A National Survey of Patient Data Capture, Management, Reporting Practice in Australian Cardiac Rehabilitation Programs.

BACKGROUND: Lack of service data for cardiac rehabilitation limits understanding of program delivery, benchmarking and quality improvement. This study aimed to describe current practices, management, utilisation and engagement with quality indicators in Australian programs. METHOD: Cardiac rehabilitation programs (n=396) were identified from national directories and networks. Program coordinators were surveyed on service data capture, management systems and adoption of published national quality indicators. Text responses were coded and classified. Logistic regression determined independent associates of the use of data for quality improvement. RESULTS: A total of 319 (81%) coordinators completed the survey. Annual patient enrolments/programs were >200 (31.0%), 51-200 (46%) and ≤50 (23%). Most (79%) programs used an electronic system, alongside paper (63%) and/or another electronic system (19%), with 21% completely paper. While 84% knew of the national quality indicators, only 52% used them. Supplementary to patient care, data were used for reports to managers (57%) and funders (41%), to improve quality (56%), support funding (43%) and research (31%). Using data for quality improvement was more likely when enrolments where >200 (Odds ratio [OR] 3.83, 95% Confidence Interval [CI] 1.76-8.34) and less likely in Victoria (OR 0.24 95%, CI 0.08-0.77), New South Wales (OR 0.25 95%, CI 0.08-0.76) and Western Australia (OR 0.16 95%, CI 0.05-0.57). CONCLUSIONS: The collection of service data for cardiac rehabilitation patient data and its justification is diverse, limiting our capacity to benchmark and drive clinical practice. The findings strengthen the case for a national low-burden approach to data capture for quality care.

Finnish sauna bathing and vascular health of adults with coronary artery disease: a randomized controlled trial.

Regular Finnish sauna use is associated with a reduced risk of cardiovascular mortality. However, physiological mechanisms underlying this association remain unknown. This study determined if an 8-wk Finnish sauna intervention improves peripheral endothelial function, microvascular function, central arterial stiffness, and blood pressure in adults with coronary artery disease (CAD). Forty-one adults (62 ± 6 yr, 33 men/8 women) with stable CAD were randomized to 8 wk of Finnish sauna use (n = 21, 4 sessions/wk, 20-30 min/session, 79°C, 13% relative humidity) or a control intervention (n = 20, lifestyle maintenance). Brachial artery flow-mediated dilation (FMD), carotid-femoral pulse wave velocity (cf-PWV), total (area under the curve) and peak postocclusion forearm reactive hyperemia, and blood pressure (automated auscultation) were measured before and after the intervention. After the sauna intervention, resting core temperature was lower (-0.27°C [-0.54, -0.01], P = 0.046) and sweat rate during sauna exposure was greater (0.3 L/h [0.1, 0.5], P = 0.003). The change in brachial artery FMD did not differ between interventions (control: 0.07% [-0.99, +1.14] vs. sauna: 0.15% [-0.89, +1.19], interaction P = 0.909). The change in total (P = 0.031) and peak (P = 0.024) reactive hyperemia differed between interventions due to a nonsignificant decrease in response to the sauna intervention and an increase in response to control. The change in cf-PWV (P = 0.816), systolic (P = 0.951), and diastolic (P = 0.292) blood pressure did not differ between interventions. These results demonstrate that four sessions of Finnish sauna bathing per week for 8 wk does not improve markers of vascular health in adults with stable CAD.NEW & NOTEWORTHY This study determined if unsupervised Finnish sauna bathing for 8 wk improves markers of vascular health in adults with coronary artery disease. Finnish sauna bathing reduced resting core temperature and improved sweating capacity, indicative of heat acclimation. Despite evidence of heat acclimation, Finnish sauna bathing did not improve markers of endothelial function, microvascular function, arterial stiffness, or blood pressure.

The acute effect of heat exposure on forearm macro- and microvascular function: Impact of measurement timing, heating modality and biological sex.

