A Novel Conceptual Model for Human Heat Tolerance.

Human "heat tolerance" has no accepted definition or physiological underpinnings; rather, it is almost always discussed in relative or comparative terms. We propose to use environmental limits to heat balance accounting for metabolic rate and clothing, that is, the environments for which heat stress becomes uncompensable for a specified metabolic rate and clothing, as a novel metric for quantifying heat tolerance.

Sex differences in thermophysiological responses of elderly to low-intensity exercise during uncompensable heat strain.

PURPOSE: The rising frequency of extreme heat events poses an escalating threat of heat-related illnesses and fatalities, placing an additional strain on global healthcare systems. Whether the risk of heat-related issues is sex specific, particularly among the elderly, remains uncertain. METHODS: 16 men and 15 women of similar age (69 ± 5 years) were exposed to an air temperature of 39.1 ± 0.3 °C and a relative humidity (RH) of 25.1 ± 1.9%, during 20 min of seated rest and at least 40 min of low-intensity (10 W) cycling exercise. RH was gradually increased by 2% every 5 min starting at minute 30. We measured sweat rate, heart rate, thermal sensation, and the rise in gastrointestinal temperature (Tgi) and skin temperature (Tsk). RESULTS: Tgi consistently increased from minute 30 to 60, with no significant difference between females and males (0.012 ± 0.004 °C/min vs. 0.011 ± 0.005 °C/min; p = 0.64). Similarly, Tsk increase did not differ between females and males (0.044 ± 0.007 °C/min vs. 0.038 ± 0.011 °C/min; p = 0.07). Females exhibited lower sweat rates than males (0.29 ± 0.06 vs. 0.45 ± 0.14 mg/m2/min; p < 0.001) in particular at relative humidities exceeding 30%. No sex differences in heart rate and thermal sensation were observed. CONCLUSION: Elderly females exhibit significantly lower sweat rates than their male counterparts during low-intensity exercise at ambient temperatures of 39 °C when humidity exceeds 30%. However, both elderly males and females demonstrate a comparable rise in core temperature, skin temperature, and mean body temperature, indicating similar health-related risks associated with heat exposure.

Adverse heat-health outcomes and critical environmental limits (Pennsylvania State University Human Environmental Age Thresholds project).

BACKGROUND: The earth's climate is warming and the frequency, duration, and severity of heat waves are increasing. Meanwhile, the world's population is rapidly aging. Epidemiological data demonstrate exponentially greater increases in morbidity and mortality during heat waves in adults ≥65 years. Laboratory data substantiate the mechanistic underpinnings of age-associated differences in thermoregulatory function. However, the specific combinations of environmental conditions (i.e., ambient temperature and absolute/relative humidity) above which older adults are at increased risk of heat-related morbidity and mortality are less clear. METHODS: This review was conducted to (1) examine the recent (past 3 years) literature regarding heat-related morbidity and mortality in the elderly and discuss projections of future heat-related morbidity and mortality based on climate model data, and (2) detail the background and unique methodology of our ongoing laboratory-based projects aimed toward identifying the specific environmental conditions that result in elevated risk of heat illness in older adults, and the implications of using the data toward the development of evidence-based safety interventions in a continually-warming climate (PSU HEAT; Human Environmental Age Thresholds). RESULTS: The recent literature demonstrates that extreme heat continues to be increasingly detrimental to the health of the elderly and that this is apparent across the world, although the specific environmental conditions above which older adults are at increased risk of heat-related morbidity and mortality remain unclear. CONCLUSION: Characterizing the environmental conditions above which risk of heat-related illnesses increase remains critical to enact policy decisions and mitigation efforts to protect vulnerable people during extreme heat events.

Nitric oxide-mediated cutaneous microvascular function is not altered in young adults following mild-to-moderate SARS CoV-2 infection.

