Nicholas Ravanelli

Heart Rate and Body Temperature Responses to Extreme Heat and Humidity With and Without Electric Fans

Patz et al1 described the projected effects of more prolonged and severe heat waves on human health. A simple, low-cost cooling device is an electric fan. A Cochrane review2 concluded “no evidence currently exists supporting or refuting the use of electric fans during heat waves” for mortality and morbidity. However, public health guidance typically warns against fan use in hot weather. Recommended upper limits range from 32.3°C (90°F) at 35% relative humidity (RH) to the high 90s (96-99°F; 35.6-37.2°C, no RH stated2). The skin-to-air temperature gradient reverses with rising environmental temperature, causing dry heat transfer toward the body via convection rather than away from it. Fan use would increase this dry heat transfer, potentially accelerating body heating3,4; however, the efficiency of sweat evaporation from the skin would be simultaneously increased. Thus, fans could still improve net heat loss. Sweat evaporation declines with increasing humidity, so in more humid environments fans may not prevent heat-induced elevations in cardiovascular (heart rate, HR) and thermal (core temperature) strain. This study examined the influence of fan use on the critical humidities at which hot environments can no longer be physiologically tolerated without rapid increases in HR and core temperature.

Should electric fans be used during a heat wave

Heat waves continue to claim lives, with the elderly and poor at greatest risk. A simple and cost-effective intervention is an electric fan, but public health agencies warn against their use despite no evidence refuting their efficacy in heat waves. A conceptual human heat balance model can be used to estimate the evaporative requirement for heat balance, the potential for evaporative heat loss from the skin, and the predicted sweat rate, with and without an electrical fan during heat wave conditions. Using criteria defined by the literature, it is clear that fans increase the predicted critical environmental limits for both the physiological compensation of endogenous/exogenous heat, and the onset of cardiovascular strain by an air temperature of ∼3-4 °C, irrespective of relative humidity (RH) for the young and elderly. Even above these critical limits, fans would apparently still provide marginal benefits at air temperatures as high as 51.1 °C at 10%RH for young adults and 48.1 °C at 10%RH for the elderly. Previous concerns that dehydration would be exacerbated with fan use do not seem likely, except under very hot (>40 °C) and dry (<10%RH) conditions, when predicted sweat losses are only greater with fans by a minor amount (∼20-30 mL/h). Relative to the peak outdoor environmental conditions reported during ten of the most severe heat waves in recent history, fan use would be advisable in all of these situations, even when reducing the predicted maximum sweat output for the elderly. The protective benefit of fans appears to be underestimated by current guidelines.

Acute acetaminophen ingestion does not alter core temperature or sweating during exercise in hot-humid conditions

Acute acetaminophen (ACT) ingestion has been reported to reduce thermal strain during cycling in the heat. In this study, nine active participants ingested 20 mg of ACT per kg of total body mass (ACT) or a placebo (PLA), 60 min prior to cycling at a fixed rate of metabolic heat production (ACT: 8.3 ± 0.3 W/kg; PLA: 8.5 ± 0.5 W/kg), which was equivalent to 55 ± 6% VO2max, for 60 min at 34.5 ± 0.1 °C, 52 ± 1% relative humidity. Resting rectal temperature (Tre; ACT: 36.70 ± 0.17 °C; PLA: 36.80 ± 0.16 °C, P = 0.24), esophageal temperature (Tes; ACT: 36.54 ± 0.22 °C; PLA: 36.61 ± 0.17 °C, P = 0.50) and mean skin temperature (Tsk; ACT: 34.00 ± 0.14 °C; PLA: 33.96 ± 0.20 °C, P = 0.70) were all similar among conditions. At end‐exercise, no differences in ΔTre (ACT: 1.12 ± 0.15 °C; PLA: 1.11 ± 0.21 °C, P = 0.92), ΔTes (ACT: 0.90 ± 0.28 °C; PLA: 0.88 ± 0.23 °C, P = 0.84), ΔTsk (ACT: 0.80 ± 0.39 °C; PLA: 0.70 ± 0.46 °C, P = 0.63), mean local sweat rate (ACT: 1.02 ± 0.15 mg/cm2/min; PLA: 1.02 ± 0.13 mg/cm2/min, P = 0.98) and whole‐body sweat loss (ACT: 663 ± 83 g; PLA: 663 ± 77 g, P = 0.995) were evident. Furthermore, ratings of perceived exertion and thermal sensation and thermal comfort were not different between ACT and PLA conditions. In conclusion, ACT ingested 60 min prior to moderate intensity exercise in hot–humid conditions does not alter physiologic thermoregulatory control nor perceived strain.

