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.

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.

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.

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.