Volker Adams obtained his PhD at the University of Konstanz in Biology and his work focused on isolation and characterization of mitochondrial contact sites in different organs. His postdoctoral training was in molecular genetics at the Institute of Molecular Genetics, Baylor College of Medicine, Houston Texas, USA. After moving to Leipzig, and taking over the position as head of the research laboratory at the Heart Center Leipzig his main research interest during the last 20 years is to understand the molecular changes in the endothelium and the skeletal muscle related to the beneficial effects of exercise training.

Steven L. Britton is a Professor of both Anesthesiology and Molecular & Integrative Physiology at the University of Michigan. Based upon the strong linkage between low exercise capacity and all-cause morbidity he hypothesized that: variation in capacity for aerobic metabolism is the central mechanistic determinant between disease and health (aerobic hypothesis). As an unbiased test of this hypothesis, Britton and Lauren G. Koch demonstrate that two-way artificial selection of rats for low and high exercise capacity also produces rats that differ for numerous disease risks, including the metabolic syndrome, fatty liver disease, Alzheimer’s degeneration, and obesity. This rat model system is shared with investigators at over 50 institutions to understand exercise as it relates to health and disease.

Since 2003, the laboratory of Dr. Yan Burelle has developed a research program focused mitochondrial physiology. The central interest of his laboratory has been to integrate multiple facets of mitochondrial biology to gain a global understanding of the importance of these organelles in physiological homeostasis, and development of human diseases, including acquired cardiac and skeletal muscle pathologies as well as genetic mitochondrial diseases. His laboratory has developed an expertise in the assessment of multiple mitochondrial functions and quality control mechanisms, which have been used not only in basic studies using animal models, but also in tissues from patients in the context of translational research.  Some of the recent work from his laboratory focuses on mechanisms involved in mitochondrial quality control in the heart, and their implication in the maintenance of mitochondrial health and cardiac response to stress. Over the years, his laboratory benefited from uninterrupted funding from CIHR, and NSERC. Dr. Burelle received salary support from FRSQ for several years and was awarded the Pfizer Cardiovascular Award, and the Merck-Frost New Investigator Award for his work. He is the author of several articles published in leading journal of his field including Autophagy, Circulation Research, and the American Journal of Respiratory and Critical Care Medicine.

Sina Coldewey is a consultant at the Department of Anaesthesiology and Intensive Care Medicine of the University Hospital Jena, Germany, since 2014. Since 2017 she is also head of the research group “Translational Septomics” at the Septomics Research Centre. She spent the early years of her medical and scientific career at Hanover Medical School. Here, she obtained her medical degree, completed her MD (Dr. med.) in molecular microbiology and her specialist training in anaesthesiology and intensive care. From 2010 to 2013, Sina Coldewey worked as a research fellow of the German Research Foundation at the William Harvey Research Institute of the Queen Mary University of London and was awarded a PhD by the University of London in 2013. Sina Coldewey is principle investigator of several projects funded by the German Research Foundation (DFG) and the Federal Ministry for Education and Research (BMBF) and member of the board of directors of the Centre for Sepsis Control & Care (CSCC) as well as the Centre of Innovation Competence (ZIK) Septomics. In her research group, physicians and scientists work together in the clinic and in the laboratory to develop novel diagnostic and therapeutic strategies for septic organ failure. To this end, the group investigates the underlying systemic and molecular mechanisms and the clinical significance of organ dysfunctions in both acute sepsis and the further course of the condition, with a specific focus on the cardiovascular system and the function of signalling lipids and metabolites.

Dr. Coleman’s research focuses on triacylglycerol biochemistry and metabolism, particularly the glycerol-3-phosphate and monoacylglycerol pathways of triacylglycerol synthesis and the enzymes that activate the long-chain fatty acids substrates of the acyltransferases involved in these pathways. Her laboratory cloned and characterized 2 novel glycerol-3-phosphate acyltransferases, GPAT2, a major GPAT in testes and GPAT 4, a major GPAT whose deficiency in mice results defective energy metabolism. Her studies of mice that are deficient in GPAT1 showed the importance of this isoform in the development of hepatic steatosis, as well as its role in diet and hormonally induced insulin resistance.
Her studies on acyl-CoA synthetases, enzymes that activate the long-chain fatty acids substrates for both glycerolipid biosynthesis and fatty acid oxidation have demonstrated that acyl-CoAs are compartmentalized within cells. Characterization of mice with tissue-specific deficiencies of acyl-CoA synthetase-1 (ACSL1) shows a requirement for this isoform in targeting fatty acids towards beta-oxidation in heart, white adipocytes, brown adipocytes, and muscle. Without ACSL1, energy metabolism in these tissues is impaired, and glucose homeostasis is compromised. Her studies are currently incorporating approaches such as metabolomics in identifying novel pathways that connect acyl-CoA metabolism with metabolically dysregulated disease states, including cardiac hypertrophy, insulin resistance, and cancer.