Vascular dysfunction has been reported in adults who have recovered from COVID-19. To date, no studies have investigated the underlying mechanisms of persistent COVID-19-associated vascular dysfunction. Our purpose was to quantify nitric oxide (NO)-mediated vasodilation in healthy adults who have recovered from SARS-CoV-2 infection. We hypothesized that COVID-19-recovered adults would have impaired NO-mediated vasodilation compared with adults who have not had COVID-19. In methods, we performed a cross-sectional study including 10 (5 men/5 women, 24 ± 4 yr) healthy control (HC) adults who were unvaccinated for COVID-19, 11 (4 men/7 women, 25 ± 6 yr) healthy vaccinated (HV) adults, and 12 (5 men/7 women, 22 ± 3 yr) post-COVID-19 (PC, 19 ± 14 wk) adults. COVID-19 symptoms severity (survey) was assessed. A standardized 39°C local heating protocol was used to assess NO-dependent vasodilation via perfusion (intradermal microdialysis) of 15 mM NG-nitro-l-arginine methyl ester during the plateau of the heating response. Red blood cell flux was measured (laser-Doppler flowmetry) and cutaneous vascular conductance (CVC = flux/mmHg) was expressed as a percentage of maximum (28 mM sodium nitroprusside + 43°C). In results, the local heating plateau (HC: 61 ± 20%, HV: 60 ± 19%, PC: 67 ± 19%, P = 0.80) and NO-dependent vasodilation (HC: 77 ± 9%, HV: 71 ± 7%, PC: 70 ± 10%, P = 0.36) were not different among groups. Neither symptom severity (25 ± 12 AU) nor time since diagnosis correlated with the NO-dependent vasodilation (r = 0.46, P = 0.13; r = 0.41, P = 0.19, respectively). In conclusion, healthy adults who have had mild-to-moderate COVID-19 do not have altered NO-mediated cutaneous microvascular function.NEW & NOTEWORTHY Healthy young adults who have had mild-to-moderate COVID-19 do not display alterations in nitric oxide-mediated cutaneous microvascular function. In addition, healthy young adults who have COVID-19 antibodies from the COVID-19 vaccinations do not display alterations in nitric oxide-mediated cutaneous microvascular function.

Skin pigmentation is negatively associated with circulating vitamin D concentration and cutaneous microvascular endothelial function.

Darkly pigmented individuals are at the greatest risk of hypovitaminosis D, which may result in microvascular endothelial dysfunction via reduced nitric oxide (NO) bioavailability and/or increased oxidative stress and inflammation. We investigated the associations among skin pigmentation (M-index; skin reflectance spectrophotometry), serum vitamin D concentration [25(OH)D], circulating inflammatory cytokine (TNF-α, IL-6, and IL-10) concentrations, and the NO contribution to local heating-induced cutaneous vasodilation (%NO-mediated vasodilation) in a diversely pigmented cohort of young adults. An intradermal microdialysis fiber was placed in the forearms of 33 healthy adults (14 men/19 women; 18-27 yr; M-index, 30-81 AU) for local delivery of pharmacological agents. Lactated Ringer's solution was perfused through the fiber during local heating-induced (39°C) cutaneous vasodilation. After attaining stable elevated blood flow, 15 mM NG-nitro-l-arginine methyl ester (l-NAME; NO synthase inhibiter) was infused to quantify %NO-mediated vasodilation. Red cell flux was measured (laser-Doppler flowmetry; LDF) and cutaneous vascular conductance (CVC = LDF/MAP) was normalized to maximal (%CVCmax; 28 mM sodium nitroprusside + 43°C). Serum [25(OH)D] and circulating cytokines were analyzed by ELISA and multiplex assay, respectively. M-index was negatively associated with [25(OH)D] (r = -0.57, P < 0.0001) and %NO-mediated vasodilation (r = -0.42, P = 0.02). Serum[25(OH)D] was positively related to %NO (r = 0.41, P = 0.02). Controlling for [25(OH)D] weakened the association between M-index and %NO-mediated dilation (P = 0.16, r = -0.26). There was a negative curvilinear relation between [25(OH)D] and circulating IL-6 (r = -0.56, P < 0.001), but not TNF-α or IL-10 (P ≥ 0.14). IL-6 was not associated with %NO-mediated vasodilation (P = 0.44). These data suggest that vitamin D insufficiency/deficiency may contribute to reduced microvascular endothelial function in healthy, darkly pigmented young adults.NEW & NOTEWORTHY Endothelial dysfunction, an antecedent to hypertension and overt CVD, is commonly observed in otherwise healthy Black adults, although the underlying causes remain unclear. We show that reduced vitamin D availability with increasing degrees of skin pigmentation is associated with reduced microvascular endothelial function, independent of race or ethnicity, in healthy young adults. Greater prevalence of vitamin D deficiency in more darkly pigmented individuals may predispose them to increased risk of endothelial dysfunction.

