Dr. Ulrik Wisloff
The current symposium clearly demonstrates that combining experimental models for cardiovascular disease with well-defined models of exercise training results in highly translatable pre-clinical findings that advance this important field of research.
For instance, Professor Ellingsen from the Norwegian University of Science and Technology demonstrated nicely how a study in rats with heart failure that went through an interval training regimen leading to remarkable cardiovascular adaptations has been translated into a clinical study involving heart failure patients; basically with “similar” findings as in rats. Furthermore, he demonstrated how exercise training regulates a protein involved in the fine tuning of cell contraction at the beat-to-beat basis; the calcium-calmodulin dependent protein kinase (CaMKII). CaMKII is known to be central for triggering lethal ventricular arrhythmias. Understanding CaMKII-regulation more completely in the heart after exercise training in healthy individuals and in individuals with cardiovascular disease will help to understand the normal physiology of the heart, how it changes during disease, and may identify new modalities of treatment.
Additionally, Professor Axel Linke (Germany) demonstrated for the first time that endurance training activates progenitor and stem cells in the heart of rats with post-infarction heart failure. These data are extremely interesting, considering ongoing clinical trials where they induce/introduce stem cells invasively into the hearts of patients.
The current symposium demonstrated that we are getting closer to understanding the mechanisms behind exercise-induced adaptations in the heart. Understanding the signaling pathways of these changes will probably contribute to the development of new molecular medicine in the future.
Exercise training: alterations at the molecular level Basic Science Track
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