Our research determines the roles of intermediary metabolism in governing integrated physiological homeostasis. In the past five years, my laboratory created a platform for metabolic analysis that includes the development of novel germline and tissue-specific mouse strains that are unable to appropriately metabolize ketone bodies, which are key integrators of mitochondrial oxidative substrate metabolism. My laboratory’s metabolic analyses of these strains include stable isotope-manipulated systems coupled with NMR and LC/MS computational metabolomics methods to quantitatively map substrate fate and measure metabolic flux. Together, the tools and approaches developed and used in the lab offer a unique window into the metabolic adaptations and maladaptations in myocardial disease, nonalcoholic fatty liver disease, and obesity/metabolic syndrome.

Åsa Gustafsson is interested in understanding the molecular pathways that regulate the life and death of cardiac myocytes. Activation of cell death pathways is a common occurrence in cardiovascular disease and contributes to the development of heart failure. Using genetic and molecular biology approaches, Dr. Gustafsson is elucidating the pathways involved in regulating mitochondrial structure, function, and degradation in myocardial cells. Specifically, she is interested in how the E3 ubiquitin ligase Parkin regulates mitochondrial turnover in cardiac myocytes. Defects in this pathway leads to accumulation of aberrant mitochondria and loss of myocytes. Dr. Gustafsson joined the Skaggs School of Pharmacy and Pharmaceutical Sciences in October 2009. Prior to coming to UCSD, she was an Assistant Professor at San Diego State University. She received her Ph.D. in Biomedical Sciences from the Department of Pharmacology at the University of California, San Diego, CA in 2001. Her postdoctoral training was done at The Scripps Research Institute in La Jolla with Dr. Roberta Gottlieb. For her contributions to cardiovascular research, she was awarded the ISHR Outstanding Investigator Award in 2014. She is also an elected Fellow of the American Heart Association and a Fellow of the International Society for Heart Research.

Ole-Jakob How is a cardiovascular physiologist at UiT, The Arctic University of Norway. His main research interest is new therapies targeting cardiac function and metabolism in acute heart failure. His Ph.D. (2006) dealt with establishing a method for measurements of cardiac efficiency in the isolated working mouse heart. Through the use of miniaturized catheters, they were the first to assess cardiac energetics using the PVA-MVO2 framework in mice. During his postdoctoral training at Department of Cardiothoracic Surgery, University Hospital Northern Norway he led the activity in the surgical laboratory. As a faculty member, he is presently head of a research group using a large animal model for assessing new therapies in acute heart failure.

Howy Jacobs is currently the Director of the Institute of Biotechnology in Helsinki, as well as holding a professorship in the University of Tampere, Finland. Educated in Cambridge, Glasgow and Pasadena, his major interests have been in the machinery of mitochondrial DNA maintenance and expression and, more recently, in the alternative respiratory chain enzymes and their potential use as a tool in research - and possibly even therapy - for disorders connected with mitochondrial dysfunction. He is a member of EMBO, a former Chief Editor of EMBO Reports, and the recipient of a number of national and international awards and distinctions. He is also passionate about the public communication of science, and is involved in several relevant media projects.

Priv.-Doz. Dr. Petra Kleinbongard, has graduated as a master of biology from the Ruhr-University Bochum and received her Ph.D. at the Heinrich-Heine University Düsseldorf/Ruhr-University Bochum where she completed her thesis on "Physiological relevance of the L-Arginine-NO-metabolism in the blood of mammals”. She then had postdoctoral training in the team and under the supervision of Prof. Dr. Malte Kelm in the Departments of Cardiology at the Universities Düsseldorf and Aachen. Her work there concerned the biology of NO, notably its origin in erythrocytes and its vasomotor function. Now, for the last nine years she is responsible for translational research on coronary microembolization and on remote ischemic conditioning in close collaboration with cardiological and cardiosurgical colleagues at the University Essen under supervision of Prof. Dr. Gerd Heusch.

