Hot ambient conditions and associated heat stress can increase mortality and morbidity, as well as increase adverse pregnancy outcomes and negatively affect mental health. High heat stress can also reduce physical work capacity and motor-cognitive performances, with consequences for productivity, and increase the risk of occupational health problems. Almost half of the global population and more than 1 billion workers are exposed to high heat episodes and about a third of all exposed workers have negative health effects. However, excess deaths and many heat-related health risks are preventable, with appropriate heat action plans involving behavioural strategies and biophysical solutions. Extreme heat events are becoming permanent features of summer seasons worldwide, causing many excess deaths. Heat-related morbidity and mortality are projected to increase further as climate change progresses, with greater risk associated with higher degrees of global warming. Particularly in tropical regions, increased warming might mean that physiological limits related to heat tolerance (survival) will be reached regularly and more often in coming decades. Climate change is interacting with other trends, such as population growth and ageing, urbanisation, and socioeconomic development, that can either exacerbate or ameliorate heat-related hazards. Urban temperatures are further enhanced by anthropogenic heat from vehicular transport and heat waste from buildings. Although there is some evidence of adaptation to increasing temperatures in high-income countries, projections of a hotter future suggest that without investment in research and risk management actions, heat-related morbidity and mortality are likely to increase.

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Purpose The present study investigated muscle metabolism and fatigue during simulated elite male ice hockey match-play. Methods Thirty U20 male national team players completed an experimental game comprising three periods of 8 × 1-min shifts separated by 2-min recovery intervals. Two vastus lateralis biopsies were obtained either during the game (n = 7) or pregame and postgame (n = 6). Venous blood samples were drawn pregame and at the end of the first and last periods (n = 14). Activity pattern and physiological responses were continuously monitored using local positioning system and heart rate recordings. Further, repeated-sprint ability was tested pregame and after each period. Results Total distance covered was 5980 ± 199 m with almost half the distance covered at high skating speeds (>17 km·h−1). Average and peak on-ice heart rate was 84% ± 2% and 97% ± 2% of maximum heart rate, respectively. Muscle lactate increased (P ≤ 0.05) more than fivefold and threefold, whereas muscle pH decreased (P ≤ 0.05) from 7.31 ± 0.04 pregame to 6.99 ± 0.07 and 7.13 ± 0.11 during the first and last periods, respectively. Muscle glycogen decreased by 53% postgame (P ≤ 0.05) with ~65% of fast- and slow-twitch fibers depleted of glycogen. Blood lactate increased sixfold (P ≤ 0.05), whereas plasma free fatty acid levels increased 1.5-fold and threefold (P ≤ 0.05) after the first and last periods. Repeated-sprint ability was impaired (~3%; P ≤ 0.05) postgame concomitant with a ~10% decrease in the number of accelerations and decelerations during the second and last periods (P ≤ 0.05). Conclusions Our findings demonstrate that a simulated ice hockey match-play scenario encompasses a high on-ice heart rate response and glycolytic loading resulting in a marked degradation of muscle glycogen, particularly in specific sub-groups of fibers. This may be of importance both for fatigue in the final stages of a game and for subsequent recovery.

This study assessed the accuracy of the technical absorbent (TA) method for measuring local sweat rate (LSR) relative to the well-established ventilated capsule (VC) method during steady-state and nonsteady-state sweating using large and small sample surface areas on the forearm and midback. Forty participants (38 males and two females) cycled at 60% peak oxygen consumption for 75 min in either a temperate [22.3 ± 0.9°C, 32 ± 17% relative humidity (RH)] or warm (32.5 ± 0.8°C, 29 ± 7% RH) environment. Simultaneous bilateral comparisons of 5-min LSR measurements using the TA and VC methods were performed for the back and forearm after 10, 30, 50, and 70 min. LSR values, measured using the TA method, were highly correlated with the VC method at all time points, irrespective of sample surface area and body region (all P < 0.001). On average, ≈ 79% of the variability observed in LSR measured with the VC method was described by the TA method. The mean difference in absolute LSR using the TA method (TA-VC with 95% confidence intervals) was -0.23 [-0.30,-0.16], -0.11 [-0.21,0.00], -0.03 [-0.14,+0.08], and +0.02 [-0.07,+0.11] mg · cm(-2) · min(-1) after 10, 30, 50, and 70 min of exercise, respectively. Duplicate LSR measurements within each method during steady-state sweating were highly correlated (TA: r = 0.96, P < 0.001, n = 20; VC: r = 0.97, P < 0.001, n = 20) with a mean bias of +0.07 ± 0.14 and +0.01 ± 0.10 mg · cm(-2) · min(-1) for TA and VC methods, respectively. The mean smallest detectable difference in LSR was 0.12 and 0.05 mg · min(-1) · cm(-2) for TA and VC methods, respectively. These data support the TA method as a reliable alternative for measuring the rate of sweat appearance on the skin surface.