Electric fan use in heat waves: Turn on or turn off?

Heat waves have been responsible for more deaths worldwide than all other natural disasters combined. In Europe, this “silent killer” caused 70000C excess deaths in 2003, and more recently 3500C people died during 2 separate heat waves in India (May 2015) and Pakistan (June 2015) (Fig. 1). Groups among the most vulnerable include the elderly, poor, and people with cardiovascular disease. Identifying simple and cost-effective cooling strategies are therefore an urgent priority. In this Discovery article, we highlight our study which was the first to assess the efficacy of the humble electric fan for mitigating cardiovascular and thermal strain in humans during simulated heat wave conditions. Despite the high cooling capacity of air conditioners (AC), the millions of tonnes of CO2 they generate annually potentially contribute to a vicious cycle of worsening future heat waves. 3 Mass ACuse has also led to electricity blackouts or brownouts during heat waves, and in some cases catastrophic exacerbations in morbidity and mortality. By contrast, electric fans have an electricity requirement that is 50-fold lower than conventional AC units (55-100 W vs 1500-5000 W). In South Korea, fans are equipped with an off-timer due to the unsubstantiated belief held since the mid-1920s that prolonged fan use can lead to asphyxiation. Meanwhile, all major international public health agencies warn against fan use during heat waves due to a similarly unsupported belief that they paradoxically increases the risk of heat related illness. Specifically, the World Health Organization (WHO) and Centers for Disease Control and Prevention (CDC) state that electric fan use above »35 C will critically exacerbate dehydration and “speed the onset” of heat exhaustion. In stark contrast, a 2012 Cochrane review identified that no empirical evidence exists to support or refute the use of fans in heat waves. In order to maintain body temperature, the human body must balance the rate of internal heat production with the rate of heat dissipation to the surrounding environment. One avenue of heat dissipation is sensible heat transfer, which in indoor environments primarily occurs via convection, following the temperature gradient between the skin surface and ambient air. When ambient air is less than skin temperature (»35 C), heat flows away from the body, but when the ambient air exceeds skin temperature this gradient is reversed and heat is instead added to the body. Since convective heat transfer increases sharply with increases in air velocity, more heat flows in to the body with forced air movement (e.g. with a fan).

Maximum Skin Wettedness following Aerobic Training with and without Heat Acclimation

