The Effect of Heat Exposure on Myocardial Blood Flow and Cardiovascular Function.

BACKGROUND: Heat extremes are associated with greater risk for cardiovascular death. The pathophysiologic mechanisms mediating this association are unknown. OBJECTIVE: To quantify the myocardial blood flow (MBF) requirements of heat exposure. DESIGN: Experimental study. (ClinicalTrials.gov: NCT04549974). SETTING: Laboratory-based. PARTICIPANTS: 61 participants, comprising 20 healthy young adults (mean age, 28 years), 21 healthy older adults (mean age, 67 years), and 20 older adults with coronary artery disease (CAD) (mean age, 70 years). INTERVENTION: Participants were heated until their core temperature increased 1.5 °C; MBF was measured before heat exposure and at every increase of 0.5 °C in core temperature. MEASUREMENTS: The primary outcome was MBF measured by positron emission tomography-computed tomography. Secondary outcomes included heart rate, blood pressure, and body weight change. RESULTS: At a core temperature increase of 1.5 °C, MBF increased in healthy young adults (change, 0.8 mL/min/g [95% CI, 0.5 to 1.0 mL/min/g]), healthy older adults (change, 0.7 mL/min/g [CI, 0.5 to 0.9 mL/min/g]), and older adults with CAD (change, 0.6 mL/min/g [CI, 0.3 to 0.8 mL/min/g]). This represented a 2.08-fold (CI, 1.75- to 2.41-fold), 1.79-fold (CI, 1.59- to 1.98-fold), and 1.64-fold (CI, 1.41- to 1.87-fold) change, respectively, from preexposure values. Imaging evidence of asymptomatic heat-induced myocardial ischemia was seen in 7 adults with CAD (35%) in post hoc analyses. LIMITATIONS: In this laboratory-based study, heating was limited to about 100 minutes and participants were restricted in movement and fluid intake. Participants refrained from strenuous exercise and smoking; stopped alcohol and caffeine intake; and withheld ß-blockers, calcium-channel blockers, and nitroglycerin before heating. CONCLUSION: Heat exposure that increases core temperature by 1.5 °C nearly doubles MBF. Changes in MBF did not differ by age or presence of CAD, but some older adults with CAD may experience asymptomatic myocardial ischemia. PRIMARY FUNDING SOURCE: Canadian Institutes of Health Research.

A dataset of proteomic changes during human heat stress and heat acclimation.

Hotter climates have important impacts on human health and performance. Yet, the cellular and molecular responses involved in human heat stress and acclimation remain understudied. This dataset includes physiological measurements and the plasma concentration of 2,938 proteins collected from 10 healthy adults, before and during passive heat stress that was performed both prior to and after a 7-day heat acclimation protocol. Physiological measurements included body temperatures, sweat rate, cutaneous vascular conductance, blood pressure, and skin sympathetic nerve activity. The proteomic dataset was generated using the Olink Explore 3072 assay, enabling a high-multiplex antibody-based assessment of protein changes based on proximity extension assay technology. The data need to be interpreted in the context of the moderate level of body hyperthermia attained and the specific demographic of young, healthy adults. We have made this dataset publicly available to facilitate research into the cellular and molecular mechanisms involved in human heat stress and acclimation, crucial for addressing the health and performance challenges posed by rising temperatures.

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 Presence of Wind Worsens the Effect of Cold Temperature on Time to Ischemia in Patients with Stable Angina.

PURPOSE: This study tested the hypothesis that the combination of cold temperature and wind further reduces time to ischemia during treadmill stress testing compared with cold temperature alone. METHODS: Eighteen participants (56 ± 9 yr) with stable angina performed four treadmill stress tests in a randomized crossover design at +20°C and -8°C, with and without a 24-km·h -1 headwind. Time to ischemia (≥1-mm ST-segment depression) and angina, rate pressure product, and total exercise duration were determined. RESULTS: At -8°C, time to ischemia was reduced by 22% (-58 s (-85 to -31 s), P < 0.01) compared with +20°C. The addition of wind at -8°C reduced time to ischemia by a further 15% (-31 s (-58 to -4 s) vs -8°C without wind, P = 0.02). The addition of wind did not affect time to ischemia at +20°C ( P = 0.38). Cold temperature and wind did not affect time to angina ( P = 0.46 and P = 0.61) or rate pressure product ( P = 0.46 and P = 0.09). Total exercise time was reduced in the presence of wind at -8°C (-29 s (-51 to -7 s), P = 0.01), but not at +20°C ( P = 0.09). CONCLUSIONS: The presence of wind reduces time to ischemia when exercise stress testing is performed in a cold environment. These results suggest that wind should be considered when evaluating the risks posed by cold weather in patients with coronary artery disease and exercise-induced ischemia.

