Featured Speakers
IBEC 2026: Exercise and Healthspan
June 1-5
Featured Speakers
Nick Betley, Ph.D.
It Is All in Your Head: Body - Brain Interactions and Beneficial Adaptations from Exercise
What makes an athlete’s performance improve? Why do some individuals improve more rapidly than others? Traditionally, increases in athletic performance are thought to occur by building the musculoskeletal, cardiovascular, and respiratory systems as an adaptive response to training. Here, we identify the brain as a critical intermediate in this process. We show that exercise changes the anatomical, physiological, and functional properties of a neuron population in the hypothalamus that is activated by exercise. We find that exercise “builds up” the excitability of these neurons, making them “stronger” with each training session. This increase in brain activity correlates with improvements in exercise performance. Blocking the activity of these hypothalamic “exercise circuits” prevents the musculoskeletal, metabolic, and endurance gains that normally occur with training while increasing the activity of these neurons after exercise essentially creates “super-mice” capable of running more than double the speed and distance of their peers!
About Dr. Betley
Nick studies how the brain and body interact to shape behavior. He began his research career as an undergraduate studying the signals and molecules that establish cell identity during development, work that led to a broader interest in how molecular programs guide nervous system assembly. At Columbia University, he investigated how neurons form connections and assemble into circuits. He later moved to Janelia Research Campus, where he worked with Scott Sternson to study the neural circuits that control feeding behavior. Since joining the University of Pennsylvania in 2015, Nick has focused on how the brain guides behavior in a changing world. Over the last decade, his lab has expanded from studying how hunger influences behavior to exploring how reciprocal signaling between the body and brain shapes behavior, with a current emphasis on how habits such as exercise alter the brain and affect behavior, health, and wellness.
Karim Bouzakri, Ph.D.
How Myokines Can Affect Beta Cell Function
Recently we have demonstrated that factors secreted from type II muscle fibers (glycolytic) and regulated by physical exercise, called myokines, have the potential to influence the physiological processes of distant organs and particularly the pancreas. Our work shows that specific myokine can improve human islets function and survival and protect them from hypoxia and inflammation.
About Dr. Bouzakri
Dr. Bouzakri received his Ph.D. at the University of Lyon, studying insulin signalling in Type 2 diabetes with Dr. Vidal. In 2004 he joined the group of Dr. Juleen Zierath at the Karolinska Institute in Stockholm, where he spent 2 years as postdoctoral Fellow. Dr. Bouzakri decided to join the European Center for the Study of Diabetes chaired by Dr. Michel Pinget in Strasbourg. There, Dr. Bouzakri was able to show that previously identified myokines may have the potential to prevent disease progression in rodent models of induced Type 2 diabetes. Dr. Bouzakri founded Ilonov in 2020 which have been selected by the very selective BaselLaunch program and became an international company based in Basel, Switzerland.
Nicholas Broskey, Ph.D.
Effect of Maternal Exercise on Infant Whole-body and Cellular Metabolism
Lifestyle interventions, such as exercise, during pregnancy have been shown to improve offspring metabolism; however, human translational studies are lacking. This presentation will explore changes in infant whole-body outcomes as well as cellular mechanisms, using human umbilical-cord mesenchymal stem cells, of how maternal exercise improves the metabolism of infants. The presentation will particularly emphasize maternal exercise as a viable strategy to offset the intergenerational risk of obesity.
About Dr. Broskey
Dr. Nicholas Broskey is an Associate Professor in the Department of Kinesiology at East Carolina University and serves as the interim Director of the East Carolina Diabetes & Obesity Institute. He conducts human translational research with a focus on skeletal muscle physiology and the integration of whole-body and cellular metabolism. Particularly, Dr. Broskey is interested in the role of mitochondria in health and disease and how exercise interventions can help ameliorate conditions of metabolic disease through changes in mitochondrial bioenergetics. His research skillset spans biochemistry, exercise physiology, and mitochondrial bioenergetics, with additional training in conducting pregnancy research and exploring the link between maternal and infant health.
We are leveraging insights from our studies on aerobic exercise and arterial aging to better understand mechanisms that preserve arterial health. Aerobic exercise promotes arterial resilience through enhanced nitric oxide bioavailability, reduced oxidative stress, and improved mitochondrial function—pathways often disrupted by cancer therapies. By identifying the molecular and functional adaptations induced by aerobic exercise in aging arteries, we aim to translate these protective mechanisms into therapeutic strategies for oncology patients who experience premature arterial aging following chemotherapy. Ultimately, this approach seeks to mitigate cardiovascular complications and improve long-term vascular health in cancer survivors.
About Dr. Clayton
I am a translational vascular physiologist focused on understanding the mechanisms that drive vascular dysfunction during normal aging and in populations experiencing premature aging, such as cancer survivors. By identifying these underlying mechanisms, our goal is to uncover therapeutic targets that can be "aimed" at with pharmacological treatments and/or lifestyle interventions (e.g., aerobic exercise). We consider aerobic exercise the gold standard for improving vascular health and are particularly interested in uncovering how it exerts its beneficial effects. We believe that insights from this work can guide the development of pharmacological therapies, especially for individuals who are unable to engage in regular exercise training.
Fernanda De Felice, Ph.D.
Unveiling the Role of FNDC5/irisin and Exercise in Alzheimer’s Disease
The development of effective therapeutic strategies for Alzheimer`s disease (AD) must take into consideration the ample spectrum of this disease, which has been associated with changes in a wide range of networks including defective hormonal signaling. We are investigating the neuroprotective role of FNDC5/irisin, a hormone produced by the muscle upon exercise, in the context of AD. FNDC5/irisin corrects synapse and memory defects in AD mouse models and was found to mediate the beneficial effects of exercise in memory in mice. Our study indicates the existence of an interesting muscle-brain axis.
