Morten A. Høydal

ORCID: 0000-0003-1804-2578
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About
Contact & Profiles
Research Areas
  • Cardiovascular Effects of Exercise
  • Cardiovascular Function and Risk Factors
  • Cardiovascular and exercise physiology
  • Cardiac electrophysiology and arrhythmias
  • Adipose Tissue and Metabolism
  • Cardiac Ischemia and Reperfusion
  • Cardiomyopathy and Myosin Studies
  • Ion channel regulation and function
  • Mitochondrial Function and Pathology
  • MicroRNA in disease regulation
  • Cardiac Arrest and Resuscitation
  • Genetics and Physical Performance
  • Signaling Pathways in Disease
  • Heart Rate Variability and Autonomic Control
  • Heme Oxygenase-1 and Carbon Monoxide
  • Fuel Cells and Related Materials
  • RNA Research and Splicing
  • Cardiac Fibrosis and Remodeling
  • Muscle metabolism and nutrition
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Anesthesia and Neurotoxicity Research
  • Advanced MRI Techniques and Applications
  • Extracellular vesicles in disease
  • Sports Performance and Training
  • Microfluidic and Bio-sensing Technologies

Norwegian University of Science and Technology
2016-2025

St Olav's University Hospital
2009-2020

The Research Council of Norway
2013-2014

University of Michigan
2007-2011

Johns Hopkins University
2011

Norwegian Veterinary Institute
2011

Wageningen University & Research
2011

University of Glasgow
2007-2011

MultiMedica
2009

University of California, San Diego
2009

Valid and reliable experimental models are essential to gain insight into the cellular molecular mechanisms underlying beneficial effects of exercise in prevention, treatment, rehabilitation lifestyle-related diseases. Studies with large changes, low variation, reproducible training outcome require individualized intensity, controlled by direct measurements maximal oxygen uptake or heart rate. As this approach is expensive time consuming, we discuss whether treadmill running speed a...

10.1097/hjr.0b013e3281eacef1 article EN European Journal of Cardiovascular Prevention & Rehabilitation 2007-12-01

Rationale: In the present study we explored mechanisms behind excitation–contraction (EC) coupling defects in cardiomyocytes from mice with type-2 diabetes (db/db). Objective: We determined whether 13 weeks of aerobic interval training could restore cardiomyocyte Ca 2+ cycling and EC coupling. Methods Results: Reduced contractility isolated sedentary db/db was associated increased diastolic sarcoplasmic reticulum (SR)-Ca leak, reduced synchrony release, transverse (T)-tubule density, lower...

10.1161/circresaha.109.199810 article EN Circulation Research 2009-08-14

Low aerobic exercise capacity is a powerful predictor of premature morbidity and mortality for healthy adults as well those with cardiovascular disease. For aged populations, poor performance on treadmill or extended walking tests indicates closer proximity to future health declines. Together, these findings suggest fundamental connection between longevity.Through artificial selective breeding, we developed an animal model system prospectively test the association survivability (aerobic...

10.1161/circresaha.111.253807 article EN Circulation Research 2011-09-16

Remote ischemic preconditioning (RIPC) has been suggested to induce cardioprotection during cardiac surgery. Maintaining proper atrial function is imperative in preventing arrhythmia and thrombus formation. Mitochondria have proposed as key targets conveying RIPC mechanisms effects. MicroRNA (miR) emerging an important regulator of mitochondrial function, arrhythmia, protection from ischemia reperfusion.This study aimed evaluate the effect on respiration miR expression human tissue.Sixty...

10.1161/circresaha.114.302751 article EN Circulation Research 2013-12-27

Purpose: A diminished mechanical efficiency (work/O2 consumed) accompanies chronic obstructive pulmonary disease (COPD), and increased has been attained by maximal strength training (MST) with an emphasis on the rate of force mobilization in concentric phase healthy subjects. This study combined these observations evaluated impact short-term MST patients COPD. Methods: Twelve COPD (FEV1 = 1.1 ± 0.1) were pretested then randomly assigned to either group (N 6) or a normal activity control 6)....

10.1249/01.mss.0000246989.48729.39 article EN Medicine & Science in Sports & Exercise 2007-02-01

Pathological forms of left ventricular hypertrophy (LVH) often progress to heart failure. Specific transcription factors have been identified that activate the gene program induce pathological LVH. It is likely apart from activating transcriptional inducers LVH, constitutive repressors need be removed during development cardiac hypertrophy. Here, we report presence Krüppel-like factor 15 (KLF15) lost in and this loss precedes progression toward We show transforming growth factor-β-mediated...

10.1074/jbc.m110.107292 article EN cc-by Journal of Biological Chemistry 2010-06-22

Abstract The response of transverse (T)‐tubules to exercise training in health and disease remains unclear. Therefore, we studied the effect on density spacing left ventricle cardiomyocyte T‐tubules normal remodeled hearts that associate with detubulation, by confocal laser scanning microscopy. First, rats increased volume 16% ( P < 0.01), preserved T‐tubule density. Thus, adapted physiologic hypertrophy. Next, a rat model metabolic syndrome pressure overload‐induced concentric...