Impact of passive heat stress and passive heat acclimation on circulating extracellular vesicles: An exploratory analysis.

NEW FINDINGS: What is the central question of this study? How does passive heat stress and subsequent heat acclimation affect the circulating concentration of extracellular vesicles? What is the main finding and its importance? Passive heat stress increased the circulating concentration of total and platelet extracellular vesicles. Seven days of hot water immersion did not modify the change in circulating concentrations of extracellular vesicles during passive heat stress. ABSTRACT: This retrospective exploratory analysis aimed to improve our understanding of the effect of passive heat stress and subsequent heat acclimation on the circulating concentration of extracellular vesicles (EVs). Healthy young adults (four females and six males, 25 ± 4 years of age, 1.72 ± 0.08 m in height and weighing 71.6 ± 9.0 kg) were heated with a water-perfused suit before and after seven consecutive days of hot water immersion. Pre-acclimation, participants were heated until oesophageal temperature increased to ∼1.4°C above baseline values. Post-acclimation, participants were heated until oesophageal temperature reached the same absolute value as the pre-acclimation visit (∼38.2°C). Venous blood samples were obtained before and at the end of passive heating to quantify plasma concentrations of EVs from all cell types (CSFE+ ), all cell types except erythrocytes (CSFE+ MHCI+ ), platelets (CSFE+ MHCI+ CD41+ ), endothelial cells (CSFE+ MHCI+ CD62e+ ), red blood cells (CSFE+ CD235a+ ) and leucocytes (CSFE+ MHCI+ CD45+ ) via flow cytometry. Passive heat stress increased the concentration of CFSE+ EVs (46,150,000/ml [3,620,784, 88,679,216], P = 0.036), CFSE+ MHCI+ EVs (28,787,500/ml [9,851,127, 47,723,873], P = 0.021) and CSFE+ MHCI+ CD41+ EVs (28,343,500/ml [9,637,432, 47,049,568], P = 0.008). The concentration of CSFE+ MHCI+ CD62e+ EVs (94,230/ml [-55,099, 243,559], P = 0.187), CSFE+ CD235a+ EVs (-1,414/ml [-15,709, 12,882], P = 0.403) or CSFE+ MHCI+ CD45+ EVs (-192,915/ml [-690,166, 304,336], P = 0.828) did not differ during heat stress. The change in circulating EVs during passive heat stress did not differ after heat acclimation (thermal state × acclimation interactions, all P ≥ 0.180). These results demonstrate that passive heat stress increases the circulating concentration of total and platelet EVs and that passive heat acclimation does not alter this increase.

Successful endoscopic removal of foreign body lacerating into the duodenum.

Video 1The endoscope was advanced under direct visualization to the third part of the duodenum. A foreign body consistent with a ballpoint pen was identified in the duodenum. The sharp end of the pen formed a deep laceration through the second portion of the duodenum. The blunt end of the pen was ulcerated into the third portion of the duodenum with 2 additional pressure ulcers located in close proximity. Removal of the pen was first attempted using a snare without success. The foreign body was then successfully removed with a rat tooth. The second portion of the duodenum showed minimal oozing with contained deep laceration. The third portion of the duodenum showed 2 pressure ulcers.

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.

Passive heat acclimation does not modulate processing speed and executive functions during cognitive tasks performed at fixed levels of thermal strain.

This study evaluated if passive controlled hyperthermia heat acclimation modulates cognitive performance during passive heat stress. Eight healthy adults (25 ± 4 years) underwent 7 consecutive days of hot water immersion (core temperature ≥38.6 °C) and a 7-day time-control period. On days 1 and 7 of heat acclimation, participants performed a digital Stroop test at baseline, when core temperature reached 38.6 °C, and after 60 minutes at a core temperature ≥38.6 °C to evaluate reaction time during tasks targeting processing speed (reading and counting) and executive functions (inhibition and switching). On days 1 and 7 of the time-control intervention, participants performed the Stroop test with equivalent amounts of time separating each task as for heat acclimation. During day 1 of heat acclimation, reaction time was quicker during the reading (-44 ms [-71 to -17], P < 0.01) and counting (-39 ms [-76 to -2], P = 0.04) tasks when the rectal temperature reached 38.6 °C, but after a further 60 minutes of heat exposure, reaction time only remained quicker during the reading task (-56 ms [-83 to -29], P < 0.01). Changes in reaction time during heat exposure were unaffected by subsequent heat acclimation (interaction, all P ≥ 0.09). In conclusion, 7 days of heat acclimation does not modulate processing speed and executive functions during passive heat exposure. Novelty: Whether heat acclimation improves cognitive performance during heat exposure remains unclear. We tested the hypothesis that heat acclimation modulates reaction time during cognitive tasks performed at matched levels of thermal strain. Despite the classical signs of heat acclimation, reaction time during heat exposure is unaffected by heat acclimation.