Utility of the Heat Index in defining the upper limits of thermal balance during light physical activity (PSU HEAT Project).

Extreme heat events and consequent detrimental heat-health outcomes have been increasing in recent decades and are expected to continue with future climate warming. While many indices have been created to quantify the combined atmospheric contributions to heat, few have been validated to determine how index-defined heat conditions impact human health. However, this subset of indices is likely not valid for all situations and populations nor easily understood and interpreted by health officials and the public. In this study, we compare the ability of thresholds determined from the National Weather Service's (NWS) Heat Index (HI), the Wet Bulb Globe Temperature (WBGT), and the Universal Thermal Climate Index (UTCI) to predict the compensability of human heat stress (upper limits of heat balance) measured as part of the Pennsylvania State University's Heat Environmental Age Thresholds (PSU HEAT) project. While the WBGT performed the best of the three indices for both minimal activities of daily living (MinAct; 83 W·m-2) and light ambulation (LightAmb; 133 W·m-2) in a cohort of young, healthy subjects, HI was likewise accurate in predicting heat stress compensability in MinAct conditions. HI was significantly correlated with subjects' perception of temperature and humidity as well as their body core temperature, linking perception of the ambient environment with physiological responses in MinAct conditions. Given the familiarity the public has with HI, it may be better utilized in the expansion of safeguard policies and the issuance of heat warnings during extreme heat events, especially when access to engineered cooling strategies is unavailable.

Heat exposure limits for young unacclimatized males and females at low and high humidity.

Little is known about the separate and combined influences of humidity conditions, sex, and aerobic fitness on heat tolerance in unacclimatized males and females. The purpose of the current study was to describe heat tolerance, in terms of critical WBGT (WBGTcrit), in unacclimatized young males and females in hot-dry (HD) and warm-humid (WH) environments. Eighteen subjects (9 M/9F; 21 ± 2 yr) were tested during exercise at 30% V̇O2max in a controlled environmental chamber. Progressive heat stress exposures were performed with either (1) constant dry-bulb temperature (Tdb) of 34 and 36 °C and increasing ambient water vapor pressure (Pa) (Pcrit trials; WH); or (2) constant Pa of 12 and 16 mmHg and increasing Tdb (Tcrit trials; HD). Chamber Tdb and Pa, and subject esophageal temperature (Tes), were continuously monitored throughout each trial. After a 30-min equilibration period, progressive heat stress continued until subject heat balance could no longer be maintained and a clear rise in Tes was observed. Absolute WBGTcrit and WBGTcrit adjusted to a metabolic rate of 300 W (WBGT300), and the difference between WBGTcrit and occupational exposure limits (OEL; ΔOEL) was assessed. WBGTcrit, WBGT300, and ΔOEL were higher in WH compared to HD (p < 0.0001) for females but were the same between environments for males (p ≥ 0.21). WBGTcrit was higher in females compared to males in WH (p < 0.0001) but was similar between sexes in HD (p = 0.44). When controlling for metabolic rate, WBGT300 and ΔOEL were higher in males compared to females in WH and HD (both p < 0.0001). When controlling for sex, V̇O2max was not associated with WBGT300 or ΔOEL for either sex (r ≤ 0.12, p ≥ 0.49). These findings suggest that WBGTcrit is higher in females compared to males in WH, but not HD, conditions. Additionally, the WBGTcrit is lower in females, but not males, in HD compared to WH conditions.

