Nandrolone decanoate impairs exercise-induced cardioprotection: role of antioxidant enzymes
Related Experiment Video
Updated: Aug 9, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Elen Aguiar Chaves1, Pedro Paulo Pereira-Junior, Rodrigo Soares Fortunato
1Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Brazil. chavesea@yahoo.com.br
Abstract:
The beneficial effects of exercise in reducing the incidence of cardiovascular diseases are well known and the abuse of anabolic androgenic steroids (AAS) has been associated to cardiovascular disorders. Previous studies showed that heart protection to ischemic events would be mediated by increasing the antioxidant enzyme activities. Here, we investigated the impact of exercise and high doses of the AAS nandrolone decanoate (DECA), 10 mgkg(-1) body weight during 8 weeks, in cardiac tolerance to ischemic events as well as on the activity of antioxidant enzymes in rats. After a global ischemic event, hearts of control trained (CT) group recovered about 70% of left ventricular developed pressure, whereas DECA trained (DT), control sedentary (CS) and DECA sedentary (DS) animals recovered only about 20%. Similarly, heart infarct size was significantly lower in the CT group compared to animals of the three other groups. The activities of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) were significantly higher in CT animals than in the other three groups, whereas catalase activity was not affected in any group. Together, these results indicate that chronic treatment with DECA cause an impairment of exercise induction of antioxidant enzyme activities, leading to a reduced cardioprotection upon ischemic events.
Related Concept Videos
Exercise and Cardiovascular Response
Light to moderate physical activity initiates a series of interconnected responses in the body. The heart rate modestly increases in anticipation of the workout, followed by widespread vasodilation as oxygen consumption by skeletal muscles increases. This results in decreased peripheral resistance, increased capillary blood flow, and accelerated...
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Drugs Affecting Neurotransmitter Synthesis
Heart Failure Drugs: β-Blockers