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Dive into the research topics where Warrick J. Inder is active.

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Featured researches published by Warrick J. Inder.


Medicine and Science in Sports and Exercise | 2011

Disproportionate Exercise Load and Remodeling of the Athlete's Right Ventricle

Andre La Gerche; Hein Heidbuchel; Andrew T. Burns; Don J. Mooney; Andrew J. Taylor; Heinz Pfluger; Warrick J. Inder; A. MacIsaac; David L. Prior

PURPOSE There is evolving evidence that intense exercise may place a disproportionate load on the right ventricle (RV) when compared with the left ventricle (LV) of the heart. Using a novel method of estimating end-systolic wall stress (ES-σ), we compared the RV and LV during exercise and assessed whether this influenced chronic ventricular remodeling in athletes. METHODS For this study, 39 endurance athletes (EA) and 14 nonathletes (NA) underwent resting cardiac magnetic resonance (CMR), maximal oxygen uptake (VO2), and exercise echocardiography studies. LV and RV end-systolic wall stress (ES-σ) were calculated using the Laplace relation (ES-σ = Pr/(2h)). Ventricular size and wall thickness were determined by CMR; invasive and Doppler echo estimates were used to measure systemic and pulmonary ventricular pressures, respectively; and stroke volume was quantified by Doppler echocardiography and used to calculate changes in ventricular geometry during exercise. RESULTS In EA, compared with NA, resting CMR measures showed greater RV than LV remodeling. The ratios RV ESV/LV ESV (1.40 ± 0.23 vs 1.26 ± 0.12, P = 0.007) and RV mass/LV mass (0.29 ± 0.04 vs 0.25 ± 0.03, P = 0.012) were greater in EA than in NA. RVES-σ was lower at rest than LVES-σ (143 ± 44 vs 252 ± 49 kdyn · cm, P < 0.001) but increased more with strenuous exercise (125% vs 14%, P < 0.001), resulting in similar peak exercise ES-σ (321 ± 106 vs 286 ± 77 kdyn · cm, P = 0.058). Peak exercise RVES-σ was greater in EA than in NA (340 ± 107 vs 266 ± 82 kdyn · cm, P = 0.028), whereas RVES-σ at matched absolute workloads did not differ (P = 0.79). CONCLUSIONS Exercise induces a relative increase in RVES-σ which exceeds LVES-σ. In athletes, greater RV enlargement and greater wall thickening may be a product of this disproportionate load excess.


The Journal of Clinical Endocrinology and Metabolism | 2011

A Longitudinal Study of Plasma and Urinary Cortisol in Pregnancy and Postpartum

Caroline Jung; Jui T. Ho; David J. Torpy; Anne Rogers; Matthew P. Doogue; John G. Lewis; Raymond J. Czajko; Warrick J. Inder

CONTEXT There is a paucity of longitudinal data on plasma and urinary cortisol levels during pregnancy using modern assays. Furthermore, conflicting data exist as to the effect of the low-dose oral contraceptive pill (OCP) on cortisol. DESIGN, SUBJECTS, AND MEASUREMENTS: We conducted a prospective longitudinal study on morning plasma cortisol (total and free), corticosteroid-binding globulin (CBG), and 24-h urinary free cortisol (UFC) levels in 20 pregnant women during the first, second, and third trimesters and 2-3 months postpartum compared with 12 subjects on low-dose OCP and 15 nonpregnant subjects not taking the OCP (control group). RESULTS A progressive rise in total plasma cortisol, CBG, and 24-h UFC was demonstrated during pregnancy, peaking during the third trimester (mean 3-fold rise compared with controls). Plasma free cortisol increased 1.6-fold by the third trimester. In the OCP group, total plasma cortisol and CBG were 2.9- and 2.6-fold elevated, respectively, whereas 24-h UFC and plasma free cortisol were not significantly different from controls. Compared with liquid chromatography-mass spectrometry, a commercial immunoassay underestimated mean total plasma cortisol concentrations by 30% during second and third trimesters and in OCP users and overestimated UFC levels by 30-35% during pregnancy. CONCLUSIONS Our study demonstrated elevations in total plasma cortisol and CBG concentrations during pregnancy and with low-dose OCP use. Pregnancy was also associated with significant increases in plasma free cortisol and UFC, suggesting that the rise in total plasma cortisol is contributed to by up-regulation of the maternal hypothalamic-pituitary-adrenal axis in addition to elevated CBG.


