Search

Background: Heat stress impacts are an escalating global health concern. Public health bodies such as the World Health Organization (WHO) warn that certain medications impair thermoregulation, with limited supporting evidence. Our aim was to investigate whether medications listed by the WHO increase core temperature responses during heat stress., Methods: For this systematic review and meta-analysis, MEDLINE, PubMed, Scopus, CINAHL, Web of Science, and EMBASE were searched up to Jan.30, 2024. Randomised studies exposing humans to exertional and/or passive heat stress that investigated a drug identified by WHO compared to no drug/placebo were eligible. The primary outcome was core temperature (e.g., rectal, oesophageal, aural, tympanic). We assessed risk of bias (Cochrane's Risk of Bias 2) and certainty of evidence (GRADE). The study was pre-registered on PROSPERO (CRD42020170684)., Findings: Thirty-five studies were included enrolling 353 individuals (16 women; 4.5%). Twenty-seven unique medications were tested. The average age of participants across studies was <30 years, and only one study included a clinical population. Under heat stress, there was moderate quality evidence that drugs with high anticholinergic properties increased core temperature at air temperatures ≥30°C (+0.42°C; 95% CI 0.04, 0.79°C; p = 0.03) alongside reduced sweating, although evidence is limited to the drug atropine. Similarly, non-selective beta-blockers (+0.11°C; 95% CI 0.02, 0.19°C; p = 0.02), adrenaline (+0.41°C; 95% CI 0.21, 0.61°C) and anti-Parkinson's agents (+0.13°C; 95% CI 0.07, 0.19°C; p = 0.02) elevated core temperature. Antidepressants, diuretics, or drugs with weak anticholinergic effects did not alter core temperature responses., Interpretation: Current evidence supports strong anticholinergics, non-selective beta-blockers, adrenaline, and anti-Parkinson's agents impairing thermoregulation during heat stress. No evidence indicated thermoregulation is impacted by other WHO-listed medications. Evidence is predominantly limited to healthy young men, with short heat stress exposures. Studies over longer durations, in women, older adults and those with chronic diseases are required to better inform the pharmaceutical management of patients during hot weather., Funding: This study was supported by a National Health and Medical Research Council (NHMRC) Investigator Grant (2021/GNT2009507; Holder: O. Jay)., Competing Interests: KLB reports grants from the NIH, Wellcome Trust, honoraria for keynote talks and travel support from the World Health Organization to attend meetings, conferences and give keynote talks. KLB is also the Chair of the US National Academy of Sciences Board on Environmental Change and Society. All of KLBs declarations are outside the scope of the submitted work. LK acknowledges funding from the National Institutes of Health (NIH; AG067471) outside of the submitted work. OJ acknowledges funding from the National Health and Medical Research Council (NHMRC 2021/GNT2009507) for the submitted work. OJ also reports grants from the Wellcome Trust and Resilience NSW, consulting fees from a National Institutes of Health grant, expert testimony for the National Rugby League, support for attending meetings and travel from the Global Heat and Health Information Network and Minderoo Foundation – all of which are outside the scope of the submitted work., (© 2024 The Author(s).)

To assess the impact of acute caffeine ingestion on thermoregulatory responses during steady-state exercise under moderate heat stress conditions in caffeine-habituated and nonhabituated individuals. Twenty-eight participants [14 habituated (HAB) (4 females) and 14 nonhabituated (NHAB) (6 females)] cycled at a fixed metabolic heat production (7 W·kg -1 ) for 60 min on two separate occasions 1 h after ingesting 1 ) 5 mg·kg -1 caffeine (CAF) or 2 ) 5 mg·kg -1 placebo (PLA), in a double-blinded, randomized, and counterbalanced order. Environmental conditions were 30.6 ± 0.9°C, 31 ± 1% relative humidity (RH). The end-exercise rise in esophageal temperature (ΔT es ) from baseline was greater with CAF in the HAB group (CAF = 0.88 ± 0.29°C, PLA = 0.62 ± 0.34°C, P < 0.001), but not in the NHAB group (CAF = 1.00 ± 0.42°C, PLA = 1.00 ± 0.39°C, P = 0.94). For a given change in mean body temperature, rises in % of maximum skin blood flow were attenuated with CAF on the forearm ( P = 0.015) and back ( P = 0.021) in the HAB group, but not in the NHAB group ( P ≥ 0.65). Dry heat loss was similar in the HAB (CAF = 31 ± 5 W·m -2 , PLA = 33 ± 7 W·m -2 ) and NHAB groups (CAF = 31 ± 3 W·m -2 , PLA 30 ± 4 W·m -2 ) ( P ≥ 0.37). There were no differences in whole body sweat losses in both groups (HAB: CAF = 0.59 ± 0.15 kg, PLA = 0.56 ± 0.17 kg, NHAB:CAF = 0.53 ± 0.19 kg, PLA 0.52 ± 0.19 kg) ( P ≥ 0.32). As the potential for both dry and evaporative heat loss was uninhibited by caffeine, we suggest that the observed ΔT es differences with CAF in the HAB group were due to alterations in internal heat distribution. Our findings support the common practice of participants abstaining from caffeine before participation in thermoregulatory research studies in compensable conditions. NEW & NOTEWORTHY We provide empirical evidence that acute caffeine ingestion exerts a thermoregulatory effect during exercise in the heat in caffeine-habituated individuals but not in nonhabituated individuals. Specifically, caffeine habituation was associated with a greater rise in esophageal temperature with caffeine compared with placebo, which appears to be driven by a blunted skin blood flow response. In contrast, no thermoregulatory differences were observed with caffeine in nonhabituated individuals. Caffeine did not affect sweating responses during exercise in the heat.

