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.
Forty per cent of critically ill patients are affected by intensive care unit-acquired weakness (ICU-AW), to which skeletal muscle wasting makes a substantial contribution. This can impair outcomes in hospital, and can cause long-term physical disability after hospital discharge. No effective mitigating strategies have yet been identified.
Application of a repetitive vascular occlusion stimulus (RVOS) a limb pressure cuff inducing brief repeated cycles of ischaemia and reperfusion, can limit disuse muscle atrophy in both healthy controls and bed-bound patients recovering from knee surgery. We wish to determine whether RVOS might be effective in mitigating against muscle wasting in the ICU. Given that RVOS can also improve vascular function in healthy controls, we also wish to assess such effects in the critically ill. We here describe a pilot study to assess whether RVOS application is safe, tolerable, feasible and acceptable for ICU patients.
This is a randomised interventional feasibility trial. Thirty-two ventilated adult ICU patients with multiorgan failure will be recruited within 48 h of admission and randomised to either the intervention arm or the control arm. Intervention participants will receive RVOS twice daily (except only once on day 1) for up to 10 days or until ICU discharge.
Serious adverse events and tolerability (pain score) will be recorded; feasibility of trial procedures will be assessed against pre-specified criteria and acceptability by semi-structured interview. Together with vascular function, muscle mass and quality will be assessed using ultrasound and measures of physical function at baseline, on days 6 and 11 of study enrolment, and at ICU and hospital discharge. Blood and urine biomarkers of muscle metabolism, vascular function, inflammation and DNA damage/repair mechanism will also be analysed. The Health questionnaire will be completed 3 months after hospital discharge.
If this study demonstrates feasibility, the derived data will be used to inform the design (and sample size) of an appropriately-powered prospective trial to clarify whether RVOS can help preserve muscle mass/improve vascular function in critically ill patients.
Vitamin D deficiency (Â25nmol/L) and insufficiency (Â50nmol/L) has become an increasingly popular topic. Current research focusses upon the potential ergogenic effects of vitamin D (vitD) in sporting performance; however, the relationship between vitD (dietary intake and nutritional status) and bone health within a University athlete cohort remains under-investigated. Therefore, the aims of this Thesis were to (1) examine vitD status longitudinally across the University competitive seasons and; (2) examine the implications that vitD deficiency/ insufficiency may have upon physical performance parameters or bone health.
In the first study, fifty-seven competitive University level- athletes from varied sports were observed from autumn to spring. Radial bone mineral density (BMD) and physical performance parameters were investigated; for the analysis of vitD and parathyroid hormone, blood samples were collected. Within the cohort 7% presented with deficiency during the autumn; increasing to 44% during spring. However, this did not have a significant effect upon physical performance and bone health despite an average status of 31.5±16.4 nmol/L in spring.
In the second study, 34 University athletes and sixteen sedentary students were recruited and followed from spring to summer. Whole body, hip and tibial scans were conducted to determine BMD and bone mineral content (BMC). Physical performance parameters including jump height, aerobic fitness, muscular strength and blood biochemistry were also collected. During the summer term, 26% of the cohort were vitD insufficient. Moreover, an insufficient vitD status was associated with a lowered jump height (p=0.015) but not aerobic fitness (p=0.07). There was also a significant positive relationship between vitD status, femoral neck BMC (r=0.685; pÂ0.02) and BMD (r=0.679; pÂ0.02). Our results show that BMD was higher in weight bearing athletes. The final study found that racket sport athletes had a significantly superior bone profile in their dominant arm when contrasted to controls.
Overall, these findings suggest that an insufficient vitD status was associated with lower indices of muscular power and aerobic fitness in University students. Therefore, being vitD replete may not only play an important role in musculoskeletal health but could also be a key determining factor in athletic performance.