Fredrik Hjulstad Bækkerud’s research looks at the effect of exercise on mitochondrial function in diabetes, coronary artery disease and heart failure with preserved ejection fraction.
- Exercise prevents muscular and mitochondrial dysfunction in heart failure with preserved ejection fraction.
- Exercise the day before reduces cardiac mitochondrial function during heart surgery.
Interval training improves energy production in the diabetic heart.
Thesis: Mitochondrial function and exercise in cardiovascular diseases
Candidate: Fredrik Hjulstad Bækkerud
Time: August 27, 2019 at 12:15
Place: St. Olavs hospital, Bevegelsessenteret: Seminarrom BS31
Link to university website (in Norwegian)
(1) Rats with heart failure with preserved ejection fraction have reduced mitochondrial density in their calf muscles. High-intensity exercise prevents this dysfunction, according to Bækkerud’s first article. Exercise also prevents dysfunction of the mitochondrial respiration in the diaphragm.
The study also looks at respiratory and limb skeletal muscular function, and shows that exercise can prevent several of the adverse muscular effects of diastolic heart failure. The study includes 22 rats who developed heart failure with preserved ejection fraction, of which half performed regular high-intensity exercise during the course of the study. They were compared to ten healthy non-exercised control rats.
(2) Exercise 24 hours prior to coronary artery bypass grafting might make the heart more susceptible to damage during and following surgery. Mitochondrial respiration in both the left ventricle and right atrium was lower following surgery in those who exercised. Moreover, troponin T levels were higher, and the apoptosis-related marker caspase 3 was increased by 50 %.
The pilot study includes 20 patients scheduled for elective CABG. Half of them were randomized to moderate intensity exercise the day before.
(3) Eight weeks of high-intensity interval training ameliorated some, but not all, mitochondrial dysfunctions in the hearts of mice with type 2 diabetes. The activity in complexes I, II and IV of mitochondrial respiration were attenuated by up to 50 % in the diabetic mice. Exercise corrected the impairments in complexes II and IV. The exercise, however, did not repair the mitochondria’s reduced ability to absorb calcium.
The study included 17 healthy mice and 30 mice genetically predisposed to developing diabetes. Half of the mice with diabetes trained 10×4-minute intervals at 90% of maximum capacity five days a week for eight weeks.
(1) Bowen, T. S., Rolim, N. P., Fischer, T., Bækkerud, F. H., Medeiros, A., Werner, S., Brønstad, E., Rognmo, Ø., Mangner, N., Linke, A., Schuler, G., Silva, G. J. J., Wisløff, U., & Adams, V. (2015). Heart failure with preserved ejection fraction induces molecular, mitochondrial, histological, and functional alterations in rat respiratory and limb skeletal muscle. European journal of heart failure, 17(3), 263-272.
(2) Smenes, B. T., Bækkerud, F. H., Slagsvold, K. H., Hassel, E., Wohlwend, M., Pinho, M., Høydal, M., Wisløff, U., Rognmo, Ø., & Wahba, A. (2018). Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial. Interactive cardiovascular and thoracic surgery, 27(1), 95-101.
(3) Bækkerud, F. H., Salerno, S., Ceriotti, P., Morland, C., Storm-Mathisen, J., Bergersen, L. H., Høydal, M. A., Catalucci, D., & Stølen, T. O. (2019). High Intensity Interval Training Ameliorates Mitochondrial Dysfunction in the Left Ventricle of Mice with Type 2 Diabetes. Cardiovascular toxicology, 1-10.