About Dr. De Felice
Fernanda De Felice is a Professor at the Center for Neurosciences Studies & Departments of Biomedical and Molecular Sciences at Queen’s University, Canada. In 2024 De Felice has been nominated Tier 1 Canada Research Chair in Brain Resilience. She further holds a position at the Federal University of Rio de Janeiro and at IDOR, Brazil. De Felice has been investigating Alzheimer’s disease (AD) and its intersection with hormones and physical exercise. De Felice conducted seminal work on the mechanisms leading to defective hormonal signaling in Alzheimer’s disease. Her studies, along with clinical observations, have contribute to understand how neuronal dysfunction occurs in the brains of AD patients and are contributing to comprehend how lifestyle interventions, in particular physical exercise, have the potential to preserve brain health and prevent or delay AD. De Felice is a fellow of the John Simon Guggenheim Memorial Foundation. She serves as Senior Editor of Neuropharmacology and is Associate Editor of Alzheimer’s & Dementia.
Human skeletal muscle displays remarkable cellular heterogeneity that extends beyond traditional myosin heavy chain–based fiber classification. By integrating single-fiber transcriptomic and proteomic profiling with single-cell analyses, we reveal multidimensional variation among myofibers in metabolic and regulatory programs. Muscle contractions elicit fiber-specific transcriptional responses that may radiate from recruited to non-recruited fibers. Cellular deconstruction of the muscle microenvironment uncovers an exercise-induced histaminergic signaling axis mediated by mast cells. Together, these findings redefine cellular heterogeneity in skeletal muscle and reveal novel intercellular mechanisms underpinning exercise-induced muscle adaptation.
About Dr. Derave
Wim Derave is a full professor at the Department of Movement and Sports Sciences at Ghent University (Belgium), where he teaches and leads a dynamic research team in exercise physiology, sport nutrition and muscle metabolism. Since 2005, Wim established his own laboratory in Ghent, which has taken a lead in the research regarding beta-alanine supplementation and the role of carnosine in skeletal muscle, both with respect to sport as to chronic metabolic diseases. An emerging research topic of his group relates to the development of an MRI-based - thus non-invasive - evaluation of muscle fiber type composition, and its applications towards sports and health. In 2017, Wim spent a 6-month sabbatical at the Gold Coast (Australia) as a visiting professor of Griffith University. Wim Derave has authored more than 200 peer-reviewed international scientific publications.
All life on Earth evolved with temporal pressures. Circadian clocks respond to these pressures by maintaining 24h biological schedules in the body. Modern technologies, such as artificial light at night, enable human activity to transcend the natural day-night cycle. However, this challenges circadian clocks and leads to metabolic dysfunction. In healthcare shift workers, we dissect the impacts of temporally uncoupling human activities, such as meals, sleep, and exercise, from the day-night cycle on aspects of metabolism and physiology.
About Dr. Erickson
Dr. Erickson is a young investigator at the Translational Research Institute, which is part of AdventHealth in Orlando, Fl. Her broad research interest is understanding the role of exercise in the prevention and treatment of metabolic disease. She specifically focuses on how circadian-related mechanisms modify physiology and metabolism in humans, which applications to shiftwork. Erickson received doctoral training in exercise physiology from the University of Georgia, followed by postdoctoral fellowships in metabolism and obesity at the Cleveland Clinic and Pennington Biomedical Research Center.
Zhenji Gan, Ph.D.
Skeletal Muscle Mitochondrial Remodeling in Exercise and Diseases
Skeletal muscle exhibits remarkable metabolic plasticity, with mitochondria playing a central role in adapting to energy demands during exercise. My talk will focus on the pivotal regulatory role of mitochondria in skeletal muscle: (1) the elucidation of new mitochondrial sensing mechanisms that regulate skeletal muscle remodeling in response to exercise or muscle disuse; (2) the discovery that skeletal muscle fiber transformation and remodeling are determined by mitochondrial function; and (3) the identification of mitochondrial quality control in skeletal muscle as a critical mechanism regulating the crosstalk between muscle and other organs, offering new insights into the regulation of systemic energy homeostasis.
About Dr. Gan
Zhenji Gan, Ph.D., is a Professor at the Model Animal Research Center, Medical School of Nanjing University. His research focuses on mitochondrial biology and skeletal muscle metabolism, with particular emphasis on how mitochondrial regulation impacts exercise adaptation and metabolic disease. He has published extensively in leading journals such as Nature Cell Biology, Science Translational Medicine, Journal of Clinical Investigation, Nature Communications, Science Advances, and PNAS, and is a recipient of China’s National Distinguished Young Scholar award. His laboratory aims to uncover novel molecular mechanisms underlying muscle function and systemic energy homeostasis.
Brian Glancy, Ph.D.
Sustaining Power: Building Energy Networks in Striated Muscle
Skeletal muscle is the most abundant tissue in humans and faces near instantaneous changes in demand for force production lasting from seconds to minutes to hours. Initiating and maintaining muscle contraction requires rapid, coordinated movement of signals and material within and among various structures located throughout the relatively large muscle cell. This talk will focus on how energy is distributed throughout striated muscle cells to sustain muscle contractions, deficits in which have been implicated in many pathologies including diabetes and muscular dystrophy as well as aging. In particular, I will discuss how the structure and function of the cellular energy distribution system are optimized as part of the integrated muscle cell to maintain energy homeostasis during the large change in energy demand caused by the onset of muscle contraction.
