ORCID Profile
0000-0003-3603-7852
Current Organisation
University of Sydney
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Publisher: American Physiological Society
Date: 2020
DOI: 10.1152/AJPREGU.00177.2019
Abstract: During heat stress, the skin vasculature can greatly increase conductance secondary to vasodilation. The subsequent increase in skin blood flow allows for convective heat transfer from the core to the skin and between the skin surface and the surrounding environment. Measurement of skin blood flow, therefore, provides valuable information regarding heat exchange between the body and the environment. In addition, assessment of skin blood flow can be used to study vascular control mechanisms. Most often, skin blood flow is measured by venous occlusion plethysmography, Doppler ultrasound, laser-Doppler flowmetry, and, more recently, optical coherence tomography. However, important delimitations to each of these methods, which may be dependent on the research question, must be considered when responses from these approaches are interpreted. In this brief review, we discuss these methods of skin blood flow measurement and highlight potential sources of error and limitations. We also provide recommendations to guide the interpretation of skin blood flow data.
Publisher: Wiley
Date: 05-2022
Publisher: Springer Science and Business Media LLC
Date: 25-02-2016
DOI: 10.1038/JP.2016.16
Abstract: The objectives of this study were to assess (i) the agreement between servo-control temperature (Tfeedback) and rectal temperature (Tre) and (ii) the distribution of regional skin temperatures (Tsk) of neonates nursed under a radiant warmer (RW) in a neonatal intensive care unit. An observational study of 13 neonates nursed under a RW device set to servo-control mode (Tfeedback set-point: 36.5 °C) who were monitored for Tfeedback, Tre and Tsk at six sites for a period of 105 min. Mean bias for Tfeedback relative to Tre was +0.01 °C, but 95% limits of agreement were ±0.99 °C, and only 66% of Tfeedback values were within the acceptable limits determined a priori (±0.5 °C). Tfeedback was maintained within a range of 1.4 °C (35.9 to 37.3 °C), whereas the range observed for regional skin temperatures spanned from 9.5 °C (27.3 to 36.8 °C foot) to 4.8 °C (33.1 to 37.9 °C chest). Although Tfeedback is maintained within narrow limits, the level of agreement with Tre is poor. In addition, large fluctuations in regional skin temperatures occur with a consistent caudal-to-rostral temperature gradient, irrespective of Tfeedback.
Publisher: American Physiological Society
Date: 2021
DOI: 10.1152/AJPHEART.00536.2020
Abstract: It is generally accepted that older adults display an impaired cardiovascular response to heat stress, and it has been suggested that this impaired response contributes to their increased risk of mortality during extreme heat events. Seminal studies have shown that cutaneous vasodilation, the redistribution of blood flow from visceral organs, and the increase in cardiac output are blunted in older adults during passive heating. The blunted rise of cardiac output was initially attributed to an inability to maintain stroke volume, suggesting that cardiac systolic and/or diastolic function does not adequately respond to the constraints of heat stress in older adults. Recent studies evaluated potential mechanisms underlying these seminal findings and their results challenge some of these initial observations. Notably, stroke volume is maintained during heat exposure in older adults and studies have provided evidence for preserved cardiac systolic and diastolic functions in this population. Nonetheless, a blunted increase in cardiac output during heat exposure remains a consistent observation in older adults, although it is now attributed to a blunted increase in heart rate. Recent studies have also evaluated the possibility that the attenuated capacity of aged skin to vasodilate contributes to a blunted increase in cardiac output during heat stress. The objective of this Mini-Review is to highlight these recent advances and challenge the long-standing view that the control of stroke volume during heat exposure is compromised in older adults. By doing so, our intent is to stimulate future studies to evaluate several unanswered questions in this area of research.
Publisher: American Physiological Society
Date: 05-2022
DOI: 10.1152/JAPPLPHYSIOL.00800.2021
Abstract: Heat therapy has been shown to improve markers of cardiometabolic health in preclinical and clinical studies. However, the effects of heat therapy in in iduals with type 2 diabetes mellitus (T2DM) remain understudied. We examined the acute effect of hot water immersion on glucose tolerance, flow-mediated dilation, reactive hyperemia, inflammatory markers, and heat shock proteins in adults with T2DM. Hot water immersion did not acutely improve the markers studied.
