Related Experiment Video
Updated: Sep 17, 2025

08:09
A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
9.9K
Resistance Training Protects against Cardiac Damage in Doxorubicin-Induced Cardiotoxicity in Rats
Claudia Morais Sequeira1, Jefferson Fernandes Evangelista1, Renata Alves1
1Department of Pharmacology and Psychobiology, Rio de Janeiro State University, Rio de Janeiro, BRAZIL.
Medicine and Science in Sports and Exercise
|July 1, 2025
Summary
Resistance training (RT) can protect the heart from doxorubicin (DOX)-induced damage by improving cardiac structure and mitochondrial dynamics. This study shows RT mitigates DOX cardiotoxicity in rats.
Area of Science:
- Cardiology
- Exercise Physiology
- Molecular Biology
Background:
- Doxorubicin (DOX) is a potent chemotherapy agent.
- DOX causes dose-dependent cardiotoxicity, potentially leading to heart failure.
- Protecting the heart during DOX treatment is a critical clinical challenge.
Purpose of the Study:
- To investigate if resistance training (RT) can mitigate doxorubicin-induced cardiac damage.
- To examine the effects of RT on proteins regulating muscle anabolism, catabolism, and mitochondrial dynamics in the left ventricle.
- To assess RT's impact on DOX cardiotoxicity markers.
Main Methods:
- Male Sprague Dawley rats were divided into control, DOX/sedentary, and DOX/RT groups.
- DOX or saline was administered daily for ten days.
- RT involved ladder climbing with weights for eight weeks, starting concurrently with DOX administration.
Main Results:
- RT significantly reduced mortality and prevented cardiac fiber atrophy and fibrosis caused by DOX.
- RT mitigated cardiomyocyte ultrastructural damage, including sarcomere misalignment and mitochondrial injury.
- RT modulated proteins involved in mitochondrial dynamics, increasing PGC1α expression and affecting Mfn2 and FIS1 levels.
Conclusions:
- Resistance training demonstrates potential as a protective strategy against doxorubicin-induced cardiotoxicity.
- RT may protect the heart by modulating proteins associated with mitochondrial dynamics.
- Further research can explore RT's clinical application in cancer patients undergoing DOX therapy.
Related Concept Videos
Exercise and Cardiovascular Response
1.1K
Exercise significantly impacts cardiovascular response, which is crucial for understanding patient health and designing effective treatment plans.
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...
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...
1.1K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
524
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
524
Heart Failure Drugs: Inotropic Agents
743
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
743