Journal of Applied Physiology | 2010

Pulmonary transit of agitated contrast is associated with enhanced pulmonary vascular reserve and right ventricular function during exercise

Andre La Gerche; A. MacIsaac; Andrew T. Burns; Don J. Mooney; Warrick J. Inder; Jens-Uwe Voigt; Hein Heidbuchel; David L. Prior

Pulmonary transit of agitated contrast (PTAC) occurs to variable extents during exercise. We tested the hypothesis that the onset of PTAC signifies flow through larger-caliber vessels, resulting in improved pulmonary vascular reserve during exercise. Forty athletes and fifteen nonathletes performed maximal exercise with continuous echocardiographic Doppler measures [cardiac output (CO), pulmonary artery systolic pressure (PASP), and myocardial velocities] and invasive blood pressure (BP). Arterial gases and B-type natriuretic peptide (BNP) were measured at baseline and peak exercise. Pulmonary vascular resistance (PVR) was determined as the regression of PASP/CO and was compared according to athletic and PTAC status. At peak exercise, athletes had greater CO (16.0 ± 2.9 vs. 12.4 ± 3.2 l/min, P < 0.001) and higher PASP (60.8 ± 12.6 vs. 47.0 ± 6.5 mmHg, P < 0.001), but PVR was similar to nonathletes (P = 0.71). High PTAC (defined by contrast filling of the left ventricle) occurred in a similar proportion of athletes and nonathletes (18/40 vs. 10/15, P = 0.35) and was associated with higher peak-exercise CO (16.1 ± 3.4 vs. 13.9 ± 2.9 l/min, P = 0.010), lower PASP (52.3 ± 9.8 vs. 62.6 ± 13.7 mmHg, P = 0.003), and 37% lower PVR (P < 0.0001) relative to low PTAC. Right ventricular (RV) myocardial velocities increased more and BNP increased less in high vs. low PTAC subjects. On multivariate analysis, maximal oxygen consumption (VO(2max)) (P = 0.009) and maximal exercise output (P = 0.049) were greater in high PTAC subjects. An exercise-induced decrease in arterial oxygen saturation (98.0 ± 0.4 vs. 96.7 ± 1.4%, P < 0.0001) was not influenced by PTAC status (P = 0.96). Increased PTAC during exercise is a marker of pulmonary vascular reserve reflected by greater flow, reduced PVR, and enhanced RV function.


Clinical Endocrinology | 2012

Measurement of salivary cortisol in 2012 – laboratory techniques and clinical indications

Warrick J. Inder; Goce Dimeski; Anthony W. Russell

The utility of measuring salivary cortisol has become increasingly appreciated since the early 1980s. Salivary cortisol is a measure of active free cortisol and follows the diurnal rhythm of serum or plasma cortisol. The saliva sample may be collected by drooling or through the use of absorbent swabs which are placed into the mouth until saturated. Salivary cortisol is therefore convenient for patients and research participants to collect noninvasively on an outpatient basis. Several assay techniques have been used to measure salivary cortisol, including radioimmunoassay and more recently liquid chromatography–tandem mass spectrometry. The analytical sensitivity varies between these assay methods, as does the potential for cross‐reactivity with other steroids. The interpretation of salivary cortisol levels relies on rigorous standardization of sampling equipment, sampling protocols and assay technology with establishment of a local reference range. Clinically, the commonest use for salivary cortisol is measuring late‐night salivary cortisol as a screening test for Cushings syndrome. Several studies have shown diagnostic sensitivities and specificities of over 90%, which compares very favourably with other screening tests for Cushings syndrome such as the 24‐h urinary‐free cortisol and the 1‐mg overnight dexamethasone suppression test. There are emerging roles for the use of salivary cortisol in diagnosing adrenal insufficiency, particularly in conditions associated with low cortisol–binding globulin levels, and in the monitoring of glucocorticoid replacement. Finally, salivary cortisol has been used extensively as a biomarker of stress in a research setting, especially in studies examining psychological stress with repeated measurements.


Medicine and Science in Sports and Exercise | 1998

The effect of glycerol and desmopressin on exercise performance and hydration in triathletes.

Warrick J. Inder; Maureen P. Swanney; R. A. Donald; Timothy C. R. Prickett; John Hellemans

