Abstract
New findings:
What is the central question of this study? The current literature indicates the oxidative stress as playing a major role in the iron-overload. Although exercise is a well-established approach to treat/prevent cardiovascular diseases, its effects on iron-overload are not known. What is the main finding and its importance? Moderate-intensity aerobic training had benefits on a rodent model of iron-overload cardiomyopathy by improving the heart antioxidant capacity. After further confirmation by translational and clinical studies, we should consider using this non-pharmacological, high accessible and easy executable adjuvant approach allied to other therapies for improving the life quality of iron-overloaded patients.
Abstract:
Iron is an essential micronutrient in several life processes, but its excess can damage organs due to oxidative stress, with cardiomyopathy being the leading cause of death in iron overloaded patients. Although exercise has long been considered as cardioprotective tool, its effects on the iron overload are not known. This study was designed to investigate the effects of moderate-intensity aerobic training in rats previously submitted to chronic iron overload. Wistar rats received intraperitoneal injections of iron-dextran 100 mg/kg, 5 days/week for 4-weeks and then, rats were kept sedentary or exercised (60 min/day, progressive aerobic training, 60-70% maximal speed, 5 days/week on a treadmill) for the following 8-weeks. Thereafter, haemodynamics was recorded and blood sample, liver and heart were collected. Myocardial mechanics of papillary muscles was assessed in vitro, and cardiac remodelling was evaluated by histology and immunoblotting. Iron overload led to liver iron deposition, fibrosis and increased serum alanine aminotransferase and aspartate aminotransferase. Moreover, cardiac iron accumulation was accompanied by impaired myocardial mechanics, increased cardiac collagen type I and lipid peroxidation (TBARS), and CK-MB release to serum. Although exercise did not influence iron levels, tissue injury markers were significantly reduced. Likewise, myocardial contractility and inotropic responsiveness were improved in exercised rats, in association with increased endogenous antioxidant enzyme catalase. In conclusion, moderate-intensity aerobic exercise was associated with attenuated oxidative stress and cardiac damage in a rodent model of iron overload, thereby suggesting its potential role as a non-pharmacological adjuvant therapy for iron overload cardiomyopathy. This article is protected by copyright. All rights reserved.