Purpose To quantify how maximum skin wettedness (&ohgr;max); that is, the determinant of the boundary between compensable and uncompensable heat stress, is altered by aerobic training in previously unfit individuals and further augmented by heat acclimation. Methods Eight untrained individuals completed an 8-wk aerobic training program immediately followed by 8 d of hot/humid (38°C, 65%RH) heat acclimation. Participants completed a humidity ramp protocol pretraining (PRE-TRN), posttraining (POST-TRN), and after heat acclimation (POST-HA), involving treadmill marching at a heat production of 450 W for 105 min in 37.5°C, 2.0 kPa (35%RH). After attaining a steady-state esophageal temperature (Tes), humidity increased 0.04 kPa·min−1. An upward inflection in Tes indicated the upper limit of physiological compensability (Pcrit), which was then used to quantify &ohgr;max. Local sweat rate, activated sweat gland density, and sweat gland output on the back and arm were simultaneously measured throughout. Results Peak aerobic capacity increased POST-TRN by approximately 14% (PRE-TRN: 45.8 ± 11.8 mL·kg−1·min−1; POST-TRN: 52.0 ± 11.1 mL·kg−1·min−1, P < 0.001). &ohgr;max values became progressively greater from PRE-TRN (0.72 ± 0.06) to POST-TRN (0.84 ± 0.08; P = 0.02), to POST-HA (0.95 ± 0.05; P = 0.03). These shifts in &ohgr;max were facilitated by a progressively greater local sweat rate and activated sweat gland density from PRE-TRN (0.84 ± 0.21 mg·cm−2·min−1; 67 ± 20 glands per square centimeter) to POST-TRN (0.96 ± 0.21 mg·cm−2·min−1, P = 0.03; 86 ± 27 glands per square centimeter; P = 0.009), to POST-HA (1.15 ± 0.21 mg·cm−2·min−1; P < 0.001; 98 ± 35 glands per square centimeter; P < 0.001). No differences in sweat gland output were observed. Conclusions A greater &ohgr;max occurred after 8 wk of aerobic training, but &ohgr;max was further augmented with heat acclimation, indicating only a partially increased heat loss capacity with training. These &ohgr;max values may assist future predictions of heat stress risk in untrained/trained unacclimated individuals and trained heat-acclimated individuals.

Heat stress and fetal risk. Environmental limits for exercise and passive heat stress during pregnancy: a systematic review with best evidence synthesis

Objective Pregnant women are advised to avoid heat stress (eg, excessive exercise and/or heat exposure) due to the risk of teratogenicity associated with maternal hyperthermia; defined as a core temperature (Tcore) ≥39.0°C. However, guidelines are ambiguous in terms of critical combinations of climate and activity to avoid and may therefore unnecessarily discourage physical activity during pregnancy. Thus, the primary aim was to assess Tcore elevations with different characteristics defining exercise and passive heat stress (intensity, mode, ambient conditions, duration) during pregnancy relative to the critical maternal Tcore of ≥39.0°C. Design Systematic review with best evidence synthesis. Data sources EMBASE, MEDLINE, SCOPUS, CINAHL and Web of Science were searched from inception to 12 July 2017. Study eligibility criteria Studies reporting the Tcore response of pregnant women, at any period of gestation, to exercise or passive heat stress, were included. Results 12 studies satisfied our inclusion criteria (n=347). No woman exceeded a Tcore of 39.0°C. The highest Tcore was 38.9°C, reported during land-based exercise. The highest mean end-trial Tcore was 38.3°C (95% CI 37.7°C to 38.9°C) for land-based exercise, 37.5°C (95% CI 37.3°C to 37.7°C) for water immersion exercise, 36.9°C (95% CI 36.8°C to 37.0°C) for hot water bathing and 37.6°C (95% CI 37.5°C to 37.7°C) for sauna exposure. Conclusion The highest individual core temperature reported was 38.9°C. Immediately after exercise (either land based or water immersion), the highest mean core temperature was 38.3°C; 0.7°C below the proposed teratogenic threshold. Pregnant women can safely engage in: (1) exercise for up to 35 min at 80%–90% of their maximum heart rate in 25°C and 45% relative humidity (RH); (2) water immersion (≤33.4°C) exercise for up to 45 min; and (3) sitting in hot baths (40°C) or hot/dry saunas (70°C; 15% RH) for up to 20 min, irrespective of pregnancy stage, without reaching a core temperature exceeding the teratogenic threshold.