BACKGROUND Hydration is an important determinant of athletic performance, and glycerol-containing solutions have been demonstrated to produce a state of hyperhydration. Secretions of arginine vasopressin (AVP) and/or other renal mechanisms may account for reduced urine output following glycerol ingestion. This study examined the effect of glycerol and the AVP analog desmopressin (DDAVP) on hydration and exercise performance in triathletes ingesting routine volumes of prerace fluids. METHODS Eight male triathletes ages 19 to 43 participated. After determination of their VO(2peak), each athlete completed a strenuous exercise protocol three times involving 60 min of exercise at 70% VO(2peak) followed immediately by an incremental increase in workload every 2 min until exhaustion. RESULTS Pretreatment with 1 gxkg(-1) glycerol or 20 microgram of DDAVP intranasally failed to produce hyperhydration or any enhancement of athletic performance. There was a significant difference in reduction in body mass between DDAVP and control (P < 0.05) but no change in sweat volume. No physiologically relevant differences in plasma sodium, renin, or hemoglobin were seen with either active agent. Plasma osmolality did have a different time course in response to exercise following glycerol (P < 0.03) owing to a smaller incremental increase. Urine osmolality was also raised at baseline following glycerol (P < 0.05). Responses to exercise of plasma AVP, cortisol, and indices of carbohydrate metabolism were similar, although AVP was elevated following DDAVP administration (P < 0.01) owing to assay cross-reactivity. CONCLUSION Although maintaining adequate hydration remains important for the endurance athlete, the routine use of either glycerol of DDAVP before athletic training or competition in a thermoneutral environment does not seem to confer any advantage over conventional fluid replacement.


The Journal of Clinical Endocrinology and Metabolism | 2014

Continuous Subcutaneous Hydrocortisone Infusion Therapy in Addison's Disease: A Randomized, Placebo-Controlled Clinical Trial

Lucia Gagliardi; Marni A. Nenke; Tilenka R. J. Thynne; Jenny von der Borch; Wayne Rankin; David Henley; Jane Sorbello; Warrick J. Inder; David J. Torpy

CONTEXT Patients with Addisons disease (AD) report impaired subjective health status (SHS). Since cortisol exhibits a robust circadian cycle that entrains other biological clocks, impaired SHS may be due to the noncircadian cortisol profile achieved with conventional glucocorticoid replacement. Continuous subcutaneous hydrocortisone infusion (CSHI) reproduces a circadian cortisol profile, but its effects on SHS have not been objectively evaluated. OBJECTIVE The aim of this study was to determine the effect of CSHI on SHS in AD. SETTING AND DESIGN This was a multicentre, double-blind, placebo-controlled trial of CSHI vs oral glucocorticoid therapy. Participants received in random order 4 weeks of: CSHI and oral placebo, and subcutaneous placebo and oral hydrocortisone, separated by a 2-week washout period. SHS was assessed using the Short-Form 36 (SF-36), General Health Questionnaire (GHQ-28), Fatigue Scale (FS), Gastrointestinal Symptom Rating Scale (GSRS); and Addisons Quality of Life Questionnaire (AddiQoL). Participants were asked their (blinded) treatment preference. Twenty-four hour urine free cortisol (UFC) and diurnal salivary cortisol collections compared cortisol exposure during each treatment. RESULTS Ten participants completed the study. Baseline SHS scores (mean ± SE) were consistent with mild impairment: SF-36 physical component summary 48.4 (± 2.4), mental component summary 53.3 (± 3.0); GHQ-28 18.1 (± 3.3); GSRS 3.7 (± 1.6), and AddiQoL 94.7 (± 3.7). FS was similar to other AD cohorts 13.5 (± 1.0) (P = 0.82). UFC between treatments was not different (P = 0.87). The salivary cortisol at 0800 h was higher during CSHI (P = 0.03), but not at any other time points measured. There was no difference between the treatments in the SHS assessments. Five participants preferred CSHI, four oral hydrocortisone, and one was uncertain. CONCLUSIONS Biochemical measurements indicate similar cortisol exposure during each treatment period, although a more circadian pattern was evident during CSHI. CSHI does not improve SHS in AD with good baseline SHS. This casts some doubt on the potential benefit of circadian cortisol delivery on SHS in AD.


Clinical Endocrinology | 2006

11β Hydroxysteroid dehydrogenase type 1 is expressed and is biologically active in human skeletal muscle

Christina Jang; Varuni R. Obeyesekere; Rodney J. Dilley; F. P. Alford; Warrick J. Inder

Objective  No data exist regarding the distribution and oxoreductase enzyme activity of 11β hydroxysteroid dehydrogenase type 1 (11β HSD‐1) in fresh human skeletal muscle. We aimed to investigate the mRNA and protein expression of 11β HSD‐1 in fresh skeletal muscle, confirm its biological activity and determine its relationship with hexose‐6‐phosphate dehydrogenase (H6PDH). We also examined the muscle fibre localization of 11β HSD‐1.


Clinical Endocrinology | 2009

Dexamethasone administration inhibits skeletal muscle expression of the androgen receptor and IGF‐1 – implications for steroid‐induced myopathy

Warrick J. Inder; Christina Jang; Varuni R. Obeyesekere; F. P. Alford

Context  Glucocorticoids are a well‐recognized cause of muscle weakness. The early effects of glucocorticoids on skeletal muscle (SkM) androgen and IGF‐1 pathways have not been previously investigated in human subjects.