About Dr. Glancy
Brian Glancy graduated with a B.A. in Sport Science from the University of the Pacific prior to receiving a Master’s degree in Kinesiology and a Ph.D. in Exercise Science from Arizona State University working with Wayne Willis. He was a postdoctoral fellow with Robert Balaban at the National Heart, Lung, and Blood Institute from 2009 to 2016. Dr. Glancy became an Earl Stadtman Investigator at the NIH with a dual appointment between NHLBI and NIAMS in 2016 and became a tenured Senior Investigator in 2023. He is a member of the American College of Sports Medicine and the American Physiological Society.
Bret Goodpaster, Ph.D.
Molecular Transducers Orchestrate the Physiological Responses to Acute Exercise
The dramatic increase in energy demand by cardiac and skeletal muscle during an acute bout of exercise require an orchestrated response across many cells, tissues, and organs. This inter-organ crosstalk, aka exercise physiology, requires inter-cellular and inter-organ coordination to acutely alter blood flow and increase energy supply, and to prepare the body for the next bout of exercise, i.e., training responses. We present novel data from the Molecular Transducers of Physical Activity Consortium (MoTrPAC) to highlight these responses and adaptations to both endurance and resistance exercise.
About Dr. Goodpaster
Dr. Goodpaster’s primary research is in the pathophysiology of obesity, insulin resistance, diabetes, and aging, and to help decipher biological mechanisms underlying the health benefits of exercise. He has received a number of awards and honors for his work, including the Nathan Shock Award from the National Institute of Aging in 2008, for his work investigating the role of muscle fat infiltration in aging and muscle quality. He is particularly well known for “the athlete’s paradox” which has shifted the paradigm in Type 2 diabetes research to investigate, how and why does fat accumulation in muscle cause insulin resistance in some subjects but not others? He currently serves as a PI on the Molecular Transducers of Physical Activity Consortium (MoTrPAC). Dr. Goodpaster obtained a B.S. in Biology from Purdue, and after completing a Pre-doctoral Fellowship at Maastricht University in the Netherlands, received his Ph.D. in Human Bioenergetics from Ball State University in 1995.
Laurie Goodyear, Ph.D.
Exercise-Induced Adaptations to Adipose Tissue and the Regulation of Systemic Metabolism
Exercise training has beneficial effects of systemic metabolism, and recent data suggest that adaptations to adipose tissue play a critical role in these responses. This presentation will discuss molecular adaptations that occur in adipose tissue in response to exercise training, including studies in mice, rats, and humans. Omics data on training effects on adipose tissue will be discussed, as will sex differences in the training response.
About Dr. Goodyear
Laurie Goodyear is a Senior Investigator at the Joslin Diabetes Center and Professor of Medicine at Harvard Medical School. She holds several positions at Joslin Diabetes Center, including Co-Head of the Section on Integrative Physiology and Metabolism, Director the Fellowship Committee, Director of the Animal Physiology Core and founder and director of the Human Exercise Physiology Research Laboratory at Joslin. The long-standing goal of the Goodyear laboratory is to elucidate the molecular basis for the benefits of exercise on health. Regular physical activity can have a plethora of beneficial effects including improved glycemic control, improved lipid profiles, and reduced rates of cardiovascular disease, Alzheimer’s disease, and other complications. The importance of exercise therefore cannot be understated, especially in people with obesity and type 2 diabetes. Her group has been at the forefront of basic and translational research aimed at determining mechanisms for many of these important effects of exercise, publishing more than 200 primary papers and reviews investigating cell systems, rodent models, and human subjects.
Danny Green, Ph.D.
Do We Need a Box Warning for Incretin Agonists: Must Be Taken with Resistance Exercise?
The optimal intervention for health benefit in overweight and obesity would induce a sustained decrease in fat mass, whilst maintaining or increasing lean body mass, strength, fitness and cardiovascular health. Incretin therapies show exceptional promise in decreasing fat mass, but also decrease lean mass, possibly predisposing some individuals to accelerated age-related sarcopenia and frailty. This talk will address the potentially critical adjuvant role of exercise, particularly resistance training, during and after incretin therapy, alongside presentation of initial findings of the Tirzepatide and Resistnce Exercise (TREx) trial.
About Dr. Green
Danny, a Winthrop Professor in the School of Human Sciences (Sport and Exercise Science) at The University of Western Australia, is a cardiovascular exercise physiologist specializing in chronic disease prevention. His research spans all ages, from preventing atherosclerosis in obese youth to optimizing exercise and medication for heart disease, stroke, diabetes and heart failure. He leads UWA’s Cardiovascular Research Group, which develops early disease detection and personalized prevention strategies through transdisciplinary collaborations in science, engineering, and medicine.
David Hood, Ph.D.
Effect of Exercise on the Regulation of Lysosome Biogenesis and Function in Muscle
Lysosomes are relatively ignored organelles in the skeletal muscle millieu, despite their important roles as cell signaling hubs, and in mediating dysfunctional cargo degradation. Lysosomes accumulate with age and in muscle disuse, but their function appears to diminish. In contrast, we have shown that the biogenesis of healthy lysosomes can occur in response to chronic exercise, and that this is regulated by transcription factors such as TFEB and TFE3. This talk will discuss the role of exercise in regulating lysosome content and function in muscle.