NEW FINDINGS: What is the central question of this study? Do measurement timing, heating modality and biological sex modulate the acute effect of heat exposure on brachial artery flow-mediated dilatation and postocclusion reactive hyperaemia? What is the main finding and its importance? The acute effect of heat exposure on brachial artery flow-mediated dilatation and postocclusion reactive hyperaemia is: (1) transient and short lasting; (2) different between forearm and whole-body heating; (3) unaffected by forearm heating during whole-body heating; and (4) not different but not always equivalent between males and females. These findings provide a useful basis for future studies to investigate the acute effect of heat exposure on vascular function. ABSTRACT: The aim of this study was to gain a better understanding of the acute effect of heat exposure on brachial artery flow-mediated dilatation (FMD) and postocclusion reactive hyperaemia (PORH) by: characterizing the time course of changes post-heating; comparing forearm and whole-body heating; determining the impact of forearm heating during whole-body heating; and comparing males and females. Twenty adults (11 males and nine females; 28 ± 6 years of age) underwent two forearm [10 min electric blanket (EB) or 30 min hot water immersion (WI)] and two whole-body [60 min water-perfused suit with forearm covered (WBH-C) or uncovered (WBH-U)] heating modalities. The FMD and PORH were measured before and after (≤5, 30, 60, 90 and 120 min) heating. The FMD increased from baseline 30 min after EB, and 30 and 90 min after WI. In contrast, FMD decreased from baseline immediately after both WBH modalities. Peak PORH increased immediately after WI and both WBH modalities. Total PORH did not differ after WI, whereas it decreased immediately after both WBH modalities. Covering the forearm during WBH did not alter acute changes in FMD or PORH. Changes in FMD and PORH did not differ statistically between males and females during each heating modality, although the observed differences could not always be considered equivalent. These results demonstrate that the acute effect of heat exposure on brachial artery FMD and PORH is: (1) transient and short lasting; (2) different between forearm heating and WBH; (3) unaffected by direct forearm heating during WBH; and (4) not different but not always equivalent between males and females.

Extreme Heat and Adverse Cardiovascular Outcomes in Australia and New Zealand: What Do We Know?

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.

Acute effect of passive heat exposure on markers of cardiometabolic function in adults with type 2 diabetes mellitus.

Heat therapy is a promising strategy to improve cardiometabolic health. This study evaluated the acute physiological responses to hot water immersion in adults with type 2 diabetes mellitus (T2DM). On separate days in randomized order, 13 adults with T2DM [8 males/5 females, 62 ± 12 yr, body mass index (BMI): 30.1 ± 4.6 kg/m2] were immersed in thermoneutral (34°C, 90 min) or hot (41°C, core temperature ≥38.5°C for 60 min) water. Insulin sensitivity was quantified via the minimal oral model during an oral glucose tolerance test (OGTT) performed 60 min after immersion. Brachial artery flow-mediated dilation (FMD) and reactive hyperemia were evaluated before and 40 min after immersion. Blood samples were drawn to quantify protein concentrations and mRNA levels of HSP70 and HSP90, and circulating concentrations of cytokines. Relative to thermoneutral water immersion, hot water immersion increased core temperature (+1.66°C [+1.47, +1.87], P < 0.01), heart rate (+34 beats/min [+24, +44], P < 0.01), antegrade shear rate (+96 s-1 [+57, +134], P < 0.01), and IL-6 (+1.38 pg/mL [+0.31, +2.45], P = 0.01). Hot water immersion did not exert an acute change in insulin sensitivity (-0.3 dL/kg/min/µU/mL [-0.9, +0.2], P = 0.18), FMD (-1.0% [-3.6, +1.6], P = 0.56), peak (+0.36 mL/min/mmHg [-0.71, +1.43], P = 0.64), and total (+0.11 mL/min/mmHg × min [-0.46, +0.68], P = 0.87) reactive hyperemia. There was also no change in eHSP70 (P = 0.64), iHSP70 (P = 0.06), eHSP90 (P = 0.80), iHSP90 (P = 0.51), IL1-RA (P = 0.11), GLP-1 (P = 0.59), and NF-κB (P = 0.56) after hot water immersion. The physiological responses elicited by hot water immersion do not acutely improve markers of cardiometabolic function in adults with T2DM.NEW & NOTEWORTHY Heat therapy has been shown to improve markers of cardiometabolic health in preclinical and clinical studies. However, the effects of heat therapy in individuals 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.

Extreme Heat and Cardiovascular Health: What a Cardiovascular Health Professional Should Know.

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.

Thermoregulation During Pregnancy: a Controlled Trial Investigating the Risk of Maternal Hyperthermia During Exercise in the Heat.

OBJECTIVES: Despite the well-established benefits of exercise, pregnant women are discouraged from physical activity in hot/humid conditions to avoid hyperthermia (core temperature (Tcore) ≥ 39.0 °C). Recent epidemiological evidence also demonstrates greater risk of negative birth outcomes following heat exposure during pregnancy, possibly due to thermoregulatory impairments. We aimed to determine (1) the risk of pregnant women exceeding a Tcore of 39.0 °C during moderate-intensity exercise in the heat; and (2) if any thermoregulatory impairments are evident in pregnant (P) versus non-pregnant (NP) women. METHODS: 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. RESULTS: The highest rectal temperature observed in a pregnant individual 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). CONCLUSION: 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.

Electric fan use for cooling during hot weather: a biophysical modelling study.

