Passive heat therapy: a promising preventive measure for people at risk of adverse health outcomes during heat extremes.

The world is experiencing increased frequency, duration, and severity of life-threatening heat extremes. Most hospitalizations and excess deaths during extreme heat events are associated with preexisting diseases in older adults. As climate change persists, the global population ages and the number of individuals with chronic diseases expands, more people are at risk of adverse health outcomes during extreme heat events. Therefore, proactive preventive measures are urgently needed to mitigate heat-related health risks within these populations. In this context, passive heat therapy (e.g., hot baths, saunas, and water-perfused suits) emerges as a promising countermeasure to improve physiological resilience to a warming planet. Passive heating improves cardiovascular function and overall health in older adults and individuals living with chronic diseases, offering the prospect of reducing cardiovascular strain during hotter days. Moreover, some studies suggest that passive heat therapy can be an effective strategy for heat acclimation (i.e., improved thermoregulation). This review describes the existing literature on the effects of passive heat therapy on cardiovascular and thermoregulatory responses in individuals with higher heat-related health risks and explores the use of passive heating as a strategy for heat acclimation to mitigate health risks during extreme heat events.NEW & NOTEWORTHY Passive heat therapy improves cardiovascular function and health in middle-aged and older adults living with or without chronic diseases. In addition, preliminary studies indicate that passive heat interventions can induce heat acclimation, improving thermoregulatory responses. Thus, passive heat therapy could serve as a preventive measure for people at risk of adverse health outcomes during extreme heat events, improving resilience to ongoing climate change.

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.

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.

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.

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.

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.

Hemostatic responses to exercise, dehydration, and simulated bleeding in heat-stressed humans.

Heat stress followed by an accompanying hemorrhagic challenge may influence hemostasis. We tested the hypothesis that hemostatic responses would be increased by passive heat stress, as well as exercise-induced heat stress, each with accompanying central hypovolemia to simulate a hemorrhagic insult. In aim 1, subjects were exposed to passive heating or normothermic time control, each followed by progressive lower-body negative pressure (LBNP) to presyncope. In aim 2 subjects exercised in hyperthermic environmental conditions, with and without accompanying dehydration, each also followed by progressive LBNP to presyncope. At baseline, pre-LBNP, and post-LBNP (<1, 30, and 60 min), hemostatic activity of venous blood was evaluated by plasma markers of hemostasis and thrombelastography. For aim 1, both hyperthermic and normothermic LBNP (H-LBNP and N-LBNP, respectively) resulted in higher levels of factor V, factor VIII, and von Willebrand factor antigen compared with the time control trial (all P < 0.05), but these responses were temperature independent. Hyperthermia increased fibrinolysis [clot lysis 30 min after the maximal amplitude reflecting clot strength (LY30)] to 5.1% post-LBNP compared with 1.5% (time control) and 2.7% in N-LBNP ( P = 0.05 for main effect). Hyperthermia also potentiated increased platelet counts post-LBNP as follows: 274 K/µl for H-LBNP, 246 K/µl for N-LBNP, and 196 K/µl for time control ( P < 0.05 for the interaction). For aim 2, hydration status associated with exercise in the heat did not affect the hemostatic activity, but fibrinolysis (LY30) was increased to 6-10% when subjects were dehydrated compared with an increase to 2-4% when hydrated ( P = 0.05 for treatment). Central hypovolemia via LBNP is a primary driver of hemostasis compared with hyperthermia and dehydration effects. However, hyperthermia does induce significant thrombocytosis and by itself causes an increase in clot lysis. Dehydration associated with exercise-induced heat stress increases clot lysis but does not affect exercise-activated or subsequent hypovolemia-activated hemostasis in hyperthermic humans. Clinical implications of these findings are that quickly restoring a hemorrhaging hypovolemic trauma patient with cold noncoagulant fluids (crystalloids) can have serious deleterious effects on the body's innate ability to form essential clots, and several factors can increase clot lysis, which should therefore be closely monitored.

Acute heat stress reduces biomarkers of endothelial activation but not macro- or microvascular dysfunction in cervical spinal cord injury.