About Dr. Hood
Dr. Hood is a former 3-term NSERC Tier I Canada Research Chair in Cell Physiology and was the Founder of the Muscle Health Research Centre, the leading centre in Canada for the study of muscle health and disease. He has published >200 peer reviewed articles and is recognized internationally for his work on mitochondrial biogenesis and turnover. He has given 160 presentations both nationally and internationally and has directly supervised >200 trainees at the graduate, undergraduate and post-doctoral levels. He has been the recipient of numerous awards, including the Canadian Society for Exercise Physiology (CSEP) Honour Award (2010) and the Michel Sarrazin award from the Canadian Physiological Society (2025). In the last 5 years he has accrued more than $2M in research funding.
Physical activity and social engagement are both important factors for maintaining brain health in aging and dance is a form of physical activity that involves both. This talk will provide a brief overview of the literature on effects of dance on the brain. This will be followed by results from a trial using dance-based intervention groups to investigate the effects of adding movement and social engagement twice weekly for 12 weeks in dyads of older adults with mild cognitive impairment and early-stage dementia and their care partners. Future directions and opportunities will also be addressed.
About Dr. Hugenschmidt
Christina Hugenschmidt, Ph.D., is the Rebecca E. Shaw Professor and Director of the Memory Counseling Program and Associate Professor of Gerontology and Geriatric Medicine at Wake Forest University School of Medicine. She is a neuroscientist committed to research that maintains dignity and purpose for older adults across the range of physical and cognitive function they experience. Her research investigates how age-related changes in movement and metabolism interact with the brain and cognition, and the potential of lifestyle interventions to support healthy brain and body function in aging. Her work on arts and aging with her close collaborator and former Kennedy Center Citizen Artist Fellow Christina Soriano, MFA, MBA has led to community collaborations and unique outreach opportunities.
Lee Jones, Ph.D.
A Translational Approach to Understand How Exercise Influences Cancer Pathogenesis
There is significant interest in whether exercise can suppress the pathogenesis of cancer. In this talk, Dr. Jones will discuss current evidence on the exercise - anger pathogenesis link, focusing on recent phase 1-type trials evaluating the biological activity of exercise on normal and tumor tissue biomarkers in distant tissues including the breast, prostate, and colon. He will also overview how high resolution data collection in these trials have facilitated correlative investigation of exercise therapy via the adoption of a systems approach. Conduct of these trials and correlative science analysis has been facilitated by a digitized, decentralized, patient-centric approach.
About Dr. Jones
Lee Jones, Ph.D., is a Professor and Head of the Exercise-Oncology Program in the Beckman Research Institute of the City of Hope in Los Angeles. His academic career has focused on a translational approach to elucidating the effects and mechanisms of controlled exercise therapy on cancer pathogenesis. His team has leveraged large observational data sets to perform several novel analyses investigating the relationship between exercise and cancer incidence and prognosis. In related analyses, he has linked clinical annotation of exercise with tumor molecular characterization to examine whether the influence of exercise on cancer outcomes differs based on tumor features. In translation to the clinic, his team has published multiple landmark prospective clinical trials investigating the tolerability and safety of exercise therapy across the entire cancer trajectory (i.e., prevention to advanced disease). In close adherence with the team's translational framework for rigorous development of exercise therapy as an anticancer strategy, they have recently completed the first phase 1-type trials to evaluate the maximum feasibility (tolerability) and biological efficacy of exercise therapy in several oncology settings. The lab has also leveraged biospecimen collection in these trials to conduct correlative studies to elucidate the mechanistic underpinnings of exercise therapy via the adoption of a systems-levek approach.
William Kraus, M.D.
Drug Repurposing to Mimic the Effects of Exercise Training for Targeted Health Effects
As background, I will discuss how we have used three large clinical trials to understand the effects of exercise training mode, intensity and amount on insulin sensitivity and other components of the metabolic syndrome. Then, I will discuss how we have used an accompanying biorepository to develop multi-omic platforms to understand mechanisms for these responses and to identify molecular targets for drug repurposing mimicking the health effects of exercise training.
About Dr. Kraus
William E. Kraus, M.D., is Professor of Medicine, Division of Cardiology, Duke University School of Medicine. His research is focused on understanding cellular signaling pathways and mechanisms responsible for the adaptive responses of skeletal muscle to normal physiologic stimuli - such as exercise training - and to maladaptive responses to pathophysiologic stimuli - such as in congestive heart failure, skeletal muscle atrophy associated with chronic spaceflight and aging. As such he uses immunohistochemistry, fiber typing, muscle enzymology, muscle primary cell culture from humans and various molecular biological methods (genetics, gene expression profiling, and metabolic profiling) to understand the mechanisms underlying human skeletal muscle adaptation to disease and exercise training and the interactions thereof. We are using these techniques to identify molecular targets in skeletal muscle for which we might identify developed drugs to repurpose for reproducing some of the health benefits of exercise training for those that cannot or will not participate in regular exercise.
Kent Langston, Ph.D.
Causes and Consequences of Physiological Inflammation in Skeletal Muscle
We previously demonstrated that appropriate regulation of physiological inflammation by regulatory T cells (Tregs) is required for the muscle-specific and organism-level metabolic adaptations and improved performance typical of exercise training. But why does exercise induce muscle inflammation at all? This talk will highlight our recent work uncovering mechanical stress as a key driver of physiological inflammation in skeletal muscle.
About Dr. Langstson
Dr. Langston is an Assistant Professor of Pathology at Yale School of Medicine and a member of the Yale Center for Research on Aging (Y-Age). He received his Ph.D. from Harvard University for his work in Dr. Tiffany Horng's laboratory on metabolic regulation of macrophage activation and tolerance. He completed his postdoctoral training with Drs. Diane Mathis and Christophe Benoist in the Department of Immunology at Harvard Medical School. At Yale, the Langston laboratory is further defining the cellular and molecular features of exercise-induced inflammatory responses in youth and during aging – an endeavor that is partly supported by an NIA/NIH K22 award – with an emphasis on elucidating how non-parenchymal cells sense exercise and regulate its benefits. An ultimate goal of this work is to design exercise-inspired interventions to combat modern afflictions associated with chronic inflammation, improve regeneration and performance after injury, reduce the pathology of musculoskeletal diseases, and combat age-related frailty (i.e., increase healthspan).
