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.

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.

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.

Core temperature and heart rate at the upper limit of the prescriptive zone.

The expressed goal of limiting workplace heat stress exposures to a core temperature (Tc ) of 38°C traces back to a 1969 World Health Organization Technical Report (WHO Series 412). The actual goal was to limit exposures to the upper limit of the prescriptive zone (ULPZ). To explore the physiological strain at the ULPZ, progressive heat stress protocol data from Penn State University (PSU) and University of South Florida (USF) below and at the ULPZ were used to articulate the relation of Tc and heart rate (HR) to metabolic rate (MR) with consideration of acclimatization state, clothing, exposure condition (PreULPZ vs. ULPZ), and sex. Regression models demonstrated the association of MR and sex with Tc and HR. At the ULPZ, women had systematically higher values of Tc and HR than men at the same MR likely due to higher relative demands. There was no effect for acclimatization state and clothing. As expected for individuals, Tc was practically constant below the ULPZ and HR exhibited increasing values approaching the ULPZ. At 490 W, the high MR cited in the WHO document, the mean Tc for men was near the 38°C limit with systematically lower Tc at lower MRs.

Distribution of upper limit of the prescriptive zone values for acclimatized and unacclimatized individuals.

Heat stress has an adverse impact on worker health and well-being, and the effects will increase with more frequent and severe heat events associated with global warming. Acclimatization to heat stress is widely considered to be a critical mitigation strategy and wet bulb globe temperature- (WBGT-) based occupational standards and guidelines contain adjustments for acclimatization. The purpose here was to 1) compare the mean values for the upper limit of the prescriptive zone (ULPZ, below which the rise in core temperature is minimal) between unacclimatized and acclimatized men and women; 2) demonstrate that the change in the occupational exposure limit (ΔOEL) due to acclimatization is independent of metabolic rate; 3) examine the relation between ΔOEL and body surface area (BSA); and 4) compare the exposure-response curves between unacclimatized and acclimatized populations. Empirically derived ULPZ data for unacclimatized participants from Pennsylvania State University (PSU) and acclimatized participants from University of South Florida (USF) were used to explore the difference between unacclimatized and acclimatized heat exposure limits. The findings provide support for a constant 3°C WBGT OEL decrease to account for unacclimatized workers. Body surface area explained part of the difference in ULPZ values between men and women. In addition, the pooled PSU and USF data provide insight into the distribution of individual values for the ULPZ among young, healthy unacclimatized and acclimatized populations in support of occupational heat stress guidelines.NEW & NOTEWORTHY Occupational exposure limit guidelines using wet bulb globe temperature (WBGT) distinguish between acclimatized and unacclimatized workers with about a 3°C difference between them. For the first time, empirical data from two laboratories provide support for acclimatization state adjustments. Using a constant difference rather than increasing differences with metabolic rate better describes the limit for unacclimatized participants. Furthermore, the lower upper limit of the prescriptive zone (ULPZ) values set forth for women do not relate to fitness level but are partly explained by their smaller body surface area (BSA). An examination of individual ULPZ values suggests that many unacclimatized individuals should be able to sustain safe work at the exposure limit for acclimatized workers.

Nitric oxide-mediated cutaneous microvascular function is not altered in middle-aged-to-older adults following mild SARS-CoV-2 infection: A pilot study.

We tested the hypothesis that post-COVID-19 adults (PC) would have impaired cutaneous nitric oxide (NO)-mediated vasodilation compared to controls (CON). We performed a cross-sectional study including 10 (10 F/0 M, 69 ± 7 years) CON and 7 (2 F/5 M, 66 ± 8 years) PC (223 ± 154 days post-diagnosis). COVID-19 symptoms severity (survey) was assessed (0-100 scale for 18 common symptoms). NO-dependent cutaneous vasodilation was induced by a standardized 42°C local heating protocol and quantified via perfusion of 15 mM NG-nitro-L-arginine methyl ester during the plateau of the heating response (intradermal microdialysis). Red blood cell flux was measured with laser-Doppler flowmetry. Cutaneous vascular conductance (CVC = flux/mm Hg) was presented as a percentage of maximum (28 mM sodium nitroprusside +43°C). All data are means ± SD. The local heating plateau (CON: 71 ± 23% CVCmax vs. PC: 81 ± 16% CVCmax , p = 0.77) and NO-dependent vasodilation (CON: 56 ± 23% vs. PC: 60 ± 22%, p = 0.77) were not different between groups. In the PC group neither time since diagnosis nor peak symptom severity (46 ± 18 AU) correlated with NO-dependent vasodilation (r < 0.01, p = 0.99 and r = 0.42, p = 0.35, respectively). In conclusion, middle-aged and older adults who have had COVID-19 did not have impaired NO-dependent cutaneous vasodilation. Additionally, in this cohort of PC, neither time since diagnosis nor symptomology were related to microvascular function.

