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Delineating the cellular mechanisms of improvements in endothelial cell function following heat therapy
Secondary Supervisor(s): Dr Mark Turner
University of Registration: Coventry University
BBSRC Research Themes:
Project Outline
Cardiovascular disease is the leading global cause of death, with endothelial function a key marker and predictor of vascular health. Although endothelial function declines with age, this can be mitigated by healthy lifestyle behaviours such as exercise. However, exercise adherence is poor, with many failing to meet physical activity guidelines, highlighting the need for complementary therapies to improve cardiovascular health.
Our group has shown that heat therapy (e.g., sauna, hot baths) induces significant, long-lasting improvements in endothelial function, in some cases exceeding those seen with exercise. Yet, the mechanisms by which heat confers these benefits, and whether they differ from exercise-induced pathways, remain unclear. Advancing this knowledge will support more targeted prescription of exercise and heat-based therapies, particularly for populations who may struggle with traditional exercise interventions.
Evidence suggests exercise improves endothelial function via circulating signalling factors, including nitric oxide, growth factors, and inflammatory cytokines. For heat therapy, initial findings show overlapping but less well-defined mechanisms. Our in-vivo data indicate that nitric oxide and inflammatory signalling cascades are activated following heat exposure.
This project will use ex-vivo endothelial cell culture models to determine the cellular mechanisms underlying heat therapy's vascular benefits and to compare these with exercise-induced pathways. By exposing cultured endothelial cells to serum collected post-exercise and post-heat therapy, we will identify and isolate key molecular signalling mechanisms.