Impact of passive heat acclimation on markers of kidney function during heat stress.

NEW FINDINGS: What is the central question of this study? Does passive heat acclimation alter glomerular filtration rate and urine-concentrating ability in response to passive heat stress? What is the main finding and its importance? Glomerular filtration rate remained unchanged after passive heat stress, and heat acclimation did not alter this response. However, heat acclimation mitigated the reduction in urine-concentrating ability and reduced the incidence of albuminuria in young healthy adults after passive heat stress. Collectively, these results suggest that passive heat acclimation might improve structural integrity and reduce glomerular permeability during passive heat stress. ABSTRACT: Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26 ± 5 years of age; 72.7 ± 8.6 kg; 172.4 ± 7.5 cm) underwent passive heat stress before and after a 7 day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133 ± 41 ml min-1 ; post, 127 ± 51 ml min-1 ; P = 0.99) and after (pre, 129 ± 46 ml min-1 ; post, 130 ± 36 ml min-1 ; P = 0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P < 0.01), but heat acclimation did not alter this response. In comparison to baseline, free water clearance was greater after passive heating before (pre, -0.86 ± 0.67 ml min-1 ; post, 0.40 ± 1.01 ml min-1 ; P < 0.01) but not after (pre, -0.16 ± 0.57 ml min-1 ; post, 0.76 ± 1.2 ml min-1 ; P = 0.11) heat acclimation. Furthermore, passive heating increased the fractional excretion rate of potassium (P < 0.03) but not sodium (P = 0.13) or chloride (P = 0.20). Lastly, heat acclimation reduced the fractional incidence of albuminuria after passive heating (before, 58 ± 51%; after, 8 ± 29%; P = 0.03). Collectively, these results demonstrate that passive heat stress does not alter the glomerular filtration rate. However, heat acclimation might improve urine-concentrating ability and filtration within the glomerulus.

Seven days of hot water heat acclimation does not modulate the change in heart rate variability during passive heat exposure.

We examined if the change in heart rate variability during passive heat exposure is modified by hot water heat acclimation (HA). Sixteen healthy adults (28 ± 5 years, 5 females/11 males) underwent heat exposure in a water-perfused suit, before and after 7 days of HA (60 min at rectal temperature ≥38.6 °C). During passive heat exposure, heart rate, the standard deviation of NN intervals (SDNN), the square root of the mean squared differences of successive NN intervals (RMSSD), and the power in the high-frequency range (HF) were measured. No difference in heart rate (P = 0.22), SDNN (P = 0.87), RMSSD (P = 0.79), and HF (P = 0.23) was observed at baseline. The increase in HR (pre-HA, 43 ± 10; post-HA, 42 ± 9 bpm; P = 0.57) and the decrease of SDNN (pre-HA, -54.1 ± 41.0; post-HA, -52.2 ± 36.8 ms; P = 0.85), RMSSD (pre-HA, -70.8 ± 49.5; post-HA, -72.7 ± 50.4 ms; P = 0.91) and HF (pre-HA, -28.0% ± 14.5; post-HA, -23.2% ± 17.1%; P = 0.27) were not different between experimental visits at fixed increases in esophageal temperature. These results suggest that 7 consecutive days of hot water HA does not modify the change in heart rate variability indices during passive heat exposure. Novelty: It remains unclear if HA alters the change in heart rate variability that occurs during passive heat exposure. At matched levels of thermal strain, 7 consecutive days of hot water immersion did not modulate the change in indices of heart rate variability during passive heat exposure.

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.

Acute Vascular Benefits of Finnish Sauna Bathing in Patients With Stable Coronary Artery Disease.