Metabolism- and sex-dependent critical WBGT limits at rest and during exercise in the heat.

Critical environmental limits are environmental thresholds above which heat gain exceeds heat loss and body core temperature (Tc) cannot be maintained at equilibrium. Those limits can be represented as critical wet-bulb globe temperature (WBGTcrit), a validated index that represents the overall thermal environment. Little is known about WBGTcrit at rest and during low-to-moderate intensity exercise, or sex differences in WBGTcrit, in unacclimated young adults. The following hypotheses were tested: 1) WBGTcrit progressively decreases as metabolic heat production (Mnet) increases, 2) no sex differences in WBGTcrit occur at rest, and 3) WBGTcrit is lower during absolute-intensity exercise but higher at relative intensities in women than in men. Thirty-six participants [19 men (M)/17 women (W); 23 ± 4 yr] were tested at rest, during light, absolute-intensity exercise (10 W), or during moderate, relative-intensity exercise [30% maximal oxygen consumption (V̇o2max)] in an environmental chamber. Dry-bulb temperature was clamped as relative humidity or ambient water vapor pressure was increased until an upward inflection was observed in Tc (rectal or esophageal temperature). Sex-aggregated WBGTcrit was lower during 10 W (32.9°C ± 1.7°C, P < 0.0001) and 30% V̇o2max (31.6°C ± 1.1°C, P < 0.0001) exercise versus at rest (35.3°C ± 0.8°C), and lower at 30% V̇o2max versus 10 W (P = 0.01). WBGTcrit was similar between sexes at rest (35.6°C ± 0.8°C vs. 35.0°C ± 0.8°C, P = 0.83), but lower during 10 W (31.9°C ± 1.7°C vs. 34.1°C ± 0.3°C, P < 0.01) and higher during 30% V̇o2max (32.4°C ± 0.8°C vs. 30.8°C ± 0.9°C, P = 0.03) exercise in women versus men. These findings suggest that WBGTcrit decreases as Mnet increases, no sex differences occur in WBGTcrit at rest, and sex differences in WBGTcrit during exercise depend on absolute versus relative intensities.

Skin pigmentation and vitamin D-folate interactions in vascular function: an update.

PURPOSE OF REVIEW: Vitamin D and folate promote vascular endothelial health and may therefore help mitigate the development of cardiovascular disease (CVD). Ultraviolet radiation (UVR) exposure stimulates cutaneous vitamin D synthesis but degrades the bioactive metabolite of folate, 5-methyltetrahydrofolate (5-MTHF). Skin melanin absorbs UVR, thereby modulating the impact of UVR exposure on vitamin D and 5-MTHF metabolism. This review presents recent findings regarding the inter-relations among UVR, skin pigmentation, folate and vitamin D, and endothelial function. RECENT FINDINGS: Evidence for roles of folic acid or vitamin D supplementation on CVD endpoints is inconsistent, although preclinical and clinical studies have demonstrated the efficacy of both micronutrients for improving endothelial function. Vitamin D deficiency is most prevalent in darkly pigmented individuals living in relatively low-UVR environments. Conversely, there is a negative relation between accumulated UVR exposure and serum folate concentration in lightly pigmented adults. The interactions among UVR and bioavailable folate and vitamin D differentially impact endothelial function in differently pigmented skin. SUMMARY: UVR exposure disparately impacts folate and vitamin D metabolism in differently pigmented skin depending upon regional UVR intensity and seasonality. These findings present new clinical research questions regarding the interactions among UVR, skin pigmentation, folate and vitamin D bioavailability, and endothelial health.

Examining "race" in physiology.

Racial disparities in cardiovascular and cerebrovascular health outcomes are well described, and recent research has shed light on the mechanistic underpinnings of those disparities. However, "race" is a social construct that is poorly defined and continually evolving and is historically based on faulty premises. The continued categorization by race in physiological research suggests that there are inherent differences between races, rather than addressing the specific underlying factors that result in health disparities between groups. The purpose of this Perspectives article is to provide a brief history of the genesis of categorization by race, why such categorization should be reconsidered in physiology research, and offer recommendations to more directly investigate the underlying factors that result in group disparities in cardiovascular and cerebrovascular health.