Dr. E. Douglas Lewandowski is currently a Professor in the Center for the Metabolic Origins of Disease and Director of Cardiovascular Translational Research at the Sanford Burnham Prebys Medical Discovery Institute at Lake Nona with a joint appointment at Florida Hospital as Senior Principal Investigator at the Translational Research Institute for Metabolism and Diabetes (TRI-MD). He is a recipient of the Method to Extend Research in Time Award (MERIT R37) from the National Heart Lung and Blood Institute (NHLBI) of the National Institutes of Health. He was named an Established Investigator of the American Heart Association and is an elected Fellow of the American Association for the Advancement of Sciences (AAAS), the International Society for Heart Research (FISHR), the American Heart Association (FAHA), and the American Physiological Society. He has served on and chaired numerous grant review panels and has served on numerous editorial boards including Circulation, Circulation Research, Journal of Molecular and Cellular Cardiology, and the American Journal of Physiology.
Dr. Lewandowski holds a B.A. from the University of Chicago and a PhD from the University of Texas Southwestern Medical Center. He has held faculty appointments at the Baylor College of Medicine in Houston TX, Harvard Medical School in Boston, MA, and the University of Illinois College of Medicine at Chicago. Before arriving at SBP, he was the Director of the UIC Center for Cardiovascular Research and the Interim Head of the Department of Physiology and Biophysics at the University of Illinois College of Medicine at Chicago.

Dr Andrew Murray is a University Senior Lecturer in Mammalian Physiology at the University of Cambridge, and the WYNG Fellow in Natural Sciences at Trinity Hall. Prior to this he studied for his first degree in Biochemistry and a DPhil in Physiology at the University of Oxford, working with Professor Kieran Clarke and supported by the British Heart Foundation. In Oxford, Andrew was instrumental in the development and testing of a novel, orally-available ketone ester supplement, which has been shown to enhance physical and cognitive performance through effects on mitochondrial function in vivo. This supplement, ΔG^TM, will be commercially-available as a performance supplement from late 2017.
Andrew leads the Mitochondrial Physiology group at the Department of Physiology, Development and Neuroscience, and is a co-Principal Investigator of the Xtreme Everest Oxygen Research Consortium. Andrew has an interest in the mitochondrial response to chronic hypoxia both in disease states and in healthy humans at high altitude. His group carried out studies of mitochondrial function at extreme high altitude during the Caudwell Xtreme Everest 2007 and Xtreme Everest 2 2013 medical research expeditions. Andrew and his group recently reported findings relating the unique metabolism of a high-altitude adapted population, the Sherpa, to genetic differences in this population, thereby revealing a functional mechanism of high-altitude adaptation that has undergone natural selection in a human population.

Dr. Peterson is a native of central Wisconsin, USA. She received her B.S. from Georgetown University graduating magna cum laude and winning the Francis Graham medal for academic and athletic achievement. She earned her medical degree from Washington University and did her residency in internal medicine and fellowship in cardiology at Barnes Hospital in St. Louis. She is the Director of Cardiac Rehabilitation and peak oxygen consumption (VO₂) testing at Barnes Hospital, and she is on the board of the Society for Heart and Vascular Metabolism.
Her research focus is to better understand nonischemic myocardial derangements in humans in order to learn how to make the myocardium function better. In doing so, Dr. Peterson employs multimodality imaging — Positron Emission Tomography, echocardiography, magnetic resonance imaging and spectroscopy — to quantify myocardial abnormalities and their responses to treatments. She has investigated the effects of obesity on myocardial perfusion, metabolism, and efficiency on the human heart. She was also the first to describe the effects of sex on these cardiac physiology measures in humans. More recently, she has been investigating the effects of diet and dietary supplement treatment on heart and skeletal muscle function in heart failure as well as novel lipid biomarkers of cardiac disease.

Peter Rehling is the Director of the Department for Cellular Biochemistry at the University Medical Center Göttingen, Germany. In addition, he is a Max Planck Institute for Biophysical Chemistry Research Fellow. He obtained his Ph.D. from the Ruhr-University Bochum, Germany. His postdoctoral research was carried out in the labs of W.-H. Kunau (Ruhr-University Bochum) and S.D. Emr (Howard Hughes Medical Institute, University of California, San Diego, USA). He became a group leader at the University of Freiburg and was appointed as a professor and Chair of the Department of Cellular Biochemistry in 2007.