Cardiovascular diseases (CVD) are highly prevalent in spinal cord injury (SCI), and peripheral vascular dysfunction might be a contributing factor. Recent evidence demonstrates that exposure to heat stress can improve vascular function and reduce the risk of CVD in uninjured populations. We therefore aimed to examine the extent of vascular dysfunction in SCI and the acute effects of passive heating. Fifteen participants with cervical SCI and 15 uninjured control (CON) participants underwent ultrasound assessments of vascular function and venous blood sampling for biomarkers of endothelial activation (i.e., CD62e+) and apoptosis (i.e., CD31+/42b-) before and after a 60-min exposure to lower limb hot water immersion (40°C). In SCI, macrovascular endothelial function was reduced in the brachial artery [SCI: 4.8 (3.2)% vs. CON: 7.6 (3.4)%, P = 0.04] but not the femoral artery [SCI: 3.7 (2.6)% vs. CON: 4.0 (2.1)%, P = 0.70]. Microvascular function, via reactive hyperemia, was ~40% lower in SCI versus CON in both the femoral and brachial arteries ( P < 0.01). Circulating concentrations of CD62e+ were elevated in SCI versus CON [SCI: 152 (106) microparticles/µl vs. CON: 58 (24) microparticles/µl, P < 0.05]. In response to heating, macrovascular and microvascular function remained unchanged, whereas increases (+83%) and decreases (-93%) in antegrade and retrograde shear rates, respectively, were associated with heat-induced reductions of CD62e+ concentrations in SCI to levels similar to CON ( P = 0.05). These data highlight the potential of acute heating to provide a safe and practical strategy to improve vascular function in SCI. The chronic effects of controlled heating warrant long-term testing. NEW & NOTEWORTHY Individuals with cervical level spinal cord injury exhibit selectively lower flow-mediated dilation in the brachial but not femoral artery, whereas peak reactive hyperemia was lower in both arteries compared with uninjured controls. After 60 min of lower limb hot water immersion, femoral artery blood flow and shear patterns were acutely improved in both groups. Elevated biomarkers of endothelial activation in the spinal cord injury group decreased with heating, but these biomarkers remained unchanged in controls.

Folic acid supplementation does not attenuate thermoregulatory or cardiovascular strain of older adults exposed to extreme heat and humidity.

NEW FINDINGS: What is the central question of this study? Does folic acid supplementation alleviate thermoregulatory and cardiovascular strain of older adults during exposure to extreme heat and humidity? What is the main finding and its importance? Folic acid supplementation for 6 weeks did not affect whole-limb blood flow/vasodilatation, core and skin temperatures, heart rate, blood pressure and cardiac output. Thus, 6 weeks of folic acid supplementation does not alleviate thermoregulatory or cardiovascular strain of healthy older adults exposed to extreme heat and humidity. ABSTRACT: Folic acid supplementation reverses age-related reductions in cutaneous vasodilatation during passive heating. However, it is unknown if folic acid supplementation alleviates thermoregulatory and cardiovascular strain experienced by older adults during heat exposure. We evaluated the effect of folic acid supplementation on thermoregulatory and cardiovascular responses of nine healthy older adults (61-72 years, 3 males/6 females) exposed to extreme heat and humidity. Participants rested at 42°C while relative humidity was increased from 30% to 70% in 2% increments every 5 min. The protocol was performed before (CON) and after (FOLIC) 6 weeks of folic acid supplementation (5 mg day-1 ). Local cutaneous vascular conductance (CVC, laser-Doppler flowmetry), forearm vascular conductance (FVC, Doppler ultrasound), mean skin and oesophageal temperatures, heart rate, blood pressure and cardiac output were measured. Folic acid supplementation increased fasting serum folate concentrations (P < 0.01). Absolute CVC was greater throughout the protocol following supplementation (CON: 1.29 ± 0.16 units mmHg-1 vs. FOLIC: 1.65 ± 0.24 units mmHg-1 , P < 0.01). However, normalized CVC (CON: 54 ± 8% vs. FOLIC: 59 ± 7%, P = 0.22), FVC (CON: 3.47 ± 0.76 ml mmHg-1 vs. FOLIC: 3.40 ± 0.56 ml mmHg-1 , P = 0.93), mean skin (P = 0.81) and oesophageal (CON: 36.87 ± 0.28°C vs. folic: 36.90 ± 0.25°C, P = 0.98) temperatures, heart rate (CON: 83 ± 10 beats min-1 vs. FOLIC: 84 ± 8 beats min-1 , P = 0.64), blood pressure (P = 0.71) and cardiac output (P = 0.20) were unaffected by folic acid supplementation. These results demonstrate that 6 weeks of folic acid supplementation does not alleviate thermoregulatory or cardiovascular strain of healthy older adults exposed to extreme heat and humidity.

Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated haemorrhagic challenge.

NEW FINDINGS: What is the central question of this study? Combined increases in skin and core temperatures reduce tolerance to a simulated haemorrhagic challenge. The aim of this study was to examine the separate and combined influences of increased skin and core temperatures upon tolerance to a simulated haemorrhagic challenge. What is the main finding and its importance? Skin and core temperatures increase during many occupational settings, including military procedures, in hot environments. The study findings demonstrate that both increased skin temperature and increased core temperature can impair tolerance to a simulated haemorrhagic challenge; therefore, a soldier's tolerance to haemorrhagic injury is likely to be impaired during any military activity that results in increased skin and/or core temperatures. Tolerance to a simulated haemorrhagic insult, such as lower-body negative pressure (LBNP), is profoundly reduced when accompanied by whole-body heat stress. The aim of this study was to investigate the separate and combined influence of elevated skin (Tskin ) and core temperatures (Tcore ) on LBNP tolerance. We hypothesized that elevations in Tskin as well as Tcore would both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both Tskin and Tcore were elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i) control, with neutral Tskin (34.3 ± 0.5°C) and Tcore (36.8 ± 0.2°C); (ii) primarily skin hyperthermia, with high Tskin (37.6 ± 0.2°C) and neutral Tcore (37.1 ± 0.2°C); (iii) primarily core hyperthermia, with neutral Tskin (35.0 ± 0.5°C) and high Tcore (38.3 ± 0.2°C); and (iv) combined skin and core hyperthermia, with high Tskin (38.8 ± 0.6°C) and high Tcore (38.1 ± 0.2°C). The LBNP tolerance was quantified via the cumulative stress index (in millimetres of mercury × minutes). The LBNP tolerance was reduced during the skin hyperthermia (569 ± 151 mmHg min) and core hyperthermia trials (563 ± 194 mmHg min) relative to control conditions (1010 ± 246 mmHg min; both P < 0.05). However, LBNP tolerance did not differ between skin hyperthermia and core hyperthermia trials (P = 0.92). The lowest LBNP tolerance was observed during combined skin and core hyperthermia (257 ± 106 mmHg min; P < 0.05 relative to all other trials). These data indicate that elevated skin temperature, as well as elevated core temperature, can both contribute to reductions in LBNP tolerance in heat-stressed individuals. However, heat stress-induced reductions in LBNP tolerance are greatest in conditions when both skin and core temperatures are elevated.

Acute limb heating improves macro- and microvascular dilator function in the leg of aged humans.

