divided into sedentary, exercise-trained and detrained groups (n=8 for each group). Hyperten-sion was induced by subcutaneous injection of deoxy corti-costerone acetate (DOCA) in a dose of 50 mg/kg body weight suspended in 0.3ml olive oil, once weekly for 4 weeks and drinking water with 1% NaCl. Rats in exercise-trained groups practiced moderate intensity treadmill exercise for 6 weeks. Rats in detrained groups practiced moderate intensity exercise for 4 weeks and remained sedentary for 2 weeks. After 6 weeks, blood samples were collected for measuring serum levels of tumor necrosis factor-alpha (TNF-a), interleukin-10 (IL-10), malondialdehyde (MDA) and total antioxidant capacity (TAC). Then, systolic and diastolic arterial blood pressures were measured by invasive technique and mean arterial blood pressure (MAP) was calculated. Lastly, rats were sacrificed and heart was excised for assessing myocardial contractility (MC) and heart rate (HR) by Langendorff isolated perfused heart.
Results: Exercise training for six weeks resulted in reduc-tion of MAP and HR and improvement of MC and all the measured biochemical parameters in hypertensive rats com-pared to sedentary hypertensive ones. This improvement of hypertension and cardiac performance by exercise training for six weeks is possibly by restoring the balance between pro- and anti-inflammatory cytokines, and attenuating oxidative stress. Training of hypertensive rats for four weeks and detraining for two weeks preserved the beneficial effects of exercise on MAP, TNF-a , MDA and TAC, but the improvement was reversed in HR and IL-10.
Conclusion: Exercise detraining for two weeks did not completely lose the benefit of exercise in controlling hyper-tension in rats.