BACKGROUND: In hot weather, electric fans can potentially provide effective cooling for people, with lower greenhouse gas emissions and cost than air conditioning. However, international public health organisations regularly discourage fan use in temperatures higher than 35°C, despite little evidence. We aimed to determine humidity-dependent temperature thresholds at which electric fans would become detrimental in different age groups. METHODS: We used biophysical modelling to determine the upper humidity-dependent temperature thresholds at which fan use would become detrimental (ie, worsen heat stress) for healthy young adults (aged 18-40 years), healthy older adults (aged ≥65 years), and older adults taking anticholinergic medication. We also obtained hourly environmental data for the period Jan 1, 2007, to Dec 31, 2019, for 108 populous cities to determine the number of days fan use would be effective for cooling, standardised to a 31-day hot weather month. We established simplified temperature thresholds for future fan use recommendations on the basis of temperatures below which fan use would never have been detrimental between Jan 1, 2007, and Dec 31, 2019, across all prevailing levels of ambient humidity. FINDINGS: According to our model, fan use would have been beneficial on 30·0 (96·6%) of 31 hot weather days for healthy young adults and 29·4 (94·9%) of 31 hot weather days for both older adults and older adults taking anticholinergic medication between Jan 1, 2007, and Dec 31, 2019. Adherence to the current WHO recommendation of fan use below temperatures of 35°C only, fan use would have been recommended on 27·2 days (87·7%) of 31 hot weather days. According to our simplified thresholds for fan use (at temperatures <39·0°C for healthy young adults, <38·0°C for healthy older adults, and <37·0°C for older adults taking anticholinergic medication), fan use would have been recommended on 29·6 (95·5%) of 31 hot weather days in healthy young adults, 29·4 (94·8%) days in healthy older adults, and 28·8 (93·0%) days in older adults taking anticholinergic medication between Jan 1, 2007, and Dec 31, 2019. INTERPRETATION: Electric fan use, particularly for healthy young adults, would not have worsened heat stress on the majority of study days between 2007 and 2019. Our newly proposed thresholds for fan use provide simple guidelines that improve future heatwave fan use recommendations. FUNDING: None.

Blunted sweating does not alter the rise in core temperature in people with multiple sclerosis exercising in the heat.

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 (Tre), mean skin (Tsk) temperature, and local sweat rate (LSR) on the upper back (LSRback) and forearm (LSRarm) 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 ΔTre between 0.2 and 0.5°C. The time to reach a ΔTre 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, ΔTre (P = 0.13), ΔTsk (P = 0.45), LSRback (P = 0.69), and LSRarm (P = 0.54) was similar to CON, but ΔTb (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, ΔTre (P = 0.52), ΔTsk (P = 0.06), LSRback (P = 0.59), and LSRarm (P = 0.08) were similar, but ΔTb (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.

Cardiovascular control during heat stress in older adults: time for an update.

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.

Improved neural control of body temperature following heat acclimation in humans.

KEY POINTS: With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7 day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans. ABSTRACT: Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14 healthy adults (nine men and five women, aged 27 ± 5 years) during passive heat stress performed before and after a 7 day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54 L h-1 (0.32, 0.75), P < 0.01] and reduced resting core temperature [-0.29°C (-0.40, -0.18), P < 0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [-0.21°C (-0.34, -0.08), P < 0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [-0.18°C (-0.35, -0.01), P = 0.04] and local sweat rate [-0.13°C (-0.24, -0.01), P = 0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating.

Skin blood flow measurements during heat stress: technical and analytical considerations.

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.

Impaired Thermoregulatory Function during Dynamic Exercise in Multiple Sclerosis.

INTRODUCTION: 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. METHODS: Sweating and skin blood flow responses were compared between 12 individuals 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) for 60 min in a climate-controlled room (25°C, 30% RH). RESULTS: Individuals 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·min·°C; CON, 0.86 ± 0.30 mg·cm·min·°C; 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). CONCLUSION: 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.

Core temperature is not elevated at rest in people with relapsing-remitting multiple sclerosis.

PURPOSE: 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. METHOD: 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 (Tre) and esophageal (Teso) temperature and resting oxygen consumption (VO2) was measured in MS (n = 28) and CON (n = 27) groups who completed the 25 °C and 30 °C trials. Tympanic membrane (Ttym) temperature was measured in MS (n = 16) and CON (n = 15) groups in the 30 °C condition. A modified fatigue impact scale (MFIS) questionnaire was used to assess subjective measures of psychosocial, physical and cognitive fatigue in the 30 °C condition. RESULTS: Irrespective of ambient temperature, no group differences were observed for Tre (MS: 37.07 ±â€¯0.30 °C; CON: 37.18 ±â€¯0.30 °C; P = 0.29), Teso (MS: 36.84 ±â€¯0.42 °C; CON: 36.92 ±â€¯0.29 °C; P = 0.36) or resting VO2 (MS: 3.89 ±â€¯0.18 ml⋅kg-1⋅min-1; CON: 3.98 ±â€¯0.17 ml⋅kg-1⋅min-1; P = 0.67). Similarly, no group differences were observed for Ttym (MS: 36.52 ±â€¯0.38 °C; CON: 36.61 ±â€¯0.33 °C; P = 0.55) in the 30 °C condition. Resting Tre did not correlate with subjective measures of fatigue: physical: r = -0.11, P = 0.67; cognitive: r = -0.14, P = 0.60; and psychosocial: r = 0.05, P = 0.84. CONCLUSION: 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 Tre and any subjective measures of fatigue in a subset of participants with MS.