BACKGROUND: Finnish sauna bathing habits are associated with a decreased risk of cardiovascular mortality. The physiologic adaptations mediating this association remain to be fully elucidated. This study tested the hypothesis that Finnish sauna bathing acutely improves peripheral flow-mediated dilation (FMD) in middle-aged and older adults with stable coronary artery disease (CAD). METHODS: Twenty-two adults (20 male, 2 female; 67 ± 10 years) with stable CAD underwent 2 periods of 10 minutes in a Finnish sauna (81.3 ± 2.7°C, 23 ± 3% humidity) separated by 10 minutes of thermoneutral rest. Before and 51 ± 8 minutes after sauna bathing, brachial artery FMD and postocclusive reactive hyperemia (PORH) were evaluated by means of Doppler ultrasound. RESULTS: Sauna bathing increased core temperature (mean +0.66°C [95% CI 0.54-0.77], P < 0.01) and heart rate (+27 beats/min [24-29], P < 0.01), and decreased systolic (-19 mm Hg [-31 to -6]; P < 0.01) and diastolic (-6 mm Hg [-11 to -1], P < 0.01) blood pressures. Brachial artery FMD was greater after sauna bathing (+1.21% [0.16-2.26], P = 0.04), whereas PORH was unchanged (peak: +0.51 mL/min/mm Hg [-0.13 to 1.15], P = 0.11; area under the curve: +0.21 mL/mm Hg [-0.12 to 0.54]; P = 0.19). CONCLUSIONS: A typical Finnish sauna bathing session acutely improves peripheral FMD in middle-aged and older adults with stable CAD.

Impact of Finnish sauna bathing on circulating markers of inflammation in healthy middle-aged and older adults: A crossover study.

OBJECTIVES: Finnish sauna bathing is associated with a reduced risk of adverse health outcomes. The acute physiological responses elicited by Finnish sauna bathing that could explain this association remain understudied. This study characterized the acute effect of Finnish sauna bathing on circulating markers of inflammation in healthy middle-aged and older adults. DESIGN: With the use of a crossover study design, 20 healthy middle-aged and older adults (9 men/11 women, 66 ±â€¯6 years old) performed 3 interventions in random order: 1) 1 x 10 min of Finnish sauna bathing (80 °C, 20 % humidity); 2) 2 x 10 min of Finnish sauna bathing; 3) a time-control period during which participants sat outside of the sauna for 10 min. MAIN OUTCOMES: Venous blood samples were obtained before (≤15 min) and after (∼65 min) each intervention to determine circulating concentrations of interleukin 6 (IL-6), interleukin 1 receptor antagonist (IL-1RA), and C-reactive protein (CRP). RESULTS: IL-6 increased in response to 2 x 10 min of sauna bathing (+0.92 pg/mL [+0.16, +1.68], P = 0.02), but not following the 1 x 10 min session (+0.17 pg/mL [-0.13, +0.47], P = 0.26). IL1-RA increased during the 1 x 10 min (+51.27 pg/mL [+20.89, +81.65], P < 0.01) and 2 x 10 min (+30.78 pg/mL [+3.44, +58.12], P = 0.03) sessions. CRP did not change in response to either sauna session (P = 0.34). CONCLUSION: These results demonstrate that typical Finnish sauna bathing sessions acutely increase IL-6 and IL1-RA in healthy middle-aged and older adults.

Cardiac function during heat stress: impact of short-term passive heat acclimation.