About Dr. Larsen
Steen Larsen is an Associate Professor at the University of Copenhagen, specializing in mitochondrial biology. His work investigates how physical activity modulates mitochondrial function and how various drugs influence mitochondrial health. His research, primarily conducted in humans, aims to uncover mechanisms that could lead to improved treatments for metabolic diseases and enhanced physical performance. He is also affiliated as a guest Professor at the Medical University in Bialystok, Poland. He has been publishing more than 130 scientific papers in peer-reviewed journals.
Brian McDonagh Ph.D.
Exercise-induced Mitochondrial Remodelling: Insights from the Model Organism C. elegans
- Excercise generates endogenous ROS required for the adaptive response to exercise.
- Exercise induced redox signalling promotes mitochondrial ER contact site assembly required for changes in mitochondrial dynamics.
- Aging and loss of dedicated peroxidases Peroxiredoxins results in disrupted mitochondrial fusion.
- Peroxiredoxins play a key role in exercise induced redox signalling that is blunted with age.
About Dr. McDonagh
Brian is a lecturer in the Discipline of Physiology at the University of Galway, Ireland and previously worked as a lecturer in Musculoskeletal Biology at the University of Liverpool. He has extensive experience in the analysis and handling of large data “omic” experiments from a variety of different platforms including proteomics, RNA-Seq and ribosomal profiling. His research interests include understanding the adaptive response to exercise and ageing in skeletal muscle. In particular he is trying to understand the redox dependent cellular signalling pathways that regulate mitochondrial dynamics including the assembly of mitochondrial ER contact sites (MERCS). MERCS assembly is promoted during exercise but disrupted in a number of age-related conditions leading to disturbed intracellular homeostasis. Currently the research group are using a number of approaches to target MERCS assembly including exercise, selective microRNAs and targeting the ER stress response using the nematode C. elegans, animal and cell models.
Benjamin Miller, Ph.D.
Context Specificity of Metformin Treatment on Mitochondrial Energetics and Healthspan (There and Back Again)
We previously showed that metformin blunted the positive effects of exercise training in human subjects. We hypothesized that the effects of metformin are likely dependent on mitochondrial energetics. This talk highlights the translation and reverse translation of our findings exploring exercise and metformin interactions.
About Dr. Miller
Dr. Miller received a Ph.D. from UC-Berkeley and completed a post-doc at the Muscle Research Center in Copenhagen, Denmark. In 2018, he moved from Colorado State University to the Aging and Metabolism Research Program at the Oklahoma Medical Research Foundation (OMRF). Dr. Miller’s expertise is in skeletal muscle, aging, mitochondria, stable isotope labeling, proteostasis and drug and lifestyle (primarily exercise) interventions. His work with tracers and in muscle aging is nationally recognized and has led to many collaborations, extensive mentoring, and leadership positions. Dr. Miller’s work is almost exclusively focused on prolonging the period spent in good health (i.e., healthspan) by targeting mitochondrial energetics and proteostatic maintenance. The Miller lab is truly translational in that the studies span from pre-clinical models to clinical trials and back. The Miller lab has focused on training the next generation of scientists and many from the lab have gone on to their own exceptional careers.
Jill Morris, Ph.D.
Importance of the Acute Exercise Response and Brain Health
It is important to understand the acute physiological changes that occur in response to exercise that are relevant to brain health outcomes. Each bout of exercise triggers changes in biomarkers that may be directly relevant to the long-term health outcomes in exercise interventions. However, these acute responses have not been well-explored in older adults, especially those with cognitive impairment, or within the context of risk factors for cognitive decline. This talk will explore key aspects of the acute exercise response that are important for the design and interpretation of current and ongoing clinical trials.
About Dr. Morris
Dr. Morris is an Associate Professor in the Department of Neurology at the University of Kansas Medical Center. She Co-Directs the KU Alzheimer’s Disease Research Center Biomarker Core and serves as Director of the KU Alzheimer’s Disease Research Center Developmental Projects Program. Dr. Morris’ research is focused on relationship between systemic and brain energy metabolism and Alzheimer's Disease. Her lab leverages translational approaches including cell models, blood based biomarkers, and neuroimaging and she has led multiple NIH funded clinical trials focused on exercise, metabolism, and brain health.
Kevin Murach, Ph.D.
The Age-Dependent Multi-Omic Myonuclear Response to a Skeletal Muscle Hypertrophic Stimulus
A detailed analysis of how muscle fiber nuclei (myonuclei) respond to a hypertrophic stimulus would provide a critical step toward understanding age-dependent skeletal muscle plasticity. To this end, we used recombination-independent doxycycline-inducible myonucleus-specific fluorescent labelling, bulk RNA-sequencing, myonuclear DNA methylation analysis, multi-omic integration, and single myonucleus RNA-sequencing to define the molecular characteristics of adult (6-8 month) and aged (24 month) murine skeletal muscle after an acute mechanical overload (MOV) stimulus. These data provide a roadmap for uncovering molecular targets through which aged muscle adaptability may be enhanced.