10.1002/jcp.22559 article EN Journal of Cellular Physiology 2010-12-06

Abstract Aims Cellular processes in the heart rely mainly on studies from experimental animal models or explanted hearts patients with terminal end‐stage failure (HF). To address this limitation, we provide data excitation contraction coupling, cardiomyocyte and relaxation, Ca 2+ handling post‐myocardial‐infarction (MI) at mid‐stage of HF. Methods results Nine MI eight control without (non‐MI) were included. Biopsies taken left ventricular myocardium processed for further measurements...

10.1002/ehf2.12271 article EN cc-by ESC Heart Failure 2018-02-12

Clinical and experimental studies demonstrate that exercise training improves aerobic capacity cardiac function in heart failure, even patients on optimal treatment with angiotensin inhibitors beta-blockers, but the cellular mechanisms are incompletely understood. Since myocardial dysfunction is frequently associated impaired energy status, aim of this study was to assess effects losartan systems for production transfer failure.Maximal oxygen uptake, metabolism were assessed failure after a...

10.1016/j.cardiores.2007.06.008 article EN Cardiovascular Research 2007-06-20

Atrial fibrillation (AF) is the most common cardiac arrhythmia with a potential to cause serious complications. Mitochondria play central roles in cardiomyocyte function and have been implicated AF pathophysiology. MicroRNA (miR) are suggested influence both mitochondrial development of AF. Yet miR expression remain largely unexplored human atrial tissue. This study aims investigate right (RA) left atria (LA) patients sinus rhythm (SR). Myocardial tissue from RA LA appendages was...

10.1152/physiolgenomics.00042.2014 article EN Physiological Genomics 2014-05-14

Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic and cardiac gene expression we examined genome-wide in hearts rats artificially selected for high low running (HCR LCR, respectively) over 16 generations. The artificial selection LCR caused accumulation risk factors disease similar to metabolic syndrome seen human, whereas HCR had markedly better function. We also studied alterations response exercise training these...

10.1152/physiolgenomics.00269.2007 article EN Physiological Genomics 2008-01-03

The intercalated disc (ID) of cardiac myocytes is emerging as a crucial structure in the heart. Loss ID proteins like N-cadherin causes lethal abnormalities, and mutations cause human cardiomyopathy. A comprehensive screen for novel mechanisms failing hearts demonstrated that expression lysosomal integral membrane protein 2 (LIMP-2) increased hypertrophy heart failure both rat myocardium. Complete loss LIMP-2 genetically engineered mice did not affect development; however, these null failed...

10.1084/jem.20070145 article EN The Journal of Experimental Medicine 2007-05-07

The relationship between inborn maximal oxygen uptake (VO(2max)) and skeletal muscle gene expression is unknown. Since low VO(2max) a strong predictor of cardiovascular mortality, genes related to might also be involved in disease. To establish the expression, we performed microarray analysis soleus rats artificially selected for high- running capacity (HCR LCR, respectively). In was accompanied by aggregation risk factors similar metabolic syndrome. Although sedentary HCR were able maintain...

10.1152/physiolgenomics.90282.2008 article EN Physiological Genomics 2008-09-10

Impaired cardiac control of intracellular diastolic Ca(2+) gives rise to arrhythmias. Whereas exercise training corrects abnormal cyclic handling in heart failure, the effect on remains unstudied. Here, we studied generation and propagation spontaneous waves failing cardiomyocytes. Post-myocardial infarction failure was induced Sprague-Dawley rats by coronary artery ligation. Echocardiography confirmed left ventricular infarctions 40 ± 5%, whereas indicated increased end-diastolic pressures,...

10.1002/jcp.22771 article EN Journal of Cellular Physiology 2011-04-04

Background There is limited knowledge about atrial myocyte Ca2+ handling in the failing hearts. The aim of this study was to examine contractile function and rats with post-infarction heart failure (HF) whether aerobic interval training could reverse a potential dysfunction. Methods results Post-infarction HF induced Sprague Dawley by ligation left descending coronary artery. Atrial shortening depressed (p<0.01) time relaxation prolonged sedentary HF-rats compared healthy controls. This...

10.1371/journal.pone.0066288 article EN cc-by PLoS ONE 2013-06-14

Cardiovascular disease (CVD) remains the leading cause of death worldwide and, despite continuous advances, better diagnostic and prognostic tools, as well therapy, are needed. The human transcriptome, which is set all RNA produced in a cell, much more complex than previously thought lack dialogue between researchers industrials consensus on guidelines to generate data make it harder compare reproduce results. This European Cooperation Science Technology (COST) Action aims accelerate...

10.3390/ncrna5020031 article EN cc-by Non-Coding RNA 2019-03-29
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