PLOS ONE | 2015

Relationship between Inflammatory Cytokines and Indices of Cardiac Dysfunction following Intense Endurance Exercise

Andre La Gerche; Warrick J. Inder; T. Roberts; Maria J. Brosnan; Hein Heidbuchel; David L. Prior

Objectives Pro-inflammatory cytokines have been noted to increase following exercise but their relationship to exercise-induced cardiac dysfunction has not previously been investigated. We sought to evaluate whether exercise-induced cardiac dysfunction was associated with increases in cytokines, particularly the pro-inflammatory cytokines IL-1β, IL-12p70 and TNFα, which have been most implicated in cardiac pathology. Methods 40 well-trained endurance athletes underwent evaluation prior to and immediately following one of four endurance sporting events ranging from 3 to 11 hours duration. Cytokines (IL-1β, IL-6, IL-8, IL-10, IL-12p70 and TNFα) were analyzed by flow cytometry from serum samples collected within 50 minutes of race completion. Cardiac troponin (cTnI) and B-type natriuretic peptide were combined with an echocardiographic assessment of cardiac function, and a composite of cTnI > 0.04 μg/L, BNP increase > 10 ng/L and a decrease in right ventricular ejection (RVEF) > 10% were prospectively defined as evidence of myocardial dysfunction. Results Relative to baseline, IL-6 IL-8 and IL-10 increased 8.5-, 2.9-, and 7.1-fold, respectively, P<0.0001. Thirty-one (78%), 19 (48%) and 18 (45%) of the athletes met the pre-specified criteria for significant cTnI, BNP and RVEF changes, respectively. TNFα, IL-12p70 were univariate predictors of ΔRVEF and ΔBNP whilst none of the anti-inflammatory cytokines were significantly associated with these measures. Ten athletes (25%, all athletes competing in the endurance event of longest duration) met criteria for exercise-induced myocardial dysfunction. In these 10 athletes with myocardial dysfunction, as compared to those without, there was significantly greater post-race expression of the pro-inflammatory cytokines IL-12p70 (8.1±3.8pg/ml vs. 2.5±2.6pg/ml, P<0.0001) and TNFα (6.5±3.1pg/ml vs. 2.0±2.5pg/ml, P<0.0001). Conclusion Cardiac dysfunction following intense endurance exercise was associated with increased expression of pro-inflammatory cytokines. This does not prove a causal relationship but provides rationale for further investigations into whether inflammation mediates exercise-induced myocardial dysfunction.


European Journal of Endocrinology | 2015

MANAGEMENT OF ENDOCRINE DISEASE: Pituitary tumour apoplexy

Cristina Capatina; Warrick J. Inder; Niki Karavitaki; John A H Wass

Pituitary tumour apoplexy (PA) is a rare clinical syndrome that occurs as a result of acute haemorrhage and/or infarction within a frequently undiagnosed pituitary tumour. The sudden enlargement of the pituitary mass undergoing PA is responsible for a wide range of acute symptoms/signs (severe headache, visual loss, diplopia, hypopituitarism, impaired consciousness) which, together with the radiological evidence of a pituitary lesion, establish the diagnosis. The optimal care of PA requires involvement of a multidisciplinary team including endocrinologist, neurosurgeon, neuroophthalmologist and the management strategy that depends on the clinical manifestations, as well as the presence of co-morbidities. Prompt surgical decompression is initially indicated in cases with severe or progressive impairment of the visual acuity or the visual fields or with altered mental state and leads to visual and neurological recovery in most of the patients. The patients with mild, stable clinical picture (including those with isolated ocular palsies) can be managed conservatively (support of fluid and electrolyte balance and stress doses of steroids in most cases) with favourable visual and neurological outcome. Frequent reassessment is mandatory because the clinical course can be unpredictable; if progression of symptoms occurs, later elective surgery is indicated and is beneficial, especially in terms of visual outcome. The endocrinological outcome is less favourable, irrespective of the treatment option, with many patients remaining on long-term replacement therapy. Despite the above guidelines, clear proof of optimal outcomes in the form of randomised controlled trials is lacking. Regrowth of the pituitary tumour years after a PA episode is possible and patients require long-term surveillance.

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Jane Sorbello

Princess Alexandra Hospital

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F. P. Alford

St. Vincent's Health System

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Carmela Caputo

St. Vincent's Health System

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David L. Prior

St. Vincent's Health System

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Caroline Jung

St. Vincent's Health System

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