Scientific Programme
Sports and Exercise Medicine and Health
IS-MH06 - Diversity in mechanisms underlying impairments to exercise and recovery in Type 1 Diabetes.
Date: 03.07.2025, Time: 10:00 - 11:15, Session Room: Arco
Description
Despite insulin therapy, persons with Type 1 Diabetes (T1D) develop severe complications such as cardiovascular and renal disease; largely due to chronic dysglycemia, dyslipidemia and insulin resistance. These complications impact the quality of life and lifespan of those with T1D; estimated at 15 years less than those without T1D. Despite important advances in T1D care, there is still no cure. Given the importance of skeletal muscle and its associated microvasculture to whole-body well-being, research focused on improving our understanding of skeletal muscle health in those with T1D has the potential to create translatable, evidence-based exercise and pharmacological advances to improve the healthy lifespan of those with T1D. This proposed symposium has invited internationally recognized scientists who are leading world class research into the mechanisms underlying the development of diabetic myopathy and therapeutic strategies to mitigate this complex complication. The reputation of these researchers is highlighted below. The invited speakers will provide state of the art research on mechanisms underlying impairments to skeletal muscle health in T1D. This symposium will be attractive to all researchers interested in skeletal muscle biology, exercise physiology, diabetes, and tissue cross-talk. Keywords: diabetes, myopathy, extracellular matrix, mitochondria, muscle wasting, atrophy, inflammation, sex differences, metabolism
Chair(s)
Irena Rebalka
McMaster University, Pathology and Molecular Medicine
Canada
Speaker A
Sarah Lessard
Virginia Tech, Fralin Biomedical Research Institute
United States
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Mechanisms for impaired cardiorespiratory fitness in type 1 diabetes
Improved cardiorespiratory fitness is a key benefit of aerobic exercise training. However, individuals living with type 1 diabetes often display lower cardiorespiratory fitness (i.e. VO2max) than those without diabetes- even when exercise training levels are matched. This may indicate a resistance toward the positive metabolic and physiological adaptations that lead to improved cardiorespiratory fitness with aerobic training in people with diabetes. This presentation will outline the key clinical features of low cardiorespiratory fitness in type 1 diabetes. The potential role for chronic hyperglycemia in impaired aerobic adaptation will be discussed. In addition, hypothesized molecular mechanisms whereby chronic hyperglycemia may alter the structure and remodeling of skeletal muscle with exercise will be proposed. Specifically, the role of hyperglycemia-induced changes to the skeletal muscle extracellular matrix, and how these may alter muscle signal transduction and key muscle remodeling events with exercise will be discussed. Recent data from human participants and pre-clinical (animal and cell culture) models will be shown. Potential strategies to improve the cardiorespiratory response to exercise in people diabetes will also be considered.
Speaker B
Mauricio Krause
Federal University of Rio Grande do Sul, Physiology
Brazil
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Metabolic, inflammatory and oxidative stress responses to exercise in people with type 1 diabetes
Type 1 diabetes (T1D) is a chronically progressive autoimmune disease that affects approximately 1% of the population in the developed world. This adverse immune response is induced and promoted by the interaction of both genetic and environmental factors. Individuals with T1D shared several cardiometabolic complications such as endothelial dysfunction, changes in glomerular filtration/kidney function, low-grade inflammation, oxidative stress, blood coagulation, mitochondrial dysfunction, anabolic resistance, metabolic inflexibility, and gut microbiota dysbiosis. The treatment of these conditions and the management of glucose balance includes pharmacological, and particularly, changes in lifestyle such as exercise and nutritional interventions. Exercise is the most effective non-pharmacological tool to prevent and treat cardiometabolic diseases related to both types of diabetes. A large body of evidence has shown that the combination of resistance and aerobic exercise can improve glycemic control, metabolism, oxidative stress, inflammation, and skeletal muscle anabolic adaptations in T1D people. Despite the negative adaptations caused by T1D in the skeletal muscle (e.g., mitochondrial dysfunction, inflammation, and regeneration), exercise training can decrease glucose fluctuations, the occurrence of hypoglycemia, and improve skeletal muscle dysfunction. In this presentation, we aim to present evidence that different types of exercise can improve inflammatory status and oxidative stress, thus causing positive metabolic adaptations in mitochondrial function, insulin sensitivity, and glycemia management. In addition, we will also discuss the potential underlying mechanisms that allow exercise to reduce inflammatory-related complications in T1D people. We understand that this topic is of particular interest to people working with diabetes management since most of the conducted research involves people with type 2 diabetes. Our discussion can potentiate the interest of the researchers in the field to include more investigation on T1D, thus providing scientific shreds of evidence for new guidelines and exercise prescriptions in this population.
Speaker C
Irena Rebalka
McMaster University, Pathology and Molecular Medicine
Canada
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Disuse, recovery and repair of skeletal muscle in Type 1 Diabetes
Despite the importance of skeletal muscle to our physical and metabolic well-being, changes to skeletal muscle health in those with Type 1 Diabetes (T1D) is not well defined. Our published and preliminary data highlight alterations to muscle health in those with T1D. In particular, we have noted reduced mitochondrial function, particularly in females and a loss of mitochondrial density in older adults with T1D. Functionally, there was a loss of upper and lower body maximal voluntary contraction (quadriceps, handgrip) in those with T1D after the age of 35. In young adults with T1D, force recovery from damaging exercise was significantly delayed along with increased extracellular matrix protein content and delayed satellite cell activation. Collectively, these alterations suggest there are impairments to skeletal muscle’s ability to respond to stressors and that strategies to maximize muscle health are urgently needed to mitigate the loss of muscle health and the resulting inability to undertake activities of daily living.