A lower heart rate (HR) during heat exposure is a classic marker of heat acclimation (HA), although it remains unclear whether this adaptation occurs secondary to reduced thermal strain and/or improvements in cardiac function. We evaluated the hypothesis that short-term passive HA reduces HR and improves cardiac function during passive heating. Echocardiography was performed under thermoneutral and hyperthermic conditions in 10 healthy adults (9 men/1 woman, 29 ± 6 yr old), pre and post 7 days of controlled hyperthermia. HR (P = 0.61), stroke volume (P = 0.99), and cardiac output (P = 0.99), were similar on days 1 and 7 of HA. Core (pre: 38.17 ± 0.42, post: 38.15 ± 0.27°C, P = 0.95) and mean skin (pre: 38.24 ± 0.41, post: 38.51 ± 0.29°C, P = 0.17) temperatures were similar during hyperthermic echocardiographic assessments. Cardiac systolic function was unaffected by HA (P ≥ 0.10). HA attenuated the decrease in end-diastolic volume (pre: -18 ± 18, post: -12 ± 19 mL, P = 0.05), accentuated the greater atrial contribution to diastolic filling (pre: +11 ± 5, post: +14 ± 5%, P = 0.02), and attenuated the increase in left atrial reservoir strain rate (pre: +1.5 ± 1.2, post: +0.8 ± 0.8 1/s, P = 0.02) during heating. Nonetheless, there were no differences in HR (pre: 106 ± 12, post: 104 ± 12 beats/min, P = 0.50), stroke volume (pre: 65 ± 15, post: 68 ± 13 mL, P = 0.55), or cardiac output (pre: 6.9 ± 2.0, post: 7.1 ± 1.7 L/min, P = 0.70) during passive heating. Short-term controlled hyperthermia HA results in limited adaptations of cardiac function during passive heating.NEW & NOTEWORTHY A lower heart rate during heat exposure is a classic marker of heat acclimation (HA). It remains unknown if improved cardiac function contributes to this response. A 7-day passive HA protocol did not alter cardiac systolic function during passive heating, whereas it improved some indexes of diastolic function in young adults. Nonetheless, heart rate during heating was unaffected by HA. These results suggest that passive HA induces limited adaptations in cardiac function during passive heating.

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.

Acute effect of Finnish sauna bathing on brachial artery flow-mediated dilation and reactive hyperemia in healthy middle-aged and older adults.

Regular Finnish sauna bathing is associated with a reduced risk of all-cause and cardiovascular mortality in middle-aged and older adults. Potential acute physiological adaptations induced by sauna bathing that underlie this relationship remain to be fully elucidated. The purpose of this study was to determine if typical Finnish sauna sessions acutely improve brachial artery flow-mediated dilation (FMD) and reactive hyperemia (RH) in healthy middle-aged and older adults. Using a randomized crossover design, FMD and RH were evaluated in 21 healthy adults (66 ± 6 years, 10 men/11 women) before and after each of the following conditions: (1) 1 × 10 min of Finnish sauna bathing (80.2 ± 3.2°C, 23 ± 2% humidity); (2) 2 × 10 min of sauna bathing separated by 10 min of rest outside the sauna; (3) a time control period (10 min of seated rest outside the sauna). FMD was taken as the peak change from baseline in brachial artery diameter following 5 min of forearm ischemia, whereas RH was quantified as both peak and area-under-the-curve forearm vascular conductance postischemia. FMD was statistically similar pre to post 1 × 10 min (4.69 ± 2.46 to 5.41 ± 2.64%, P = 0.20) and 2 × 10 min of sauna bathing (4.16 ± 1.79 to 4.55 ± 2.14%, P = 0.58). Peak and area-under-the-curve forearm vascular conductance were also similar following both sauna interventions. These results suggest that typical Finnish sauna bathing sessions do not acutely improve brachial artery FMD and RH in healthy middle-aged and older adults.

Acute mesenteric ischemia in an African American patient with heterozygous factor V Leiden deficiency.

It is well documented that factor V Leiden mutation (FVL) is a common hypercoagulable risk factor in the Caucasian population. Patients with homozygous FVL mutation have an increased risk for venous thromboembolism. However, there have been few cases of heterozygous FVL mutation associated with arterial thrombosis described in the literature. Our case report presents an African American (AA) female with heterozygous FVL mutation who presented with acute arterial mesenteric ischemia.

YouTube as a source of patient education in idiopathic pulmonary fibrosis: a media content analysis.

Purpose: Idiopathic pulmonary fibrosis (IPF) is a common cause of pulmonary fibrosis, with millions of individuals affected in the world. Patients may use multiple resources to educate themselves regarding their illness, including popular social media video hosting site YouTube. We set out to determine the quality of patient education material discussing IPF available on YouTube. Methods: 100 consecutive videos were surveyed for review, of which 59 were included in the final analysis. Three independent blinded reviewers were assigned to score each video on a scoring system designed along patient education material available publicly at the American Thoracic Society and the American College of Chest Physicians. Scores by each reviewer were compared to others using means, standard deviation, Cohen's Kappa, and intra-class reliability. Results: Video content had a mean score of 5.9, SD 3.96 out of a maximum of 20 points. Cohen's Kappa between the three raters was calculated to a value of 0.92 and Interclass reliability was 0.79 (0.70-0.86, 95% CI) indicating appropriateness of comparison between the three raters. Conclusion: Patient education material regarding IPF on YouTube was found deficient in quantity and quality. Providers should be aware of the best information resources available and utilize these to educate their patients.