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1.
Can J Physiol Pharmacol ; 99(7): 752-759, 2021 Jul.
Article in English | MEDLINE | ID: mdl-33201749

ABSTRACT

Exhaustive exercise can cause subclinical inflammation to the heart, as it is an oxidative tissue that works continuously. The effect of exhaustive exercise on left and right ventricles (LVs, RVs) may be different. It is claimed that paraoxonase-1 (PON1), an antioxidant enzyme, has a cardioprotective effect on oxidative stress. Rats were separated as non-exercised controls (Con), those euthanized immediately after (E-0) and 24 h after exhaustive exercise (E-24). Cardiac troponin-I (cTnI), total antioxidant status (TAS), total oxidant status (TOS), PON1 activities, and histological findings in LV and RV of the exhausted rats were evaluated. TAS and PON1 levels were lower in LVs compared with RVs of all groups. TOS levels were high in LVs compared with RVs of all groups. In LVs, TAS levels decreased significantly in the E-0 group while PON1 activity decreased in E-0 and E-24 groups compared with controls. In LVs, TOS levels decreased significantly in E-0 and E-24 groups, but in RVs a decrease was seen only in the E-0 group. cTnI levels increased significantly in the E-0 group and decreased to control levels in the E-24 group. Considering the histological and biochemical findings, exhaustive exercise affected the heart to the maximum during and just after exhaustion, and LV was influenced more than RV.


Subject(s)
Aryldialkylphosphatase , Animals , Heart Ventricles , Male , Oxidative Stress , Rats
2.
Turk J Med Sci ; 47(6): 1940-1946, 2017 Dec 19.
Article in English | MEDLINE | ID: mdl-29306260

ABSTRACT

Background/aim: Exercise benefits the cardiovascular system, but strenuous exercise can cause cardiac damage and induce cytokine production, particularly that of interleukin-6 (IL-6). Hepcidin, which is primarily regulated by IL-6, increases after exercise. Hepcidin is a possible protective factor against the adverse effects of strenuous exercise such as oxidative stress. The aim of the study is to reveal that training increases hepcidin and attenuates increased levels of IL-6 in the hearts of exhaustively exercised rats by comparing the IL-6 and hepcidin mRNA expression levels in trained and untrained groups.Materials and methods: Thirty male Wistar albino rats were assigned to the following groups: sedentary controls (Con); untrained animals that acutely completed exhaustive exercise and were sacrificed immediately after exhaustion (UT-i) or 1 day after exhaustion (UT-1); and long-term trained animals that completed exhaustive exercise and were sacrificed immediately after exhaustion (T-i) or 1 day after exhaustion (T-1). mRNA levels were examined by reverse transcription PCR. Results: IL-6 levels significantly increased in the UT-i, T-i, and T-1 groups compared to the Con group (P = 0.000, P = 0.024, P = 0.001), with maximal IL-6 expression found in the UT-i group. Hepcidin levels significantly increased in the T-1 group (P = 0.000) compared to the control. Conclusion: Increased IL-6 levels in rats show that exhaustive exercise can cause cardiac inflammation. However, long-term training attenuated the severity of the inflammation. The possible protective effect of increased hepcidin in the trained groups can be explained by the antiinflammatory effects of IL-6 and long-term training.


Subject(s)
Hepcidins/analysis , Interleukin-6/analysis , Myocardium/metabolism , Physical Conditioning, Animal/physiology , Animals , Fatigue/metabolism , Hepcidins/genetics , Hepcidins/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Male , Polymerase Chain Reaction , Rats , Rats, Wistar
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