Dr Julie Hunt
Julie Hunt graduated with a BSc in Sports Science from the University of Brighton (2007) before achieving an MSc in Exercise Physiology from Loughborough University (2009). During this time she worked as a physiologist for British Triathlon and assisted on UK sport talent ID campaigns. Julie continued her studies at Loughborough University, completing a PhD on the peripheral vascular adaptation to resistance training with blood flow restriction. She has since held an academic post as a Lecturer in Sport and Exercise Physiology.
My research interests lie with skeletal muscle and vascular adaptations to exercise and exercise training in healthy and clinical populations. My PhD focused on the novel exercise mode of ischemic (occlusion) strength training, where application of a pressure cuff around the exercising limb reduces blood flow to the working muscle. Muscle hypertrophy and peripheral vascular remodelling occurs at low training loads (20%1RM) with blood flow restriction. Research into the mechanisms behind this type of exercise provide greater insight into the physiology of muscle and vascular growth, and can optimize treatments aimed at maintaining or improving physical function in populations (elderly, rehabilitating athletes) intolerant to high mechanical loads.
I also have a keen interest in swimming and triathlon specific performance, and have been involved in collaborative research with the English Institute of Sport.
Julie Hunt collaborates with academic and applied sport and exercise scientists:
Dr Richard Ferguson, Loughborough University
Professor Mark Lewis, Loughborough University
Dr Steve Ingham, English Institute of Sport
Dr Jamie Pringle, English Institute of Sport
New for 2014: BSc Sports & Exercise Science
The Physiological SocietyEuropean College of Sport Science
Journal articlesHunt JEA, Galeo D, Tufft G, Bunce D & Ferguson RA (2013). Time course of regional vascular adaptations to low load resistance training with blood flow restriction. Journal of Applied Physiology, 115, 3, 403-411.Taylor CW, Ingham SA, Hunt JEA, Martin NR, Lewis MP, Pringle JS, Fudge BW & Ferguson RA (under review). Sprint interval and continuous cycling induce similar increases in AMPK phosphorylation, PGC-1α and VEGF mRNA expression in trained human skeletal muscle. Journal of Applied Physiology.
Etxebarria N, Hunt JEA, Ingham SA & Ferguson RA (2013). Physiological assessment of isolated running does not directly replicate running capacity after triathlon-specific cycling. Journal of Sports Science, published ahead of print.
Hunt JEA, Walton LA & Ferguson RA (2012). Brachial artery modifications to blood flow restricted handgrip training and detraining. Journal of Applied Physiology. 112, 956-961.
Hunt JEA, Taylor CW, Martin N, Player D, Lewis MP & Ferguson RA (2013). The acute angiogenic transcriptional response to low load resistance exercise with blood flow restriction. European College of Sports Science, Barcelona.
Taylor CW, Ingham SA, Hunt JEA, Martin NR, Lewis MP, Pringle JS, Fudge BW & Ferguson RA (2013). Acute interval and continuous sprint cycling increases angiogenic gene expression in trained skeletal muscle. European College of Sports Science, Barcelona
Hunt JEA, Galeo D & Ferguson RA (2012). Popliteal artery modifications to low load plantar flexion training with blood flow restriction. The Physiological Society; The Biochemical Basis of Elite Performance, London.
Hunt JEA, Walton LA & Ferguson RA (2011). Brachial artery modifications to blood flow restricted handgrip training and detraining. ACSM 58th Annual Meeting, Denver, Colorado.
Pringle J, Hunt JEA, Dekerle J, Brickley G (2009). Critical speed, anaerobic distance capacity and swimming performance after prior heavy and severe exercise. ACSM 56th Annual Meeting, Seattle, Washington
is reduced blood pressure in the presence of a normal or raised cardiac output. The vasoplegic syndrome is
encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and
trauma, but despite this, uniform clinical definitions are lacking, which renders translational research in this area
challenging. We discuss the role of vasoplegia in these contexts and the criteria that are used to describe it are
discussed. Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen
sulphide and reactive oxygen species production, are reviewed and potential for therapeutic intervention explored.
Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the
blood vessels, are also discussed. The optimum balance between maintaining adequate systemic vascular resistance
against the potentially deleterious effects of treatment with catecholamines is as yet unclear, but development of
novel vasoactive agents may facilitate greater understanding of the role of the differing pathways in the
development of vasoplegia. In turn, this may provide insights into the best way to care for patients with this
common, multifactorial condition.