Four weeks of vitamin D supplementation improves nitric oxide-mediated microvascular function in college-aged African Americans.

Reduced nitric oxide (NO)-mediated cutaneous vasodilation, secondary to increased oxidative stress, presents in young African American (AA) compared with European American (EA) adults and may be modulated by vitamin D status. We assessed cutaneous microvascular function in 18 young, healthy (21 ± 2 yr; 9 men, 9 women) subjects before (pre, 8 AA, 10 EA) 4 wk of 2,000 IU/day oral vitamin D supplementation and in 13 subjects after (post, 7 AA, 6 EA) 4 wk of 2,000 IU/day oral vitamin D supplementation. Serum vitamin D concentrations [25(OH)D] were measured at each visit. Three intradermal microdialysis fibers placed in the ventral forearm were randomized for treatment with 10 µM Tempol, 100 µM apocynin, or lactated Ringer's solution (control). Local heating (39°C) induced cutaneous vasodilation; red cell flux was measured at each site (laser-Doppler flowmetry), and cutaneous vascular conductance (CVC = flux/MAP) was expressed as a percentage of maximum (28 mM sodium nitroprusside, +43°C) for each phase of local heating. After stable elevated blood flow was attained, 15 mM NG-nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor) was perfused at all sites to quantify the NO contribution to cutaneous vasodilation (%NO), calculated as the difference between local heating and l-NAME plateaus. Serum [25(OH)D], the magnitude of the local heating response, and %NO were all lower in AAs versus EAs (P < 0.01). Tempol (P = 0.01), but not apocynin (P ≥ 0.19), improved the local heating response and %NO. Four weeks of supplementation improved serum [25(OH)D], the local heating response, and %NO in AAs (P ≤ 0.04) but not in EAs (P ≥ 0.41). Vitamin D supplementation mitigated endothelial dysfunction, an antecedent to overt cardiovascular disease (CVD), in otherwise healthy, young AA adults.NEW & NOTEWORTHY Endothelial dysfunction, an antecedent to overt cardiovascular disease (CVD), is observed earlier and more frequently in otherwise healthy African Americans (AAs) when compared with other ethnic groups. Vitamin D may modulate endothelial function, and darkened skin pigmentation increases risk of vitamin D deficiency. We show that 4 wk of 2,000 IU/day vitamin D supplementation improves microvascular responses to local heating in AAs. Ensuring adequate vitamin D status may mitigate development of cardiovascular dysfunction in this at-risk population.

Ultraviolet Radiation Exposure, Risk, and Protection in Military and Outdoor Athletes.

Overexposure to ultraviolet radiation (UVR) from the sun is associated with deleterious health effects including, but not limited to, increased risk of skin cancers. Military personnel and those who participate in outdoor exercise or sports represent two potential populations at elevated risk of negative health consequences of UVR exposure due to large amounts of time spent outdoors, often in harsh UVR environments. Despite exposure to high and/or frequent doses of UVR in recreational and tactical athletes, adequate sun-protection practices are often disregarded or not well understood by many within these at-risk populations, resulting in heightened risk of negative UVR effects. The focus of this review is to examine the available literature regarding UVR exposure, risk of adverse health effects of UVR exposure, and sun protection practices in outdoor exercisers, athletes, and military personnel.

The vitamin D-folate hypothesis in human vascular health.