Local heating of an extremity increases blood flow and vascular shear stress throughout the arterial tree. Local heating acutely improves macrovascular dilator function in the upper limbs of young healthy adults through a shear stress-dependent mechanism but has no such effect in the lower limbs of this age group. The effect of acute limb heating on dilator function within the atherosclerotic prone vasculature of the lower limbs of aged adults is unknown. Therefore, the purpose of this study was to test the hypothesis that acute lower limb heating improves macro- and microvascular dilator function within the leg vasculature of aged adults. Nine young and nine aged adults immersed their lower limbs at a depth of ~33 cm into a heated (~42°C) circulated water bath for 45 min. Before and 30 min after heating, macro (flow-mediated dilation)- and microvascular (reactive hyperemia) dilator functions were assessed in the lower limb, following 5 min of arterial occlusion, via Doppler ultrasound. Compared with preheat, macrovascular dilator function was unchanged following heating in young adults (P = 0.6) but was improved in aged adults (P = 0.04). Similarly, microvascular dilator function, as assessed by peak reactive hyperemia, was unchanged following heating in young adults (P = 0.1) but was improved in aged adults (P < 0.01). Taken together, these data suggest that acute lower limb heating improves both macro- and microvascular dilator function in an age dependent manner. NEW & NOTEWORTHY: We demonstrate that lower limb heating acutely improves macro- and microvascular dilator function within the atherosclerotic prone vasculature of the leg in aged adults. These findings provide evidence for a potential therapeutic use of chronic lower limb heating to improve vascular health in primary aging and various disease conditions.

Biomass carbon, nitrogen and phosphorus stocks in hybrid poplar buffers, herbaceous buffers and natural woodlots in the riparian zone on agricultural land.

In many temperate agricultural areas, riparian forests have been converted to cultivated land, and only narrow strips of herbaceous vegetation now buffer many farm streams. The afforestation of these riparian zones has the potential to increase carbon (C) storage in agricultural landscapes by creating a new biomass sink for atmospheric CO2. Occurring at the same time, the storage of nitrogen (N) and phosphorus (P) in plant biomass, is an important water quality function that may greatly vary with types of riparian vegetation. The objectives of this study were (1) to compare C, N and P storage in aboveground, belowground and detrital biomass for three types of riparian vegetation cover (9-year-old hybrid poplar buffers, herbaceous buffers and natural woodlots) across four agricultural sites and (2) to determine potential vegetation cover effects on soil nutrient supply rate in the riparian zone. Site level comparisons suggest that 9-year-old poplar buffers have stored 9-31 times more biomass C, 4-10 times more biomass N, and 3-7 times more biomass P than adjacent non managed herbaceous buffers, with the largest differences observed on the more fertile sites. The conversion of these herbaceous buffers to poplar buffers could respectively increase C, N and P storage in biomass by 3.2-11.9 t/ha/yr, 32-124 kg/ha/yr and 3.2-15.6 kg/ha/yr, over 9 years. Soil NO3 and P supply rates during the summer were respectively 57% and 66% lower in poplar buffers than in adjacent herbaceous buffers, potentially reflecting differences in nutrient storage and cycling between the two buffer types. Biomass C ranged 49-160 t/ha in woodlots, 33-110 t/ha in poplar buffers and 3-4 t/ha in herbaceous buffers. Similar biomass C stocks were found in the most productive poplar buffer and three of the four woodlots studied. Given their large and varied biomass C stocks, conservation of older riparian woodlots is equally important for C balance management in farmland. In addition, the establishment of poplar buffers, in replacement of non managed herbaceous buffers, could rapidly increase biomass C, N and P storage along farm streams, which would be beneficial for water quality protection and global change mitigation.

Phytochemistry of wild populations of Panax quinquefolius L. (North American ginseng).

A survey of the phytochemistry of Panax quinquefolius L. (North American ginseng) collected from wild populations in Ontario, Quebec, Maine, Vermont, and Wisconsin was undertaken. Reverse-phase HPLC was used to determine the natural variation of levels of ginsenosides Rg1, Re, Rf, Rb1, Rc, Rb2, and Rd and their total in leaf, stem, and root of authentic wild-grown material. The totals in roots varied from 1 to 16%, with the greatest number of individual samples having 4-5% total ginsenosides. The lack of ginsenoside Rf in roots of authentic wild populations confirmed its status as a phytochemical marker differentiating American and Asian ginseng. Ten geographically isolated wild populations were collected, and several showed significant variation in the levels of major ginsenosides. There was no statistical difference in mean ginsenoside content between wild and cultivated P. quinquefolius roots at 4 years of age, suggesting there is no phytochemical justification for wild crafting. Baseline data on total ginsenoside levels for authentic wild P. quinquefolius reported here provide reference levels for quality assurance programs.