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.
University roles and responsibilities
- Programme Leader for BSc (Hons) Sport and Exercise Science
Affiliations and memberships
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
Hunt 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
Background: Blackcurrant is rich in anthocyanins that may protect against exercise-induced muscle damage (EIMD) and facilitate a faster recovery of muscle function. We examined the effects of New Zealand blackcurrant (NZBC) extract on indices of muscle damage and recovery following a bout of strenuous isokinetic resistance exercise. Methods: Using a double-blind, randomised, placebo controlled, parallel design, twenty-seven healthy participants received either a 3 g·day−1 NZBC extract (n = 14) or the placebo (PLA) (n = 13) for 8 days prior to and 4 days following 60 strenuous concentric and eccentric contractions of the biceps brachii muscle on an isokinetic dynamometer. Muscle soreness (using a visual analogue scale), maximal voluntary contraction (MVC), range of motion (ROM) and blood creatine kinase (CK) were assessed before (0 h) and after (24, 48, 72 and 96 h) exercise. Results: Consumption of NZBC extract resulted in faster recovery of baseline MVC (p = 0.04), attenuated muscle soreness at 24 h (NZBC: 21 ± 10 mm vs. PLA: 40 ± 23 mm, p = 0.02) and 48 h (NZBC: 22 ± 17 vs. PLA: 44 ± 26 mm, p = 0.03) and serum CK concentration at 96 h (NZBC: 635 ± 921 UL vs. PLA: 4021 ± 4319 UL, p = 0.04) following EIMD. Conclusions: Consumption of NZBC extract prior to and following a bout of eccentric exercise attenuates muscle damage and improves functional recovery. These findings are of practical importance in recreationally active and potentially athletic populations, who may benefit from accelerated recovery following EIMD.
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-1α 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-1α 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 1α 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.
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.
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
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.
Purpose Previous investigations to establish factors influencing the blood flow restriction (BFR) stimulus have determined cuff pressures required for complete arterial occlusion, which does not reflect the partial restriction prescribed for this training technique. This study aimed to establish characteristics that should be accounted for when prescribing cuff pressures required for partial BFR. Methods Fifty participants were subjected to incremental blood flow restriction of the upper and lower limbs by proximal pneumatic cuff inflation. Popliteal and brachial artery diameter, blood velocity and blood flow was assessed with Doppler ultrasound. Height, body mass, limb circumference, muscle–bone cross-sectional area, adipose thickness (AT) and arterial blood pressure were measured and used in different models of hierarchical linear regression to predict the pressure at which 60 % BFR (partial occlusion) occurred. Results Combined analysis revealed a difference in cuff pressures required to elicit 60 % BFR in the popliteal (111 ± 12 mmHg) and brachial arteries (101 ± 12 mmHg). MAP (r = 0.58) and AT (r = −0.45) were the largest independent determinants of lower and upper body partial occlusion pressures. However, greater variance was explained by upper and lower limb regression models composed of DBP and BMI (48 %), and arm AT and DBP (30 %), respectively. Conclusion Limb circumference has limited impact on the cuff pressure required for partial blood flow restriction which is in contrast to its recognised relationship with complete arterial occlusion. The majority of the variance in partial occlusion pressure remains unexplained by the predictor variables assessed in the present study.