Self-paced exercise performance in the heat with neck cooling, menthol application, and abdominal cooling.

OBJECTIVES: 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. DESIGN: Counter-balanced crossover design. METHODS: 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 (Tre), mean skin temperature (Tsk), whole-body thermal sensation (TSwb) and thermal sensation of the neck (TSneck) were recorded throughout. RESULTS: 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 ΔTre at the end of exercise was similar (p=0.874) for CON (0.83±0.5°C), NEC (0.85±0.5°C), ABD (0.82±0.5°C) and MEN (0.81±0.5°C). TSwb was cooler (p<0.013) in MEN (125±8mm) compared to CON (146±19mm), NEC (135±11mm) and ABD (141±16mm). CONCLUSIONS: No differences in exercise performance or thermal strain were observed in any of the cooling trials compared to the CON trial, despite significantly cooler TSwb values in the MEN and NEC trials compared to the CON trial. These findings differ from previous observations and highlight that the benefit of neck cooling may be situation dependent.

Temperature of water ingested before exercise alters the onset of physiological heat loss responses.

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 O2 consumption (V̇o2peak)] ingested 1.5°C, 37°C, or 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50% V̇o2peak for 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (Tb), 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 V̇o2peak], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in Tb was greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔTb = 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔTb = 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔTb = 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.

Cold Water Ingestion Improves Exercise Tolerance of Heat-Sensitive People with MS.

PURPOSE: Heat intolerance commonly affects the exercise capacity of people with multiple sclerosis (MS) during bouts of hot weather. Cold water ingestion is a simple cooling strategy, but its efficacy for prolonging exercise capacity with MS remains undetermined. We sought to identify whether cold water ingestion blunts exercise-induced rises in body temperature and improves exercise tolerance in heat-sensitive individuals with MS. METHODS: On two separate occasions, 20 participants (10 relapsing-remitting MS (expanded disability status scale, 2-4.5); 10 age-matched healthy controls) cycled at ∼40% V˙O2max at 30°C and 30% relative humidity until volitional exhaustion (or a maximum of 60 min). Every 15 min, participants ingested 3.2 mL·kg of either 1.5°C (CLD) or 37°C (NEU) water. Rectal (Tre) temperature, mean skin (Tsk) temperature, and heart rate (HR) were measured throughout. RESULTS: All 10 controls but only 3 of 10 MS participants completed 60 min of exercise in NEU trial. The remaining 7 MS participants all cycled longer (P = 0.006) in CLD (46.4 ± 14.2 min) compared with NEU (32.7 ± 11.5 min), despite a similar absolute Tre (NEU: 37.32°C ± 0.34°C; CLD: 37.28°C ± 0.26°C; P = 0.44), change in Tre (NEU: 0.38°C ± 0.21°C; CLD: 0.34°C ± 0.24°C), absolute Tsk (NEU: 34.48°C ± 0.47°C; CLD: 34.44°C ± 0.54°C; P = 0.82), and HR (NEU: 114 ± 20 bpm; CLD: 113 ± 18 bpm; P = 0.38) for the same exercise volume. CONCLUSIONS: Cold water ingestion enhanced exercise tolerance of MS participants in the heat by ∼30% despite no differences in Tre, Tsk or HR. These findings support the use of a simple cooling strategy for mitigating heat intolerance with MS and lend insight into the potential role of cold-afferent thermoreceptors that reside in the abdomen and oral cavity in the modulation of exercise tolerance with MS in the heat.

A comparison of thermoregulatory responses to exercise between mass-matched groups with large differences in body fat.

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 (Hprod); and 2) whether differences in adiposity should be accounted for by prescribing an exercise intensity eliciting a fixed Hprod 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 Hprod of 1) 550 W (FHP trial) and 2) 7.5 W/kg LBM (LBM trial). Changes in rectal temperature (ΔTre) and local sweat rate (LSR) were measured continuously while whole body sweat loss (WBSL) and net heat loss (Hloss) were estimated over 60 min. In the FHP trial, ΔTre (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 Hloss (LO-BF 1,867 ± 208 kJ, HI-BF 1,826 ± 224 kJ; P = 0.69) were all similar. In the LBM trial, ΔTre (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 Hloss (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 individuals demonstrate a greater ΔTre independently of differences in mass and Hprod, 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 Hprod in watts per kilogram lean body mass.