About Dr. Murach
Kevin A. Murach, Ph.D., received his undergraduate degree from the University of North Carolina at Chapel Hill, completed a master’s degree in Exercise Physiology at James Madison University in Harrisonburg, Virginia, then earned his Ph.D. in Human Bioenergetics from the Ball State Human Performance Laboratory in Muncie, Indiana. His dissertation was a collaboration with NASA aimed at optimizing the exercise prescription for astronauts on the International Space Station. Dr. Murach spent six years as a post-doctoral fellow/scholar studying muscle stem cells at the University of Kentucky Center for Muscle Biology in Lexington. He now is an Associate Professor at the University of Arkansas and PI of the Molecular Muscle Mass Regulation (M3R) Laboratory. His current research uses human muscle samples, primary cell culture, genetically modified mouse models, omics, and computation to understand the molecular cues that drive exercise adaptations and aging, and the interaction between the two.
Darrell Neufer, Ph.D.
The Quest to Measure Mitochondrial Efficiency
Mitochondrial respiration accounts for ~25% of basal metabolic rate and ~90% of ATP produced in cells. It therefore stands to reason that the efficiency at which the massive energy conversions that occur in mitochondria, and are potentially regulated, could be a major determinant of overall metabolic rate and efficiency. However, directly quantifying mitochondrial bioenergetic efficiency has been a technical challenge for more than 60 years. A novel approach will be presented that recapitulates the counterbalanced interplay among the three thermodynamic free energies that is necessary to detect potential differences in bioenergetic efficiency. Data will be presented showing that mitochondrial bioenergetic efficiency undergoes remarkable adaptative changes in response to persistent changes in energy balance.
About Dr. Neufer
Dr. Neufer is Professor and Chief, Section of Molecular Medicine, Departments of Internal Medicine and Biochemistry, and the Associate Director of the Cardiometabolic Center of Excellence, Wake Forest University School of Medicine. For more than 40 years, Dr. Neufer’s research career has integrated exercise physiology, molecular biology, metabolism, and mitochondrial bioenergetics. His lab is currently focused on deciphering the mechanisms controlling mitochondrial function under normal and metabolically compromised or stressed states, and determining how altered mitochondrial function in turn contributes to, or counterbalances against, the etiology and/or pathology of diseases related to metabolism.
Weijun Qian, Ph.D.
Integrative Profiling of Proteome and Multiple Post-Translational Modifications
This presentation will provide an overview of major regulatory posttranslational modifications (PTMs), including redox modifications, phosphorylation, acetylation, and ubiquitination, as well as current strategies for integrative profiling of the proteome and multiple PTMs from the same biological samples. Emerging approaches in single-cell and spatial proteomics will be discussed in the context of disease applications. Finally, biological applications, particularly those relevant to exercise physiology, along with integrative data analysis will be highlighted.
About Dr. Qian
Wei-Jun Qian is a Bioanalytical Chemist and a Laboratory Fellow within the Translational Omics group, Biological Sciences Division, at Pacific Northwest National Laboratory (PNNL). He receives a B.S. in Chemistry from Nanjing University, China, and a Ph.D. in Bioanalytical Chemistry from University of Florida. Dr. Qian has devoted much of his career in the development and application of advanced mass spectrometry-based proteomics to quantify protein abundances and post-translational modifications in the context of biomedical applications. He is particularly recognized for his work in redox biology, focusing on thiol-based modifications, and his efforts to apply advanced omics techniques to study complex diseases such as type 1 diabetes and pancreatic islet dysfunction. Dr. Qian has recognized for several prestigious honors, including the Presidential Early Career Award for Scientists and Engineers (PECASE) Award.
Blake Rasmussen, Ph.D.
The Impact of Physical Activity on the Human Skeletal Muscle Metabolome and Mitochondrial Function in Older Adults
Aging and physical activity significantly alter human skeletal muscle metabolism. Using a multi-omic approach, along with single nucleus RNA sequencing, we highlight the specific skeletal muscle changes in the metabolome, mitochondrial function, inflammation, and protein synthesis following 7 days of disuse atrophy in late midlife adults. We also present data showing the beneficial muscle metabolic and cellular adaptations following 12 weeks of resistance exercise training in older adults.
About Dr. Rasmussen
Dr. Rasmussen’s research is in the area of muscle, metabolic and exercise physiology. Over the past 25 years, he has been the Director of the NIH-funded Skeletal Muscle Biology Lab, published more than 150 papers, and has trained several PhD students and postdoctoral fellows. Dr. Rasmussen recently moved to UT Health San Antonio as Professor & Chair of the Department of Cellular & Integrative Physiology where he is the Leader of the Molecular Phenotyping Resource Core for the San Antonio Pepper Center and Co-Leader of the San Antonio Nathan Shock Center GeroMetabolism Core. His research focuses on uncovering the basic mechanisms regulating muscle growth and loss in humans and animal models and unraveling the cellular mechanisms responsible for how exercise, physical inactivity and nutrients impact muscle protein and cellular metabolism across the lifespan. More recently the lab has expanded into multi-omic analyses of different tissues and the effects of disuse on mitochondrial dysfunction in skeletal muscle.
Richard Simpson, Ph.D.
Exercise-mobilized Immune Cells: A Novel Cell Source for Cancer Immunotherapy
Acute bouts of exercise mobilize highly differentiated effector lymphocytes into circulation through catecholamine- and β₂-adrenergic receptor–dependent pathways. These mobilized immune cells display phenotypic and transcriptomic signatures indicative of enhanced cytotoxicity and immune surveillance. We have demonstrated that immune and therapeutic cell products manufactured from exercise-mobilized donors exhibit superior anti-tumor activity against hematologic malignancies, particularly when combined with monoclonal antibodies or bispecific T-cell engagers. Collectively, this work highlights the potential of exercise as an important adjunctive strategy to improve the efficacy of cancer immunotherapies.