Onset of cardiovascular drift during progressive heat stress in young adults (PSU HEAT project).

With climate change, humans are at a greater risk for heat-related morbidity and mortality, often secondary to increased cardiovascular strain associated with an elevated core temperature (Tc). Critical environmental limits (i.e., the upper limits of compensable heat stress) have been established based on Tc responses for healthy, young individuals. However, specific environmental limits for the maintenance of cardiovascular homeostasis have not been investigated in the context of thermal strain during light activity. Therefore, the purposes of this study were to 1) identify the specific environmental conditions (combinations of ambient temperature and water vapor pressure) at which cardiovascular drift [i.e., a continuous rise in heart rate (HR)] began to occur and 2) compare those environments to the environmental limits for the maintenance of heat balance. Fifty-one subjects (27 F; 23 ± 4 yr) were exposed to progressive heat stress across a wide range of environmental conditions in an environmental chamber at two low metabolic rates reflecting minimal activity (MinAct; 159 ± 34 W) or light ambulation (LightAmb; 260 ± 55 W). Whether systematically increasing ambient temperature or humidity, the onset of cardiovascular drift occurred at lower environmental conditions compared with Tc inflection points at both intensities (P < 0.05). Furthermore, the time at which cardiovascular drift began preceded the time of Tc inflection (MinAct P = 0.01; LightAmb P = 0.0002), and the difference in time between HR and Tc inflection points did not differ (MinAct P = 0.08; LightAmb P = 0.06) across environmental conditions for either exercise intensity. These data suggest that even in young adults, increases in cardiovascular strain precede the point at which heat stress becomes uncompensable during light activity.NEW & NOTEWORTHY To our knowledge, this study is the first to 1) identify the specific combinations of temperature and humidity at which an increase in cardiovascular strain (cardiovascular drift) occurs and 2) compare those environments to the critical environmental limits for the maintenance of heat balance. We additionally examined the difference in time between the onset of increased cardiovascular strain and uncompensable heat stress. We show that an increase in cardiovascular strain systematically precedes sustained heat storage 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.

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.

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.

Heat stress vulnerability and critical environmental limits for older adults.

The present study examined heat stress vulnerability of apparently healthy older vs. young adults and characterized critical environmental limits for older adults in an indoor setting at rest (Rest) and during minimal activity associated with activities of daily living. Critical environmental limits are combinations of ambient temperature and humidity above which heat balance cannot be maintained (i.e., becomes uncompensable) for a given metabolic heat production. Here we exposed fifty-one young (23±4 yrs) and 49 older (71±6 yrs) adults to progressive heat stress across a wide range of environments in an environmental chamber during Minimal Activity (young and older subjects) and Rest (older adults only). Heat compensability curves were shifted leftward for older adults indicating age-dependent heat vulnerablity (p < 0.01). During Minimal Activity, critical environmental limits were lower in older compared to young adults (p < 0.0001) and lower than those at Rest (p < 0.0001). These data document heat vulnerability of apparently healthy older adults and to define critical environmental limits for indoor settings in older adults at rest and during activities of daily living, and can be used to develop evidence-based recommendations to minimize the deleterious impacts of extreme heat events in this population.

Core temperature responses to compensable versus uncompensable heat stress in young adults (PSU HEAT Project).

With global warming, much attention has been paid to the upper limits of human adaptability. However, the time to reach a generally accepted core temperature criterion (40.2°C) associated with heat-related illness above (uncompensable heat stress) and just below (compensable heat stress) the upper limits for heat balance remains unclear. Forty-eight (22 men/26 women; 23 ± 4 yr) subjects were exposed to progressive heat stress in an environmental chamber during minimal activity (MinAct, 159 ± 34 W) and light ambulation (LightAmb, 260 ± 55 W) in warm-humid (WH; ∼35°C, >60% RH) and hot-dry (HD; 43°C-48°C, <25% RH) environments until heat stress became uncompensable. For each condition, we compared heat storage (S) and the change in gastrointestinal temperature (ΔTgi) over time during compensable and uncompensable heat stress. In addition, we examined whether individual characteristics or seasonality were associated with the rate of increase in Tgi. During compensable heat stress, S was higher in HD than in WH environments (P < 0.05) resulting in a greater but more variable ΔTgi (P ≥ 0.06) for both metabolic rates. There were no differences among conditions during uncompensable heat stress (all P > 0.05). There was no influence of sex, aerobic fitness, or seasonality, but a larger body size was associated with a greater ΔTgi during LightAmb in WH (P = 0.003). The slopes of the Tgi response during compensable (WH: MinAct, 0.06, LightAmb, 0.09; HD: MinAct, 0.12, LightAmb, 0.15°C/h) and uncompensable (WH: MinAct, 0.74, LightAmb, 0.87; HD: MinAct, 0.71, LightAmb, 0.93°C/h) heat stress can be used to estimate the time to reach a target core temperature from any given starting value.NEW & NOTEWORTHY This study is the first to examine heat storage and the rate of change in core temperature above (uncompensable heat stress) and just below (compensable heat stress) critical environmental limits to human heat balance. Furthermore, we examine the influence of individual subject characteristics and seasonality on the change in core temperature in warm-humid versus hot-dry environments. We provide the rate of change in core temperature, enabling projections to be made to and from any hypothetical core temperature.

