Swimming training decreased isoproterenol-induced cardiac fibrosis area by 86% in wild-type mice, but not in AMPKα2-knockout mice, demonstrating that the cardioprotective effect is AMPK-dependent.
Does swimming training prevent isoproterenol-induced cardiac fibrosis in mice, and is this effect dependent on AMPK activation?
Exercise training protects against beta-adrenergic receptor overstimulation-induced cardiac fibrosis via an AMPK-dependent reduction in oxidative stress.
Effect estimate: 86% reduction
p-value: p=<0.001
Regular exercise can protect the heart against external stimuli, but the mechanism is not well understood. We determined the role of adenosine monophosphate-activated protein kinase (AMPK) in regulating swimming exercise-mediated cardiac protection against β-adrenergic receptor overstimulation with isoproterenol (ISO) in mice. Ten-week-old AMPKα2+/+ and AMPKα2-knockout (AMPKα2-/-) littermates were subjected to 4 weeks of swimming training (50 min daily, 6 days a week) or housed under sedentary conditions. The mice received daily subcutaneous injection of ISO (5 mg/kg/d), a nonselective β-adrenergic receptor agonist, during the last 2 weeks of swimming training. Swimming training alleviated ISO-induced cardiac fibrosis in AMPKα2+/+ mice but not AMPKα2-/- mice. Swimming training activated cardiac AMPK in AMPKα2+/+ mice. Furthermore, swimming training attenuated ISO-induced production of reactive oxygen species (ROS) and expression of NADPH oxidase and promoted the expression of antioxidant enzymes in AMPKα2+/+ mice but not AMPKα2-/- mice. In conclusion, swimming training attenuates ISO-induced cardiac fibrosis by inhibiting the NADPH oxidase-ROS pathway mediated by AMPK activation. Our findings provide a new mechanism for the cardioprotective effects of exercise.
Ma et al. (Fri,) conducted a other in Isoproterenol-induced cardiac fibrosis. Swimming training vs. Sedentary conditions was evaluated on Cardiac fibrosis area (86% reduction, p=<0.001). Swimming training decreased isoproterenol-induced cardiac fibrosis area by 86% in wild-type mice, but not in AMPKα2-knockout mice, demonstrating that the cardioprotective effect is AMPK-dependent.