Publisher: Informa UK Limited
Date: 24-05-2020
Publisher: Elsevier BV
Date: 03-2019
DOI: 10.1016/J.JSAMS.2018.09.225
Abstract: To investigate whether the exercise performance benefits with neck cooling in the heat are attributable to neck-specific cooling, general body cooling, a cooler site-specific thermal perception or a combination of the above. Counter-balanced crossover design. Twelve healthy participants cycled in the heat (34°C, 30% relative humidity), at a power output (PO) self-selected to maintain a fixed rating of perceived exertion (RPE) of 16. Each participant underwent four experimental trials: no cooling (CON), neck cooling (NEC), abdominal cooling (ABD), or neck cooling with menthol (MEN). Participants cycled for 90min or until their workload reduced by <70% of their initial PO. Changes in PO, rectal temperature (T The mean reduction in PO throughout exercise was similar (p=0.431) for CON (175±10W), NEC (176 ±12W), ABD (172±13W) and MEN (174±12W). The ΔT No differences in exercise performance or thermal strain were observed in any of the cooling trials compared to the CON trial, despite significantly cooler TS
Publisher: Elsevier BV
Date: 04-2019
DOI: 10.1016/J.MSARD.2019.01.013
Abstract: To reassess the notion that people with multiple sclerosis (MS) do not demonstrate an elevated resting core temperature when measured using best-practice precision thermometry. Across two international data collection sites (Australia and USA), twenty-eight relapsing-remitting MS patients and 27 aged-matched controls (CON) were exposed to either 30 °C, 30% relative humidity (RH) (Sydney) or 25 °C, 30% RH (Dallas). Resting rectal (T Irrespective of ambient temperature, no group differences were observed for T Contrary to recent reports, resting core temperature is not elevated in relapsing-remitting MS patients compared to healthy controls when measured using precision thermometry. Furthermore, no association was observed between resting T
Publisher: Springer Science and Business Media LLC
Date: 24-06-2021
DOI: 10.1007/S40279-021-01504-Y
Abstract: Despite the well-established benefits of exercise, pregnant women are discouraged from physical activity in hot/humid conditions to avoid hyperthermia (core temperature (T Thirty participants (15 pregnant in their second trimester or third trimester) completed two separate exercise-heat exposures in a climate chamber (32 °C, 45%RH). On separate occasions, each participant cycled on a semi-recumbent cycle ergometer for 45 min at a workload representative of a moderate-intensity (1) non-weight-bearing (NON-WB), or (2) weight-bearing (WB) activity. Thermoregulatory responses were monitored throughout. The highest rectal temperature observed in a pregnant in idual was 37.93 °C. Mean end-exercise rectal temperature did not differ between groups (P:37.53 ± 0.22 °C, NP:37.52 ± 0.34 °C, P = 0.954) in the WB trial, but was lower in the P group (P:37.48 ± 0.25 °C, vs NP:37.73 ± 0.38 °C, P = 0.041) in the NON-WB trial. Whole-body sweat loss was unaltered by pregnancy during WB (P:266 ± 62 g, NP:264 ± 77 g P = 0.953) and NON-WB P:265 ± 51 g, NP:300 ± 75 g P = 0.145) exercise. Pregnant participants reported higher ratings of thermal sensation (felt hotter) than their non-pregnant counterparts in the WB trial (P = 0.002) but not in the NON-WB trial, (P = 0.079). Pregnant women can perform 45 min of moderate-intensity exercise at 32 °C, 45%RH with very low apparent risk of excessive maternal hyperthermia. No thermoregulatory impairments with pregnancy were observed.
