Key result
Preventive aerobic training in rats reduces DOX-induced cardiac atrophy, inflammation, and stress signaling.
Why the study?
Doxorubicin clinical use is limited by dose-dependent cardiotoxicity, prompting investigation into whether preventive aerobic training protects against doxorubicin-induced cardiac injury.
Does preventive aerobic training protect against doxorubicin-induced cardiotoxicity in Wistar rats?
Does preventive aerobic training protect against doxorubicin-induced cardiotoxicity in Wistar rats?
Preventive aerobic training mitigates doxorubicin-induced cardiotoxicity in a rat model by preserving redox status, reducing inflammation, and attenuating cardiac atrophy.
Should not yet change practice; hypothesis-generating for preventive aerobic training against doxorubicin cardiotoxicity.
Doxorubicin (DOX) is a highly effective chemotherapeutic agent whose clinical use is limited by dose-dependent cardiotoxicity associated with oxidative stress, inflammation, and cellular stress responses. Here, we investigated whether preventive aerobic training could protect against DOX-induced cardiac injury in Wistar rats. Animals were assigned to sedentary control (C), sedentary DOX (D), trained control (CT), and trained DOX (DT) groups. The moderate-intensity (~50–80% maximal exercise test) treadmill protocol (40 min/day, 4 days/week for 4 weeks) was performed before intraperitoneal administration of DOX (4 mg/kg, weekly for 4 weeks) or saline. Preventive training markedly improved exercise capacity (p < 0.001) and attenuated oxidative damage, maintaining antioxidant enzyme activity (GR, SOD) at control levels (p > 0.05). DOX significantly upregulated cardiac IL-6 and IL-1β expression (p < 0.01), while trained animals preserved IL-1β expression similar to controls (p > 0.99). In parallel, DOX increased cardiac HIF-1 expression (p < 0.05), indicating activation of hypoxia- and stress-related signaling pathways, an effect that was attenuated by preventive training (p > 0.99). DOX-induced cardiac atrophy was evidenced by reduced left ventricular mass (p < 0.001), which was partially prevented by training (p < 0.05). Although hematological toxicity persisted, preventive aerobic exercise effectively counteracted DOX cardiotoxicity by restoring redox homeostasis, dampening inflammation, and limiting apoptotic signaling. Collectively, these findings highlight exercise preconditioning as a promising non-pharmacological strategy in cardio-oncology to mitigate chemotherapy-associated cardiac injury.
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Ghignatti et al. (2026) studied this question. Preventive aerobic training in rats preserved antioxidant enzyme activity and reduced DOX-induced cardiac atrophy, inflammation, and stress signaling.