About Dr. Simpson
I am a full professor in the School of Nutritional Sciences and Wellness (College of Agriculture and Life Sciences) at the University of Arizona and hold joint appointments in Pediatrics (College of Medicine), Immunobiology (College of Medicine), the Arizona Cancer Center and the Bio5 Institute. I also hold the Gouri Bhattacharya Endowed Chair in Pediatric Cancer in the Steele Children’s Research Center at The University of Arizona. My research interests are concerned with the effects of exercise, stress and aging on the immune system, and how exercise can mitigate diseases such as cancer through its immune-modulating effects. Major focus areas include understanding (1) how exercise-induced adrenergic activation mobilizes immune cells that can be harvested for cancer therapy; (2) how exercise and other behavioral interventions can offset age-related decrements in the normal functioning of the immune system (immunosenescence), (3) the interplay between the immune and neuroendocrine system during high level human performance and extreme isolation (e.g. space travel), and (4) how persistent virus infections such as cytomegalovirus (CMV) can alter the phenotype and function of T-cells and NK-cells to protect the host from certain hematological malignancies.
Proper coordination between fetal muscle and bone development is essential for healthy locomotor function, yet the mechanisms by which mitochondrial dysfunction disrupts this process remain unclear. We found that mitochondrial POLG mutations markedly impair fetal osteogenesis, accompanied by widespread transcriptional defects in cytoskeletal organization, muscle proliferation, and energy metabolism. Maternal exercise significantly restored fetal bone homeostasis through activation of the apelin-APJ signaling pathway, effects that were diminished in APJ knockdown fetuses. Mechanistically, maternal exercise enhanced ATF4 activation and its interaction with RUNX2, promoting osteogenic differentiation in POLG-mutant offspring. These findings highlight a previously unrecognized muscle-to-bone endocrine axis through which maternal exercise counteracts mitochondrial mutation induced skeletal deficits.
About Dr. Son
Dr. Jun Seok Son received his Ph.D. in Nutrigenomics and Growth Biology from Washington State University in 2020, followed by a Post-Doctoral Research Associate appointment at Washington State University. He joined the University of Maryland School of Medicine in 2021 as an Assistant Professor in the Department of Obstetrics, Gynecology and Reproductive Sciences, where he leads the Perinatal Exercise Genomics Laboratory and directs the Mouse Metabolic Research Core (MMRC). He also holds a secondary appointment as Assistant Professor in the Department of Physiology. Dr. Son’s research investigates how maternal exercise, obesity, and related physiological environments shape fetal development and long-term offspring health. His work focuses on nutrient and metabolite driven epigenetic regulation of stem and progenitor cell fate, particularly the differentiation of myogenic and adipogenic lineages. By integrating multi-omics, mitochondrial genetics, and developmental physiology, his team aims to uncover mechanistic pathways that can be leveraged to improve metabolic outcomes across generations. Ultimately, his goal is to translate these insights into clinical strategies that enhance the health of mothers and children affected by obesity and metabolic dysfunction.
Paul Titchenell, Ph.D.
Activin Pathway Modulation and Quality Weight Loss
Modulation of the activin signaling pathway has emerged as a promising strategy to enhance muscle mass while promoting weight loss, addressing key challenges in obesity and metabolic disease management. Preclinical studies have demonstrated that targeting activin receptors leads to significant improvements in lean mass and metabolic health, even under conditions of caloric restriction or pharmacologic weight loss. Recent clinical data further support the translational potential of this approach, showing favorable effects on body composition and metabolic biomarkers in obese individuals. These data will be discussed during the presentation.
About Dr. Titchenell
Paul Titchenell is currently Executive Director - Head of Metabolic Physiology at Eli Lilly and Company. Dr. Titchenell is recognized for his work on insulin signaling, hepatic metabolism, and metabolic diseases such as obesity and type 2 diabetes. He earned a Ph.D. in Physiology from Penn State University and completed postdoctoral training at the Perelman School of Medicine at the University of Pennsylvania, where he later became a tenured Associate Professor and Director of the Rodent Metabolic Phenotyping Center. His research has focused on the underlying mechanisms of insulin resistance and metabolic regulation in liver, adipose tissue, and muscle. After more than a decade in academia, he recently transitioned to big pharma, where he is focused on translating scientific discoveries into new therapies for cardiometabolic disease.
Signe Torekov, Ph.D.
Healthy Weight Throughout Life (Impact of Exercise on Muscle Wasting in Obesity Therapy)
Sustaining a healthy weight across the lifespan requires interventions that integrate biological, behavioral, and environmental dimensions. Our translational research provides evidence for safe, effective, and personalized strategies that promote fat loss while preserving muscle mass, thereby supporting lifelong metabolic health and sustainable obesity treatment outcomes.
About Dr. Torekov
Professor Signe Sørensen Torekov is a leading researcher in obesity and metabolism at the University of Copenhagen. She leads the Clinical Translational Metabolism Group, studying how exercise, diet, and pharmacological treatment can help people achieve and maintain a healthy weight. Her discoveries have influenced clinical practice and international guidelines, offering new approaches to obesity treatment. Featured in The Washington Post and Danish national TV, she is an award-winning scientist, international speaker, and trusted advisor dedicated to improving health through science.
Saul Villeda, Ph.D.