Publisher: Wiley
Date: 29-10-2015
DOI: 10.1113/JP271507
Publisher: Elsevier BV
Date: 10-2023
Publisher: American Physiological Society
Date: 2019
DOI: 10.1152/AJPREGU.00028.2018
Abstract: This study sought to determine whether the temperature of water ingested before exercise alters the onset threshold and subsequent thermosensitivity of local vasomotor and sudomotor responses after exercise begins. Twenty men [24 (SD 4) yr of age, 75.8 (SD 8.1) kg body mass, 52.3 (SD 7.7) ml·min −1 ·kg −1 peak O 2 consumption (V̇o 2peak )] ingested 1.5°C, 37°C, or 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50% V̇o 2peak for 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (T b ), local sweat rate (LSR), and skin blood flow (SBF) were measured. In a subset of eight men [25 (SD 5) yr of age, 78.6 (SD 8.3) kg body mass, 48.9 (SD 11.1) ml·min −1 ·kg −1 V̇o 2peak ], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in T b was greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔT b = 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔT b = 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔT b = 0.18 (SD 0.15) °C, 0.11 (SD 0.13) °C, and 0.09 (SD 0.09) °C with 1.5°C, 37°C, and 50°C water, respectively, P = 0.07]. Conversely, the thermosensitivity of LSR and SBF was not different [LSR = 1.11 (SD 0.75), 1.11 (SD 0.75), and 1.34 (SD 1.11) mg·min −1 ·cm −2 ·°C −1 with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.46) SBF = 717 (SD 882), 517 (SD 606), and 857 (SD 904) %baseline arbitrary units (AU)/°C with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.95)]. After 15 min of exercise, LSR and SBF were greater with ingestion of 50°C than 1.5°C water [LSR = 0.40 (SD 0.17) vs. 0.31 (SD 0.19) mg·min −1 ·cm −2 ( P = 0.02) SBF = 407 (SD 149) vs. 279 (SD 117) %baseline AU ( P 0.001)], but not 37°C water [LSR = 0.50 (SD 0.22) mg·min −1 ·cm −2 SBF = 324 (SD 169) %baseline AU]. CVC was statistically unaffected [275 (SD 81), 340 (SD 114), and 384 (SD 160) %baseline CVC with 1.5°C, 37°C, and 50°C ingested water, respectively, P = 0.30]. Collectively, these results support the concept that visceral thermoreceptors modify the central drive for thermoeffector responses.
Publisher: Elsevier BV
Date: 11-2021
DOI: 10.1016/J.CJCA.2021.08.008
Abstract: As global temperatures continue to rise, extreme heat events are becoming more frequent and intense. Extreme heat affects cardiovascular health as it is associated with a greater risk of adverse cardiovascular events, especially for adults with preexisting cardiovascular diseases. Nonetheless, the pathophysiology underlying the association between extreme heat and cardiovascular risk remains understudied. Furthermore, specific recommendations to mitigate the effects of extreme heat on cardiovascular health remain limited to guide clinical practice within the context of a warming climate. The overall objective of this review article is to raise awareness that extreme heat poses a risk for cardiovascular health. Specifically, the review discusses why cardiovascular healthcare professionals should care about extreme heat, how extreme heat affects cardiovascular health, and recommendations to minimise the cardiovascular consequences of extreme heat. Future research directions are also provided to further our understating of the cardiovascular health consequences of extreme heat. A better awareness and understanding of the cardiovascular consequences of extreme heat will help cardiovascular health professionals assess the risk and optimise the care of their patients exposed to an increasingly warm climate.
