Julie Hunt

Dr Julie Hunt


Lecturer in Sport and Exercise Sciences
+44 (0)1483 689400
30 PG 00

Biography

Biography

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.

Research interests

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.

Research collaborations

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

Teaching

New for 2014: BSc Sports & Exercise Science

Affiliations

The Physiological SocietyEuropean College of Sport Science

Publication highlights

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.

Conference presentations

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

My publications

Publications

Etxebarria N, Hunt J, Ingham S, Ferguson R (2014) Physiological assessment of isolated running does not directly replicate running capacity after triathlon-specific cycling, JOURNAL OF SPORTS SCIENCES 32 (3) pp. 229-238 TAYLOR & FRANCIS LTD
Hunt JEA, Galea 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) pp. 403-411 AMER PHYSIOLOGICAL SOC
Taylor CW, Ingham SA, Hunt JEA, Martin NRW, Pringle JSM, Ferguson RA (2016) Exercise duration-matched interval and continuous sprint cycling induce similar increases in AMPK phosphorylation, PGC-1 alpha and VEGF mRNA expression in trained individuals, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY 116 (8) pp. 1445-1454 SPRINGER
Hunt JEA, Stodart C, Ferguson RA (2016) The influence of participant characteristics on the relationship between cuff pressure and level of blood flow restriction, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY 116 (7) pp. 1421-1432 SPRINGER
Hunt JEA, Walton LA, Ferguson RA (2012) Brachial artery modifications to blood flow-restricted handgrip training and detraining, JOURNAL OF APPLIED PHYSIOLOGY 112 (6) pp. 956-961 AMER PHYSIOLOGICAL SOC
Thompson EB, Farrow L, Hunt JEA, Lewis MP, Ferguson RA (2014) Brachial artery characteristics and micro-vascular filtration capacity in rock climbers, European Journal of Sport Science
Rock climbers perform repeated isometric forearm muscle contractions subjecting the vasculature to repeated ischaemia and distorted haemodynamic signals. This study investigated forearm vascular characteristics in rock climbers compared to healthy untrained controls. Eight climbers (CLIMB) (BMI; 22.3, s = 2.0 kg/m, isometric handgrip strength; 46, s = 8 kg) were compared against eight untrained controls (CON) (BMI; 23.8, s = 2.6 kg/m, isometric handgrip strength; 37, s = 9 kg). Brachial artery diameter and blood flow were measured, using Doppler ultrasound, at rest and following 5-mins ischaemia (peak diameter) and ischaemic exercise (maximal dilation) to calculate flow mediated dilation (FMD) and dilatory capacity (DC). Capillary filtration capacity was assessed using venous occlusion plethysmography. Resting (4.30, s = 0.26 vs. 3.79, s = 0.39 mm), peak (4.67, s = 0.31 vs. 4.12, s = 0.45 mm) and maximal (5.14, s = 0.42 vs. 4.35, s = 0.47 mm) diameters were greater (P
Darling A, Hart K, Gossiel F, Robertson F, Hunt J, Hill T, Johnsen S, Berry J, Eastell R, Vieth R, Lanham-New S (2017) Higher bone resorption excretion in South Asian women vs White Caucasians and increased bone loss with higher seasonal cycling of vitamin D:  results from the D-FINES cohort study, Bone 98 pp. 47-53 Elsevier
Few data exist on bone turnover in South Asian women and it is not well elucidated as to whether Western dwelling South Asian women have different bone resorption levels to that of women from European ethnic backgrounds. This study assessed bone resorption levels in UK dwelling South Asian and Caucasian women as well as evaluating whether seasonal variation in 25-hydroxyvitamin D [25(OH)D] is associated with bone resorption in either ethnic group. Data for seasonal measures of urinary N-telopeptide of collagen (uNTX) and serum 25(OH)D were analysed from n=373 women (four groups; South Asian postmenopausal n=44, South Asian premenopausal n=50, Caucasian postmenopausal n=144, Caucasian premenopausal n =135) (mean (± SD) age 48 (14) years; age range 18-79 years) who participated in the longitudinal D-FINES (Diet, Food Intake, Nutrition and Exposure to the Sun in Southern England) cohort study (2006-2007). A mixed between-within subjects ANOVA (n=192) showed a between subjects effect of the four groups (P
Ferguson Richard A., Hunt Julie, Lewis Mark P., Martin Neil R. W., Player Darren J., Stangier Carolin, Taylor Conor W., Turner Mark C. (2018) The acute angiogenic signalling response to low-load resistance exercise with blood flow restriction, European Journal of Sport Science 18 (3) pp. 397-406 Taylor & Francis
This study investigated protein kinase activation and gene expression of angiogenic factors in response to low-load resistance exercise with or without blood flow restriction (BFR). In a repeated measures cross-over design, six males performed four sets of bilateral knee extension exercise at 20% 1RM (reps per set = 30:15:15:continued to fatigue) with BFR (110?mmHg) and without (CON). Muscle biopsies were obtained from the vastus lateralis before, 2 and 4?h post-exercise. mRNA expression was determined using real-time RT?PCR. Protein phosphorylation/expression was determined using Western blot. p38MAPK phosphorylation was greater (p = 0.05) at 2?h following BFR (1.3 ± 0.8) compared to CON (0.4 ± 0.3). AMPK phosphorylation remained unchanged. PGC-1± mRNA expression increased at 2?h (5.9 ± 1.3 vs. 2.1 ± 0.8; p = 0.03) and 4?h (3.2 ± 0.8 vs. 1.5 ± 0.4; p = 0.03) following BFR exercise with no change in CON. PGC-1± protein expression did not change following either exercise. BFR exercise enhanced mRNA expression of vascular endothelial growth factor (VEGF) at 2?h (5.2 ± 2.8 vs 1.7 ± 1.1; p = .02) and 4?h (6.8 ± 4.9 vs. 2.5 ± 2.7; p = .01) compared to CON. mRNA expression of VEGF-R2 and hypoxia-inducible factor 1± increased following BFR exercise but only eNOS were enhanced relative to CON. Matrix metalloproteinase-9 mRNA expression was not altered in response to either exercise. Acute low-load resistance exercise with BFR provides a targeted angiogenic response potentially mediated through enhanced ischaemic and shear stress stimuli.
Lambden Simon, Creagh-Brown Ben C., Hunt Julie, Summers Charlotte, Forni Lui G. (2018) Definitions and pathophysiology of vasoplegic shock, Critical Care 22 (174) pp. 1-8 BioMed Central
Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which
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.
Lambden Simon, Creagh-Brown Ben C., Hunt Julie, Summers Charlotte, Forni Lui G. (2018) Definitions and pathophysiology of vasoplegic shock, Critical Care 22 174 pp. 1-8 BioMed Central Ltd.
Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which 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. © 2018 The Author(s).
Chhetri Ismita, Hunt Julie E. A., Mendis Jeewaka R., Patterson Stephen D., Puthucheary Zudin A., Montgomery Hugh E., Creagh-Brown Benedict C. (2019) Repetitive vascular occlusion stimulus (RVOS) versus standard care to prevent muscle wasting in critically ill patients (ROSProx):a study protocol for a pilot randomised controlled trial, Trials 20 456 pp. 1-14 BMC

Background

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.

Methods

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.

Discussion

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.