Peter Rehling’s research addresses the mechanisms of protein transport into mitochondria, the biogenesis of mitochondrial membrane protein complexes, and how these process are affected in mitochondrial disorders. Recent work has led him to the analysis of translational regulation in mitochondria and the integration of mitochondrial proteostasis into the cellular context.

Michael N. Sack, M.D., Ph.D. is a Senior Investigator at the NHLBI of the National Institutes of Health, Bethesda, USA. Dr. Sack undertook his training at the University of The Witwatersrand and University of Cape Town Medical Schools in South Africa. He subsequently trained at Georgetown University and at Washington University Medical Centers, in Washington DC and St. Louis, USA respectively. He held academic appointments at University College London and at The University of Cape Town prior to joining the NIH. His research focuses on the post-translational regulation of metabolism and mitochondrial functioning underpinning perturbations associated with cardiometabolic diseases.

I use non-invasive magnetic resonance spectroscopy (MRS) to investigate the etiology of insulin resistance in type 2 diabetes and specifically the causes and consequences of fat storage in heart, liver and muscle. To this end, I use cardiac and hepatic ¹H-MRS to study ectopic fat storage in these tissues and ³¹P-MRS to address energy metabolism in vivo. Applying these tools, I found that in vivo mitochondrial function is reduced in diabetic patients. Furthermore, I showed that lipid content and oxidative capacity in cardiac and skeletal muscle are modulated by endurance training and acute exercise and that high concentrations of FFA- as seen in diabetes - lead to increased fat storage. In 2010, I received a NWO-VENI award to investigate the role of hepatic mitochondrial energy and lipid metabolism in type 2 diabetes. Based on pilotwork generated in my team, I received in 2012 an EFSD research grant to investigate the muscle metabolite acetylcarnitine; this work has resulted in a recent publication where we showed that acetylcarnitine is detectable with ¹H-MRS and that levels are inversely related to insulin resistance (Lindeboom, JCI 2014). With a recent NWO-VIDI award I will investigate the interaction of NAD⁺ and acetylcarnitine and their role in protein acetylation and the development of insulin resistance.

Mervyn Singer is Professor of Medicine at University College London, UK and a Senior Investigator of the UK National Institute of Health Research. He co-chaired the recent ‘Sepsis-3’ Definitions Task Force. His research interests focus upon sepsis, mechanisms of organ failure, shock states, tissue oxygenation and novel monitoring/diagnostic/therapeutic approaches. These span preclinical investigations (with a particular interest in bioenergetics and metabolism), translational applications and clinical studies. Funding comes from the Wellcome Trust, UK Medical Research Council, EU and British Heart Foundation among others.

Heinrich Taegtmeyer is a Professor of Medicine at McGovern Medical School, The University of Texas Health Science Center at Houston. He is a practicing cardiologist with 40 years of continuous funding of his laboratory from the US Public Health Service (NHLBI). He received his medical degree (Dr. Med.) summa cum laude from the University of Freiburg (Germany), and his PhD (DPhil) from the University of Oxford (England). He trained in Medicine on the Harvard Medical Service of the Boston City Hospital and in Cardiology at the Peter Bent Brigham Hospital, also in Boston, Massachusetts. His research in cardiac metabolism resulted in 294 peer-reviewed papers which were quoted 12,000 times with an h-index of 72.

Stefan Wagner is Professor for Translational Cardiology at the University of Regensburg. He finished his medical training and received his M.D. at the Georg-August-University of Goettingen. In his thesis he investigated the role of Na/Ca exchange for cardiac Na and Ca metabolism upon reactive oxygen-species-dependent (ROS) injury. During his post-doctoral training he studied the role of Ca-Calmodulin-dependent serine/threonine kinase II (CaMKII). He identified a novel CaMKII-dependent Na entry pathway by voltage-gated Na channels (NaV1.5) and showed its relevance for cardiac Ca overload, contractile dysfunction and arrhythmias. Since his appointment at the University of Regensburg he strongly collaborates with cardiac surgeons and pharmaceutical companies to translate this findings into the clinic. He currently studies two potential CaMKII inhibitors in various animal models and human tissue. Recently, he also identified a novel link from sleep-disordered breathing to cardiac arrhythmias in patients by showing a ROS-dependent activation of CaMKII that leads to profound dysregulation of cardiac Na and Ca metabolism.