Publisher: American Physiological Society
Date: 03-2021
DOI: 10.1152/AJPREGU.00090.2020
Abstract: The purpose of this study is to determine whether thermoregulatory capacity is altered by multiple sclerosis (MS) during exercise in the heat. Sixteen MS participants (EDSS: 2.9 ± 0.9 47 ± 8 yr 77.6 ± 14.0 kg) and 14 healthy control (CON) participants (43 ± 11 yr 78.6 ± 17.0 kg) cycled at a heat production of 4 W·kg −1 for 60 min at 30°C, 30% relative humidity (RH) (Warm). A subset of eight MS (EDSS: 2.6 ± 0.5 44 ± 8 yr 82.3 ± 18.2 kg) and 8 CON (44 ± 12 yr 81.2 ± 21.1 kg) also exercised at 35°C, 30% RH (Hot). Rectal temperature (T re ), mean skin (T sk ) temperature, and local sweat rate (LSR) on the upper back (LSR back ) and forearm (LSR arm ) were measured. All CON, and only 9 of 16 and 7 of 8 MS participants completed 60 min of exercise in Warm and Hot trials, respectively. All MS participants who were unable to complete exercise stopped with a ΔT re between 0.2 and 0.5°C. The time to reach a ΔT re of 0.2°C was similar (MS: 28 ± 15 min, CON: 32 ± 18 min P = 0.51). For MS participants, completing 60-min of exercise in Warm, ΔT re ( P = 0.13), ΔT sk ( P = 0.45), LSR back ( P = 0.69), and LSR arm ( P = 0.54) was similar to CON, but ΔT b (body temperature) (MS: 0.16 ± 0.13°C, CON: 0.07 ± 0.06°C P = 0.02) and onset time (MS: 16 ± 10 min, CON: 8 ± 5 min P = 0.02) for sweating were greater in MS. Similarly, in Hot, ΔT re ( P = 0.52), ΔT sk ( P = 0.06), LSR back ( P = 0.59), and LSR arm ( P = 0.08) were similar, but ΔT b (MS: 0.19 ± 0.16°C, CON: 0.06 ± 0.04°C P = 0.04) and onset time (MS: 13 ± 7 min, CON: 6 ± 3 min P = 0.02) for sweating were greater in MS. Even at 35°C, a delayed sweating onset did not alter heat loss to sufficiently affect exercise-induced rises in core temperature. Heat intolerance with MS does not seem attributable to thermoregulatory impairments.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-2018
Publisher: Wiley
Date: 05-2021
Publisher: Elsevier BV
Date: 2024
Publisher: American Physiological Society
Date: 15-03-2016
DOI: 10.1152/JAPPLPHYSIOL.00906.2015
Abstract: We sought to determine 1) the influence of adiposity on thermoregulatory responses independently of the confounding biophysical factors of body mass and metabolic heat production (H prod ) and 2) whether differences in adiposity should be accounted for by prescribing an exercise intensity eliciting a fixed H prod per kilogram of lean body mass (LBM). Nine low (LO-BF) and nine high (HI-BF) body fat males matched in pairs for total body mass (TBM LO-BF: 88.7 ± 8.4 kg, HI-BF: 90.1 ± 7.9 kg P = 0.72), but with distinctly different percentage body fat (%BF LO-BF: 10.8 ± 3.6% HI-BF: 32.0 ± 5.6% P 0.001), cycled for 60 min at 28.1 ± 0.2°C, 26 ± 8% relative humidity (RH), at a target H prod of 1) 550 W (FHP trial) and 2) 7.5 W/kg LBM (LBM trial). Changes in rectal temperature (ΔT re ) and local sweat rate (LSR) were measured continuously while whole body sweat loss (WBSL) and net heat loss (H loss ) were estimated over 60 min. In the FHP trial, ΔT re (LO-BF: 0.66 ± 0.21°C, HI-BF: 0.87 ± 0.18°C P = 0.02) was greater in HI-BF, whereas mean LSR (LO-BF 0.52 ± 0.19, HI-BF 0.43 ± 0.15 mg·cm −2 ·min −1 P = 0.19), WBSL (LO-BF 586 ± 82 ml, HI-BF 559 ± 75 ml P = 0.47) and H loss (LO-BF 1,867 ± 208 kJ, HI-BF 1,826 ± 224 kJ P = 0.69) were all similar. In the LBM trial, ΔT re (LO-BF 0.82 ± 0.18°C, HI-BF 0.54 ± 0.19°C P 0.001), mean LSR (LO-BF 0.59 ± 0.20, HI-BF 0.38 ± 0.12 mg·cm −2 ·min −1 P = 0.04), WBSL (LO-BF 580 ± 106 ml, HI-BF 381 ± 68 ml P 0.001), and H loss (LO-BF 1,884 ± 277 kJ, HI-BF 1,341 ± 184 kJ P 0.001) were all greater at end-exercise in LO-BF. In conclusion, high %BF in iduals demonstrate a greater ΔT re independently of differences in mass and H prod , possibly due to a lower mean specific heat capacity or impaired sudomotor control. However, thermoregulatory responses of groups with different adiposity levels should not be compared using a fixed H prod in watts per kilogram lean body mass.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 03-2019
DOI: 10.1249/MSS.0000000000001821