Objectives: To examine, 1) optimal structure of break periods to mitigate physiological heat strain during rugby league play (Stage 1); and ii) effectiveness of three different cooling strategies applied during breaks (Stage 2)., Design: Counter-balanced crossover design., Methods: In 37 °C, 50% RH, 11 males completed six simulated 80-min (two 40-min halves) rugby league matches on a treadmill with different break structures: regular game (RG) (12-min halftime), 1-min or 3-min "quarter-time" breaks halfway through each half with a 12-min halftime break (R1C and R3C), a 20-min halftime break (EH), or 1-min or 3-min quarter-time breaks with a 20-min halftime break (E1C and E3C) [Stage 1]. Nine participants completed Stage 2, which assessed the application of either ice towels (ICE), an electric fan (FAN) or a misting fan (MST) during breaks in the E3C protocol which, in Stage 1, prevailed as the optimal break structure., Results: Stage 1: Irrespective of quarter-time break duration, reductions in rectal temperature (-0.24 °C ± 0.24) and heart rate (-61 ± 10 bpm) during the halftime break were greater with a 20-min compared to a 12-min break (-0.08 ± 0.13 °C, p = 0.005; -55 ± -9 bpm, p = 0.021). Stage 2: End-game rises in rectal temperature were smaller (p < 0.006) in MST (1.41 ± 0.22 °C), FAN (1.55 ± 0.36 °C) and ICE (1.60 ± 0.21 °C) than in CON (1.80 ± 0.39 °C). The end-halftime heart rate was lower (p < 0.001) in ICE (89 ± 13 bpm), MST (90 ± 10 bpm) and FAN (92 ± 13 bpm) than in CON (99 ± 18 bpm)., Conclusions: Combining an extended halftime period and quarter-time breaks with MST application is the optimal cooling strategy for rugby league players in hot, humid conditions., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Current public health guidance designed to protect individuals against extreme heat and the ongoing COVID-19 pandemic is seemingly discordant, yet during the northern hemisphere summer, we are faced with the imminent threat of their simultaneous existence. Here we examine the environmental limits of electric fan-use in the context of the United States summer as a potential stay-at-home cooling strategy that aligns with existing efforts to mitigate the spread of SARS-COV-2., Competing Interests: Declaration of competing interest This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Purpose: It is often assumed that a person with a higher mean skin temperature (Tsk) will sweat more during exercise. However, it has not yet been demonstrated whether Tsk describes any individual variability in whole-body sweat rate (WBSR) independently of the evaporative requirement for heat balance (Ereq)., Methods: One hundred forty bouts of 2-h treadmill walking completed by a pool of 21 participants (23 ± 4 yr, 174 ± 8 cm, 76 ± 11 kg, 1.9 ± 0.2 m) under up to nine conditions were analyzed. Trials employed varying rates of metabolic heat production (Hprod; 197-813 W), and environmental conditions (15°C, 20°C, 25°C, 30°C; all 50% relative humidity), yielding a wide range of Ereq (86-684 W) and Tsk values (26.9°C-34.4°C)., Results: The individual variation observed in WBSR was best described using Ereq (in watts; R = 0.784) as a sole descriptor, relative to Ereq (in watts per meter squared; R = 0.735), Hprod (in watts; R = 0.639), Hprod (in watts per meter squared; R = 0.584), ambient air temperature (Ta) (R = 0.263), and Tsk (R = 0.077; all, P < 0.001). A multiple stepwise linear regression included only Ereq (in watts; adjusted R = 0.784), with Tsk not significantly correlating with the residual variance (P = 0.285), independently of Ereq (in watts). Hprod (in watts) had similar predictive strength to Ereq (in watts) at a fixed air temperature, explaining only 5.2% at 30°C, 4.9% at 25°C, 2.7% at 20°C, and 0.5% at 15°C (all, P < 0.001) less variance in WBSR compared with Ereq. However, when data from all ambient temperatures were pooled, Hprod alone was a markedly worse predictor of WBSR than Ereq (R = 0.639 vs 0.784; P < 0.001)., Conclusions: Ereq (in watts) explained approximately four-fifths of the individual variation in WBSR over a range of ambient temperatures and exercise intensities, whereas Tsk did not explain any residual variance independently of Ereq.