Systemic Mechanisms of Exercise-induced Brain Rejuvenation
Aging drives cellular and cognitive impairments in the adult brain. It is imperative to gain mechanistic insight into what drives aging phenotypes in the brain in order to maintain, and even restore, functional integrity in the elderly. We, and others, have shown that systemic manipulations – including exercise and administration of exercise induced blood factors (exerkines) - can reverse age-related impairments in regenerative, synaptic and inflammatory processes, as well as rescue cognitive faculties in the aged brain. These studies have revealed a series of body-brain axis that mediate the influence of the systemic environment indicating tissue specific exerkines can have broad rejuvenating effect on the aging brain. Despite this potential, much is unknown as to the molecular mechanisms regulating pro-youthful effects of blood-borne exercise induced factors. I will discuss work from my research group that begins to provide mechanistic insight into the systemic and molecular drivers promoting rejuvenation in the aging brain.
About Dr. Villeda
Dr. Saul Villeda is an Associate Professor in the Department of Anatomy and Endowed Chair in Biomedical Science at the University of California San Francisco and serves as Associate Director of the Bakar Aging Research Institute. He obtained his B.S. degree from the University of California Los Angeles, his PhD degree in Neuroscience from Stanford University, and started his independent career at the University of California San Francisco as a Sandler Fellow. Dr. Villeda has made the exciting discovery that the aging process in the brain can be reversed by altering levels of circulating factors in blood. Dr. Villeda’s research is best known for the use of innovative heterochronic parabiosis and blood plasma administration approaches to investigate the influence that exposure to young blood-derived or exercise-induced circulating factors has in promoting molecular and cellular changes underlying cognitive rejuvenation. His work has garnered accolades that include a National Institutes of Health Director’s Independence Award, the W.M. Keck Foundation Medical Research Award, the Glenn Award for Research in Biological Mechanisms of Aging, and the McKnight Innovator Award in Cognitive Aging.
Seung-Hee Yoo, Ph.D.
Fbxl21 Regulates Circadian Proteostasis and Stress Response Via Degradation of Dnajb6 and Its Client Proteins
Circadian regulation of proteostasis, a key determinant of muscle health, remains largely unknown. Here, we identified DNAJB6, an Hsp40 (DnaJ) co-chaperone, as a novel substrate of the circadian E3 ligase FBXL21. FBXL21 mediated the ubiquitination-dependent proteasomal degradation of both DNAJB6 and its client proteins including Desmin; causative mutations of DNAJB6 in myopathies, however, rendered resistance to FBXL21-directed degradation. Fbxl21 KO C2C12 cells displayed aberrant accumulation of Desmin, and showed aggravated cytoplasmic accumulation of TDP-43, another DNAJB6 client protein, in response to heat shock stress. Under circadian-timed exercise as a physiological stressor, WT mice displayed a robust diurnal rhythm in G3BP1+/FUS+ stress granule formation and TDP-43 accumulation as a function of exercise timing. In contrast, the Fbxl21 hypomorph Psttm mutant mice showed elevated stress granules and TDP-43 without exercise, which was exacerbated under exercise-induced stress conditions; these abnormalities were rescued by skeletal muscle-specific FBXL21 expression. Our study elucidates a novel circadian regulatory mechanism of skeletal muscle proteostasis via FBXL21 as a chaperone-linked E3 ligase, highlighting the FBXL21-DNAJB6 axis as a potential therapeutic target for myopathies.
About Dr. Yoo
My research interest is understanding the function and mechanism of circadian clocks at levels from genes to behavior. In response to daily environmental changes imposed by Earth’s rotation, almost all species, ranging from cyanobacteria to humans, have evolved physiological and behavioral rhythms, called circadian rhythms. The harmony between our intrinsic biological timing and the daily environmental oscillation is critical to physiological well-being; conversely, disrupted circadian rhythms have been shown to cause or increase the risk of various chronic diseases. My lab focus on delineating fundamental cellular mechanisms in circadian rhythms and also deciphering physiological and pathological roles of the clock. My long-term goal is to translate such fundamental mechanistic knowledge into new drug targets and therapeutic strategies for improved prevention and treatment of chronic diseases.
Exercise profoundly impacts skeletal muscle and systemic metabolism, yet the complex molecular mechanisms underlying these adaptations remain incompletely understood. Advanced omics technologies—including genomics, transcriptomics, proteomics, and metabolomics—are revolutionizing our ability to map exercise-induced changes at unprecedented resolution, revealing intricate networks that govern muscle function and metabolic remodeling. These insights are particularly relevant for type 2 diabetes, where exercise represents a powerful therapeutic intervention with highly variable individual responses. This talk will explore how integrating multi-omics data can advance our understanding of exercise biology and pave the way for personalized training strategies that optimize metabolic health outcomes.
About Dr. Zierath
Juleen R. Zierath is Professor of Clinical Integrative Physiology at Karolinska Institutet, Stockholm, and Professor and Executive Director at the Novo Nordisk Foundation Center for Basic Metabolic Research at University of Copenhagen. She is a member of the Nobel Assembly and Nobel Committee for Physiology or Medicine, the Royal Swedish Academy of Sciences, EMBO, Academia Europaea and the Keystone Symposia Board of Directors. She has received several awards, including the Diabetes Prize for Excellence awarded by EASD and Novo Nordisk Foundation for outstanding achievements in research, the Harold Rifkin Award for Distinguished International Service in the Cause of Diabetes from the American Diabetes Association, and a Distinguished Alumnus Award and Honorary Doctorate of Science from University of Wisconsin-River Falls. Zierath performs translational research to delineate mechanisms for Type 2 Diabetes pathogenesis. Her current work is focused on the interaction between circadian rhythms and exercise training and the control of metabolism in diabetes and obesity.