Abstract: Impairments in sudomotor function during passive whole-body heating have been reported in multiple sclerosis (MS), a demyelinating disease of the CNS that disrupts autonomic function. However, the capability of the thermoregulatory system to control body temperature during exercise has never been assessed in MS. Thus, the aim of the present study was to test the hypothesis that thermoregulatory function is impaired in MS patients compared with healthy controls (CON) exercising at similar rates of metabolic heat production. Sweating and skin blood flow responses were compared between 12 in iduals diagnosed with relapsing-remitting MS (9 females, 3 males) and 12 sex-, age-, mass-, and BSA-matched CON during a single bout of cycling exercise (rate of metabolic heat production: ∼4.5 W·kg −1 ) for 60 min in a climate-controlled room (25°C, 30% RH). In iduals with MS exhibited an attenuated increase in cumulative whole-body sweat loss after 30 min (MS, 72 ± 51 g CON, 104 ± 37 g P = 0.04) and 60 min (MS, 209 ± 94 g CON, 285 ± 62 g P = 0.02), as well as lower sweating thermosensitivity (MS, 0.49 ± 0.26 mg·cm −2 ·min −1 ·°C −1 CON, 0.86 ± 0.30 mg·cm −2 ·min −1 ·°C −1 P = 0.049). Despite evidence for thermoregulatory dysfunction, there were no differences between MS and CON in esophageal or rectal temperatures at 30- or 60-min time points ( P 0.05). Cutaneous vasculature responses were also not different in MS compared with CON ( P 0.05). Taken together, MS blunts sweating responses during exercise while cutaneous vasculature responses are preserved. Altered mechanisms of body temperature regulation in persons with MS may lead to temporary worsening of disease symptoms and limit exercise tolerance under more thermally challenging conditions.
Publisher: Wiley
Date: 05-2021
Publisher: Wiley
Date: 05-2021
Publisher: Wiley
Date: 26-02-2020
DOI: 10.1113/JP279266
Publisher: Elsevier BV
Date: 06-2021
Publisher: Wiley
Date: 23-05-2017
DOI: 10.1113/EP086320
Publisher: Elsevier BV
Date: 2023
DOI: 10.1016/J.HLC.2022.10.010
Abstract: Extreme heat events are a leading natural hazard risk to human health. Under all future climate change models, extreme heat events will continue to increase in frequency, duration, and intensity. Evidence from previous extreme heat events across the globe demonstrates that adverse cardiovascular events are the leading cause of morbidity and mortality, particularly amongst the elderly and those with pre-existing cardiovascular disease. However, less is understood about the adverse effects of extreme heat amongst specific cardiovascular diseases (i.e., heart failure, dysrhythmias) and demographics (sex, ethnicity, age) within Australia and New Zealand. Furthermore, although Australia has implemented regional and state heat warning systems, most personal heat-health protective advice available in public health policy documents is either insufficient, not grounded in scientific evidence, and/or does not consider clinical factors such as age or co-morbidities. Dissemination of evidence-based recommendations and enhancing community resilience to extreme heat disasters within Australia and New Zealand should be an area of critical focus to reduce the burden and negative health effects associated with extreme heat. This narrative review will focus on five key areas in relation to extreme heat events within Australia and New Zealand: 1) the potential physiological mechanisms that cause adverse cardiovascular outcomes during extreme heat events 2) how big is the problem within Australia and New Zealand? 3) what the heat-health response plans are 4) research knowledge and translation and, 5) knowledge gaps and areas for future research.
Start Date: 2022
End Date: 2025
Funder: Canadian Institutes of Health Research
View Funded ActivityStart Date: 2022
End Date: 2025
Funder: Heart and Stroke Foundation of Canada
View Funded ActivityStart Date: 2021
End Date: 2021
Funder: Canadian Institute for Military and Veteran Health Research
View Funded ActivityStart Date: 2020
End Date: 2023
Funder: Fonds de Recherche du Québec - Santé
View Funded ActivityStart Date: 2016
End Date: 2018
Funder: Multiple Sclerosis Research Australia
View Funded Activity