The vitamin D-folate hypothesis has been proposed as an explanation for the evolution of human skin pigmentation. According to this hypothesis, a darkened skin pigment was adapted by early human populations living in equatorial Africa to protect against photodegradation of bioavailable folate by ultraviolet radiation (UVR). As humans moved away from the equator to more northern latitudes and occupied regions of lower UVR exposure and greater seasonal variation, however, depigmentation occurred to allow for adequate biosynthesis of vitamin D. Vitamin D and folate are both recognized for their evolutionary importance in healthy pregnancy and early childhood development. More recently, evidence has emerged demonstrating the importance of both vitamin D and folate in vascular health via their effects in reducing oxidative stress and improving nitric oxide (NO) bioavailability. Thus, populations with darkened skin pigmentation may be at elevated risk of vascular dysfunction and cardiovascular disease in low UVR environments due to hypovitaminosis D; particularly important as darkly-pigmented African-Americans represent an at-risk population for cardiovascular disease. Conversely, lightly pigmented populations in high UVR environments may be at risk of deleterious vascular effects of UVR-induced folate degradation. The focus of this review is to explore the currently available literature regarding the potential role of UVR in vascular health via its differential effects on vitamin D and folate metabolism, as well as the interaction between skin pigmentation, genetics, and environment in modulating the vascular influence of UVR exposure.

Sunscreen or simulated sweat minimizes the impact of acute ultraviolet radiation on cutaneous microvascular function in healthy humans.

NEW FINDINGS: What is the central question of this study? Are ultraviolet radiation (UVR)-induced increases in skin blood flow independent of skin erythema? Does broad-spectrum UVR exposure attenuate NO-mediated cutaneous vasodilatation, and does sunscreen or sweat modulate this response? What are the main findings and their importance? Erythema and vascular responses to UVR are temporally distinct, and sunscreen prevents both responses. Exposure to UVR attenuates NO-mediated vasodilatation in the cutaneous microvasculature; sunscreen or simulated sweat on the skin attenuates this response. Sun over-exposure may elicit deleterious effects on human skin that are separate from sunburn, and sunscreen or sweat on the skin may provide protection. ABSTRACT: Exposure to ultraviolet radiation (UVR) may result in cutaneous vascular dysfunction independent of erythema (skin reddening). Two studies were designed to differentiate changes in erythema from skin vasodilatation throughout the 8 h after acute broad-spectrum UVR exposure with (+SS) or without SPF-50 sunscreen (study 1) and to examine NO-mediated cutaneous vasodilatation after acute broad-spectrum UVR exposure with or without +SS or simulated sweat (+SW) on the skin (study 2). In both studies, laser-Doppler flowmetry was used to measure red cell flux, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure). In study 1, in 14 healthy adults (24 ± 4 years old; seven men and seven women), the skin erythema index and CVC were measured over two forearm sites (UVR only and UVR+SS) before, immediately after and every 2 h for 8 h post-exposure (750 mJ cm-2 ). The erythema index began to increase immediately post-UVR (P < 0.05 at 4, 6 and 8 h), but CVC did not increase above baseline for the first 4-6 h (P ≤ 0.01 at 6 and 8 h); +SS prevented both responses. In study 2, in 13 healthy adults (24 ± 4 years old; six men and seven women), three intradermal microdialysis fibres were placed in the ventral skin of the forearm [randomly assigned to UVR (450 mJ cm-2 ), UVR+SS or UVR+SW], and one fibre (non-exposed control; CON) was placed in the contralateral forearm. After UVR, a standardized local heating (42°C) protocol quantified the percentage of NO-mediated vasodilatation (%NO). The UVR attenuated %NO compared with CON (P = 0.01). The diminished %NO was prevented by +SS (P < 0.01) and +SW (P < 0.01). Acute broad-spectrum UVR attenuates NO-dependent dilatation in the cutaneous microvasculature, independent of erythema. Sunscreen protects against both inflammatory and heating-induced endothelial dysfunction, and sweat might prevent UVR-induced reductions in NO-dependent dilatation.

Sunscreen does not alter sweating responses or critical environmental limits in young adults (PSU HEAT project).