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.

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.

Validity and reliability of a protocol to establish human critical environmental limits (PSU HEAT Project).

The PSU HEAT protocol has been used to determine critical environmental limits, i.e., those combinations of ambient temperature and humidity above which heat stress becomes uncompensable and core temperature rises continuously. However, no studies have rigorously investigated the reliability and validity of this experimental protocol. Here, we assessed the 1) between-visit reliability and 2) validity of the paradigm. Twelve subjects (5 M/7W; 25 ± 4 yr) completed a progressive heat stress protocol during which they walked on a treadmill (2.2 mph, 3% gradient) in a controllable environmental chamber. After an equilibration period, either dry-bulb temperature (Tdb) was increased every 5 min while ambient water vapor pressure (Pa) was held constant (Tcrit experiments) or Pa was increased every 5 min while Tdb was held constant (Pcrit experiments) until an upward inflection in gastrointestinal temperature (Tgi) was observed. For reliability experiments, 11 subjects repeated the same protocol on a different day. For validity experiments, 10 subjects performed a Tcrit experiment at their previously determined Pcrit or vice versa. The between-visit reliability (intraclass correlation coefficient, ICC) for critical environmental limits was 0.98. Similarly, there was excellent agreement between original and validity trials for Tcrit (ICC = 0.95) and Pcrit (ICC = 0.96). Furthermore, the wet-bulb temperature at the Tgi inflection point was not different during reliability (P = 0.78) or validity (P = 0.32) trials compared with original trials. These findings support the reliability and validity of this experimental paradigm for the determination of critical environmental limits for maintenance of human heat balance.NEW & NOTEWORTHY The PSU HEAT progressive heat stress protocol has been used to identify critical environmental limits for various populations, clothing ensembles, and metabolic intensities. However, no studies have rigorously investigated the reliability and validity of this experimental model. Here, we demonstrate excellent reliability and validity of the PSU HEAT protocol.

Critical environmental limits for young, healthy adults (PSU HEAT Project).

Critical environmental limits are those combinations of ambient temperature and humidity above which heat balance cannot be maintained for a given metabolic heat production, limiting exposure time, and placing individuals at increased risk of heat-related illness. The aim of this study was to establish those limits in young (18-34 yr) healthy adults during low-intensity activity approximating the metabolic demand of activities of daily living. Twenty-five (12 men/13 women) subjects were exposed to progressive heat stress in an environmental chamber at two rates of metabolic heat production chosen to represent minimal activity (MinAct) or light ambulation (LightAmb). Progressive heat stress was performed with either 1) constant dry-bulb temperature (Tdb) and increasing ambient water vapor pressure (Pa) (Pcrit trials; 36°C, 38°C, or 40°C) or 2) constant Pa and increasing Tdb (Tcrit trials; 12, 16, or 20 mmHg). Each subject was tested during MinAct and LightAmb in two to three experimental conditions in random order, for a total of four to six trials per participant. Higher metabolic heat production (P < 0.001) during LightAmb compared with MinAct trials resulted in significantly lower critical environmental limits across all Pcrit and Tcrit conditions (all P < 0.001). These data, presented graphically herein on a psychrometric chart, are the first to define critical environmental limits for young adults during activity resembling those of light household tasks or other activities of daily living and can be used to develop guidelines, policy decisions, and evidence-based alert communications to minimize the deleterious impacts of extreme heat events.NEW & NOTEWORTHY Critical environmental limits are those combinations of temperature and humidity above which heat balance cannot be maintained, placing individuals at increased risk of heat-related illness. Those limits have been investigated in young adults during exercise at 30% V̇o2max, but not during metabolic rates that approximate those of light activities of daily living. Herein, we establish critical environmental limits for young adults at two metabolic rates that reflect activities of daily living and leisurely walking.