Thursday evening involved a refreshing expedition in extreme weather followed by a delicious dinner in traditional surroundings. Luckily, everybody survived the storm and were ready for a new day full of scientific input. Day 2 started with a session focusing on mitochondrial function. First speaker was professor Erich Gnaiger from Medical University of Innsbruck, Austria – with the most suitable tie of the day:) His scientific contribution to the field of mitochondrial physiology and pathology is quite impressive, including significant contribution to more than 200 publications. Gnaiger is also the initiator and chairman of the International Mitochondrial Physiology Society. His lesson gave insight into mitochondrial respiratory control and early defects of oxidative phosphorylation in hearts affected by heart failure. Several studies have also shown the negative effects of an inactive lifestyle on the mitochondrial function in the heart. We even learned that human beings have very much in common with pigs – although there are some differences.
The next session addressed basic mechanisms of cardiac function. Professor of Cardiac Electrophysiology Mark Boyett from the University of Manchester has been investigating the “ion channels” of the heart for several years, and held the presentation “Exercise training reduces the resting heart rate via downregulation of the funny channel, HCN4, and the funny current, If”. Further, Dr. Daniele Catalucci from Humanitas Clinical and Research Center and National Research Counsil (CNR) in Italy presented “Novel insights and new corrective strategies for the recovery of cardiac perfomance”.The calcium handling in the myocytes represents a very central part of the research activity in CERG, for instance as shown in this blog post. Several of our researchers therefore listened extra carefully when dr. Luigi Venetucci from the University of Manchester spoke about inherited calcium channelopathies in the pathophysiology of arrhytmias. This research plays an important role in the development of new drugs. However, as shown in our group, exercise training also affects the calcium handling in the myocytes, for instance with reduced phosphorylation of cytosolic CaMKII, which again is associated with improved contractile function.
Almost 40 % of heart failure patients have atrial fibrillation. Dr. Anthony J. Workman, University of Glasgow, gave us a very useful introduction to basic mechanisms of this disease, with insights from human atrial cells and cells from rabbits with heart failure. Workman and his colleagues have demonstrated that electric currents and voltage signals generated by single heart cells obtained from patients with AF are disturbed in a way that may exacerbate the disease, by so-called “electrical remodelling”. For example, the atrial cell’s refractory period is reduced, which may promote a rapid and chaotic rhythm. He also investigates the effects of beta-blockers, as well as the effect of heart failure, on electric currents, calcium movements and the proteins which regulate these, in human atrial cells and tissues.
Is cardiopulmonary exercise testing (CPET) more than VO2max? Definitely yes, according to dr. Sandy Jack, from the University of Southampton. She is a routined teacher of several CPET courses, with many of the CERG researchers as satisfied students. Her lesson highlighted the use of exercise testing in preoperative assessment and perioperative management, including prehabilitation in cancer patients undergoing major surgery. Further, research suggests that exercise enhances the effect of chemotherapy in cancer patients.
The scientific program was followed by the arrangement “Man in Extreme Environments” at Samfundet. More about that in the next blog post!
Maria Henningsen, CERG