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.

Menthol-induced activation of TRPM8 receptors increases cutaneous blood flow across the dermatome.

Topical menthol-based analgesics increase skin blood flow (SkBF) through transient receptor potential melastatin 8 (TRPM8) receptor-dependent activation of sensory nerves and endothelium-derived hyperpolarization factors. It is unclear if menthol-induced TRPM8 activation mediates a reflex change in SkBF across the dermatome in an area not directly treated with menthol. The purpose of this study was to determine the effects of localized topical menthol application on SkBF across a common dermatome. We hypothesized that SkBF would be increased with menthol at the site of application and across the dermatome (contralateral limb) through a spinal reflex mechanism. In a double blind, placebo controlled, cross-over design, 15 healthy participants (7 men; age = 22 ± 1 yrs) were treated with direct application (3 ml over 8 × 13 cm) of 5% menthol gel (Biofreeze™) or placebo gel on the L4 dermatome, separated by 48 h. Red blood cell flux was measured using laser Doppler flowmetry over the area of application, on the contralateral leg of the same dermatome, and in a separate dermatome (L5/S1) to serve as control. Cutaneous vascular conductance was calculated for each measurement site (CVC = flux/MAP). At baseline there were no differences in CVC between menthol and placebo gels, or among sites (all p > 0.05). After 30 ± 6 min, CVC increased at the treated site with menthol (0.12 ± 0.02 vs. 1.36 ± 0.19 flux/mm Hg, p < 0.01) but not the placebo (0.10 ± 0.01 vs. 0.18 ± 0.04 flux/mm Hg, p = 0.91). There was a modest increase in CVC at the contralateral L4 dermatome with menthol gel (0.16 ± 0.04 vs. 0.29 ± 0.06 flux/mm Hg, p < 0.01), but not placebo (0.11 ± 0.02 vs. 0.15 ± 0.03 flux/mm Hg, p = 0.41). There was no effect on SkBF from either treatments at the L5/S1 control dermatome (both, p > 0.05), suggesting the lack of a systemic response. In conclusion, menthol containing topical analgesic gels increased SkBF at the treated site, and modestly throughout the dermatome. These data suggest menthol-induced activation of the TRPM8 receptors induces an increase in SkBF across the area of common innervation through a localized spinal reflex mechanism.

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.

Reproducibility of the neurocardiovascular responses to common laboratory-based sympathoexcitatory stimuli in young adults.

The magnitude of blood pressure (BP) and muscle sympathetic nerve activity (MSNA) responses to laboratory stressors is commonly used to compare neurocardiovascular responsiveness between groups and conditions. However, no studies have rigorously examined the reproducibility of BP and MSNA responsiveness. Here, we assess the within-visit reproducibility of BP (finger photoplethysmography) and MSNA (microneurography) responses to isometric handgrip (HG) and postexercise ischemia (PEI) in young healthy adults (n = 30). In a subset (n = 21), we also examined the between-visit reproducibility of responsiveness to HG, PEI, and the cold pressor test (CPT). Intraclass correlation coefficients (ICCs) were used as a primary reproducibility measure (e.g., ICC >0.75 is considered very good). Within a visit, the increase in mean arterial pressure during HG [ICC = 0.85 (0.69-0.93); P < 0.001] and PEI [ICC = 0.85 (0.69-0.93); P < 0.001] demonstrated very good reproducibility. Furthermore, the between-visit reproducibility of the pressor response to HG [ICC = 0.85 (0.62-0.94); P < 0.001], PEI [ICC = 0.84 (CI = 0.58-0.94); P < 0.001], and the CPT [ICC = 0.89 (0.72-0.95) P < 0.001]) were also very good. However, there was greater variability in both the within- [HG: ICC = 0.58 (-0.22-0.85), P = 0.001; PEI: ICC = 0.33 (-0.24-0.69), P = 0.042] and between-visit reproducibility of MSNA responsiveness [HG: ICC = 0.87 (0.53-0.96), P = 0.001; PEI: ICC = 0.24 (-0.62-0.78), P = 0.27; CPT: ICC = 0.77 (0.29-0.93), P = 0.007]. The magnitude of the BP response to several standard laboratory stimuli was very good, whereas the variability of the MSNA response to these perturbations was generally less consistent, particularly during PEI. These data provide novel insight for both study design and data interpretation when comparing neurocardiovascular responsiveness between different conditions, groups, or studies, as well as before and after interventions/treatments.NEW & NOTEWORTHY The magnitude of the increases in blood pressure and muscle sympathetic nerve activity in response to sympathoexcitatory stimuli such as static handgrip, postexercise ischemia, and the cold pressor test are commonly used to assess neurocardiovascular responsiveness. However, limited studies have comprehensively examined the reproducibility of these responses. We demonstrate that the reproducibility of the pressor response to these perturbations was very good within an individual, whereas the reproducibility of the MSNA response was less consistent.