Outdoor athletes often eschew using sunscreen due to perceived performance impairments, which many attribute in part to the potential for reduced thermoregulatory heat loss. Past studies examining the impact of sunscreen on thermoregulation are equivocal. The purpose of this study was to determine the effects of mineral and chemical-based sunscreens on sweating responses and critical environmental limits in hot-dry (HD) and warm-humid (WH) environments. Nine subjects (3 M/6 F; 25 ± 2 yr) were tested with 1) no sunscreen (control), 2) chemical-, and 3) mineral-based sunscreen. Subjects were exposed to progressive heat stress with either 1) constant dry-bulb temperature (Tdb) at 34°C and increasing water vapor pressure (Pa) (WH trials) or 2) constant Pa at 12 mmHg and increasing Tdb (HD trials). Subjects walked at 4.9 ± 0.5 metabolic equivalents (METs) until an upward inflection in gastrointestinal temperature was observed (i.e., the critical environmental limit). Compared with control (39.9 ± 3.0°C), critical Tdb was not different in mineral (39.2 ± 3.5°C, P = 0.39) or chemical (39.7 ± 3.0°C, P = 0.98) sunscreen trials in HD environments. Compared with control (18.8 ± 4.0 mmHg), critical Pa was not different in mineral (18.9 ± 4.8 mmHg, P = 0.81) or chemical (19.5 ± 4.6 mmHg, P = 0.81) sunscreen trials in WH environments. Sweating rates, evaporative heat loss, skin wettedness, and sweating efficiency were not different among the three trials in the WH (all P ≥ 0.48) or HD (all P ≥ 0.87) environments. Critical environmental limits are unaffected by sunscreen application, suggesting sunscreen does not alter integrative thermoregulatory responses during exercise in the heat.NEW & NOTEWORTHY Our findings demonstrate that neither sweating nor critical environmental limits were affected by mineral-based and chemical-based sunscreen applications. The rates of change in core temperature during compensable and uncompensable heat stress were not changed by wearing sunscreen. Evaporative heat loss, efficiency of sweat evaporation, skin wettedness, and sweating rates were unaffected by sunscreen. Sunscreen did not alter integrative thermoregulatory responses during exercise in the heat.

Critical Environmental Core Temperature Limits and Heart Rate Thresholds across the Adult Age Span (PSU HEAT Project).

The frequency, duration, and severity of extreme heat events have increased and are projected to continue to increase throughout the next century. As a result, there is an increased risk of excessive heat- and cardiovascular-related morbidity and mortality during these extreme heat events. Therefore, the purposes of this investigation were to establish (1) critical environmental core temperature (Tc) limits for middle-aged adults (MA), (2) environmental thresholds that cause heart rate (HR) to progressively rise in MA and older (O) adults, and (3) examine critical environmental Tc limits and HR environmental thresholds across the adult age span. Thirty-three young (Y) (15 F; 23±3 yrs), 28 MA (17F; 51±6 yrs), and 31 O (16F; 70±3 yrs) subjects were exposed to progressive heat stress in an environmental chamber in a warm-humid (WH, 34-36°C, 50-90% rh) and a hot-dry (HD, 38°C-52°C, <30% rh) environment while exercising at a low metabolic rate reflecting activities of daily living (~1.8 METS). In both environments, there was a main effect of age on the critical environmental Tc limit and environmental HR thresholds (main effect of age all p < 0.001). Across the life span, critical environmental Tc and HR thresholds decline linearly with age in HD environments (R2 ≥ 0.3), and curvilinearly in WH environments (R2 ≥ 0.4). These data support an age-associated shift in critical environmental Tc limits and HR thresholds toward lower environmental conditions, and can be used to develop evidence-based safety guidelines to minimize future heat-related morbidity and mortality across the adult age span.

Relatively minor influence of individual characteristics on critical wet-bulb globe temperature (WBGT) limits during light activity in young adults (PSU HEAT Project).