Thermoregulatory responses to exercise at a fixed rate of heat production are not altered by acute hypoxia

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg-1·min-1] completed 45 min of cycling, once in normoxia (NORM; [Formula: see text] = 0.21) and twice in hypoxia (HYP1/HYP2; [Formula: see text]= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1) two distinctly different %V̇o2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (Hprod) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2) the same %V̇o2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different Hprod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o2peak, changes in rectal temperature (ΔTre) and changes in esophageal temperature (ΔTes) were greater at end-exercise in NORM [ΔTre: 0.76 (0.19)°C; ΔTes: 0.64 (0.22)°C] compared with HYP2 [ΔTre: 0.56 (0.22)°C, P < 0.01; ΔTes: 0.42 (0.21)°C, P < 0.01]. As a result of a greater Hprod (P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm-2·min-1] compared with HYP2 [0.71 (0.19) mg·cm-2·min-1]. However, at a fixed Hprod, ΔTre [0.75 (0.24)°C; P = 0.77] and ΔTes [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm-2·min-1] was not different (P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o2peak, determines changes in core temperature and sweating during exercise.NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o2max) does not influence changes in thermoregulatory responses.

Sustained increases in skin blood flow are not a prerequisite to initiate sweating during passive heat exposure

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiSeff) or low (LoSeff) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiSeff at 36°C (HiSeff: 99 ± 11 vs. LoSeff: 77 ± 11 min, P < 0.01) and 42°C (HiSeff: 72 ± 16 vs. LoSeff: 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions (P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating.

The optimal exercise intensity for the unbiased comparison of thermoregulatory responses between groups unmatched for body size during uncompensable heat stress

We sought to identify the appropriate exercise intensity for unbiased comparisons of changes in rectal temperature (ΔTre) and local sweat rates (LSR) between groups unmatched for body size during uncompensable heat stress. Sixteen males vastly different in body morphology were separated into two equal groups [small (SM): 65.8 ± 6.2 kg, 1.8 ± 0.1 m2; large (LG): 100.0 ± 13.1 kg, 2.3 ± 0.1 m2], but matched for sudomotor thermosensitivity (SM: 1.3 ± 0.6; LG: 1.1 ± 0.4 mg·cm−2·min−1·°C−1). The maximum potential for evaporation (Emax) for each participant was assessed using an incremental humidity protocol. On separate occasions, participants then completed 60 min of cycling in a 35°C and 70% RH environment at (1) 50% of VO2max, (2) a heat production (Hprod) of 520 W, (3) Hprod relative to mass (6 W·kg−1), and (4) Hprod relative to mass above Emax (3 W·kg−1>Emax). Emax was similar between LG (347 ± 39 W, 154 ± 15 W·m−2) and SM (313 ± 63 W, 176 ± 34 W·m−2, P > 0.12). ΔTre was greater in SM compared to LG at 520 W (SM: 1.5 ± 0.5; LG 0.8 ± 0.3°C, P < 0.001) and at 50% of VO2max (SM: 1.4 ± 0.5; LG 0.9 ± 0.3°C, P < 0.001). However, ΔTre was similar between groups when Hprod was either 6 W·kg−1 (SM: 0.9 ± 0.3; LG 0.9 ± 0.2°C, P = 0.98) and 3 W·kg−1>Emax (SM: 1.4 ± 0.5; LG 1.3 ± 0.4°C, P = 0.99). LSR was similar between LG and SM irrespective of condition, suggesting maximum LSR was attained (SM: 1.10 ± 0.23; LG: 1.07 ± 0.35 mg·cm−2·min−1, P = 0.50). In conclusion, systematic differences in ΔTre and LSR between groups unmatched for body size during uncompensable heat stress can be avoided by a fixed Hprod in W·kg−1 or W·kg−1>Emax.

The influence of body morphology on changes in core temperature during exercise in an uncompensable environment

Evidence demonstrates that for unbiased comparisons of changes in core temperature (ΔTcore) between groups unmatched for body morphology, exercise should be performed using a fixed heat production (Hprod) per unit mass in physiologically compensable environments [1]. In uncompensable conditions, it has been suggested that a fixed external workload is the primary determinant of ΔTcore [2], however in addition to not accounting for differences in Hprod relative to mass, such an approach excludes the influence of differences the surface area-to-mass ratio on the absolute maximum rate of evaporative heat loss (Emax). We examined the best method for performing unbiased comparisons of ΔTcore between groups unmatched for body morphology during exercise in an uncompensable environment.