Critical environmental limits are temperature-humidity thresholds above which heat balance cannot be maintained for a given metabolic heat production. This study examined the association between individual characteristics [sex, body surface area (AD), aerobic capacity (V̇o2max), and body mass (mb)] and critical environmental limits in young adults at low metabolic rates. Forty-four (20 M/24 F; 23 ± 4 yr) subjects were exposed to progressive heat stress in an environmental chamber at two low net metabolic rates (Mnet); minimal activity (MinAct; Mnet = ∼160 W) and light ambulation (LightAmb; Mnet = ∼260 W). In two hot-dry (HD; ≤25% rh) environments, ambient water vapor pressure (Pa = 12 or 16 mmHg) was held constant and dry-bulb temperature (Tdb) was systematically increased. In two warm-humid (WH; ≥50% rh) environments, Tdb was held constant at 34°C or 36°C, and Pa was systematically increased. The critical wet-bulb globe temperature (WBGTcrit) was determined for each condition. During MinAct, after entry of Mnet into the forward stepwise linear regression model, no individual characteristics were entered into the model for WH (R2adj = 0.01, P = 0.27) or HD environments (R2adj = -0.01, P = 0.44). During LightAmb, only mb was entered into the model for WH environments (R2adj = 0.44, P < 0.001), whereas only V̇o2max was entered for HD environments (R2adj = 0.22; P = 0.002). These data demonstrate negligible importance of individual characteristics on WBGTcrit during low-intensity nonweight-bearing (MinAct) activity with a modest impact of mb and V̇o2max during weight-bearing (LightAmb) activity in extreme thermal environments.NEW & NOTEWORTHY Our laboratory has recently published a series of papers establishing the upper ambient temperature-humidity thresholds for maintaining heat balance, termed critical environmental limits, in young adults. However, no studies have investigated the relative influence of individual characteristics, such as sex, body size, and aerobic fitness, on those environmental limits. Here, we demonstrate the contributions of sex, body mass, body surface area, and maximal aerobic capacity on critical wet-bulb globe temperature (WBGT) limits in young adults.

Within-limb variation in skin pigmentation does not influence cutaneous vasodilation.

Ultraviolet radiation (UVR) exposure acutely reduces nitric oxide (NO)-dependent cutaneous vasodilation. In addition, increased constitutive skin melanin is associated with attenuated NO-dependent cutaneous vasodilation. However, the impact of within-limb variation in skin melanization, associated with seasonal UVR exposure, on NO-dependent cutaneous vasodilation is unknown. We investigated the effect of within-limb variation in skin melanin on NO-dependent cutaneous vasodilation. Intradermal microdialysis fibers were placed in the inner-upper arm, ventral forearm, and dorsal forearm of seven adults (33 ± 14 yr; 4 M/3 F) with constitutively light skin pigmentation. Melanin-index (M-index; an index of skin pigmentation), measured via reflectance spectrophotometry, confirmed differences in sun exposure among sites. A standardized local heating (42°C) protocol induced cutaneous vasodilation. After attaining a stable elevated blood flow plateau, 15 mM NG-nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor) was infused to quantify the NO contribution. Laser-Doppler flowmetry (LDF) measured red cell flux and cutaneous vascular conductance (CVC = LDF/mean arterial pressure) and was normalized to maximal (%CVCmax; 28 mM sodium nitroprusside + 43°C local heating). Dorsal forearm M-index was higher [50.5 ± 11.8 au (arbitrary units)] compared with the ventral forearm (37.5 ± 7.4 au; P ≤ 0.03) and upper arm (30.0 ± 4.0 au; P ≤ 0.001) M-index. Cutaneous vasodilation responses to local heating were not different among sites (P ≥ 0.12). Importantly, neither the magnitude of the local heating plateau (dorsal: 85 ± 21%; ventral: 70 ± 21%; upper: 87 ± 15%; P ≥ 0.16) nor the NO-mediated component of that response (dorsal: 59 ± 15%; ventral: 54 ± 13%; upper: 55 ± 11%; P ≥ 0.79) was different among sites. These data suggest that within-limb differences in skin pigmentation secondary to seasonal UVR exposure do not alter NO-dependent cutaneous vasodilation.NEW & NOTEWORTHY Locally derived endothelial nitric oxide (NO) contributes to the full expression of cutaneous vasodilation responses. Acute ultraviolet radiation (UVR) exposure attenuates NO-mediated vasodilation of the cutaneous microvasculature. Our findings suggest that in constitutively lightly pigmented skin, variation in skin melanin due to seasonal exposure to UVR does not alter the NO contribution to cutaneous vasodilation. Seasonal UVR exposure does not impact the NO-mediated cutaneous microvascular function.