Two studies were performed to 1) characterize changes in local sweat rate (LSR) following fluid ingestion of different temperatures during exercise, and 2) identify the potential location of thermoreceptors along the gastrointestinal tract that independently modify sudomotor activity. In study 1, 12 men cycled at 50% Vo2peak for 75 min while ingesting 3.2 ml/kg of 1.5°C, 37°C, or 50°C fluid 5 min before exercise; and after 15, 30, and 45-min of exercise. In study 2, 8 men cycled at 50% Vo2peak for 75 min while 3.2 ml/kg of 1.5°C or 50°C fluid was delivered directly into the stomach via a nasogastric tube (NG trials) or was mouth-swilled only (SW trials) after 15, 30, and 45 min of exercise. Rectal (Tre), aural canal (Tau), and mean skin temperature (Tsk); and LSR on the forehead, upper-back, and forearm were measured. In study 1, Tre, Tau, and Tsk were identical between trials, but after each ingestion, LSR was significantly suppressed at all sites with 1.5°C fluid and was elevated with 50°C fluid compared with 37°C fluid (P < 0.001). The peak difference in mean LSR between 1.5°C and 50°C fluid after ingestion was 0.29 ± 0.06 mg·min(-1)·cm(-2). In study 2, LSR was similar between 1.5°C and 50°C fluids with SW trials (P = 0.738), but lower at all sites with 1.5°C fluid in NG trials (P < 0.001) despite no concurrent differences in Tre, Tau, and Tsk. These data demonstrate that 1) LSR is transiently altered by cold and warm fluid ingestion despite similar core and skin temperatures; and 2) thermoreceptors that independently and acutely modulate sudomotor output during fluid ingestion probably reside within the abdominal area, but not the mouth.

Relative to 37 °C, ICE ingestion caused disproportionately greater reductions in Esk relative to Hfluid, resulting in a lower HLnet and greater S. Mechanistically, LSR and possibly SkBF were suppressed independently of Tre or Tsk, reaffirming the concept of human abdominal thermoreception. From a heat balance perspective, recommendations for ICE ingestion during exercise in warm, dry conditions should be reconsidered.

Heat acclimation is associated with plasma volume (PV) expansion that occurs within the first week of exposure. However, prolonged effects on hemoglobin mass (Hbmass) are unclear as intervention periods in previous studies have not allowed sufficient time for erythropoiesis to manifest. Therefore, Hbmass, intravascular volumes, and blood volume (BV)-regulating hormones were assessed with 5½ weeks of exercise-heat acclimation (HEAT) or matched training in cold conditions (CON) in 21 male cyclists [(mean ± SD) age: 38 ± 9 years, body weight: 80.4 ± 7.9 kg, VO2peak: 59.1 ± 5.2 ml/min/kg]. HEAT (n = 12) consisted of 1 h cycling at 60% VO2peak in 40°C for 5 days/week in addition to regular training, whereas CON (n = 9) trained exclusively in cold conditions (<15°C). Before and after the intervention, Hbmass and intravascular volumes were assessed by carbon monoxide rebreathing, while reticulocyte count and BV-regulating hormones were measured before, after 2 weeks and post intervention. Total training volume during the intervention was similar (p = 0.282) between HEAT (509 ± 173 min/week) and CON (576 ± 143 min/week). PV increased (p = 0.004) in both groups, by 303 ± 345 ml in HEAT and 188 ± 286 ml in CON. There was also a main effect of time (p = 0.038) for Hbmass with +34 ± 36 g in HEAT and +2 ± 33 g in CON and a tendency toward a higher increase in Hbmass in HEAT compared to CON (time × group interaction: p = 0.061). The Hbmass changes were weakly correlated to alterations in PV (r = 0.493, p = 0.023). Reticulocyte count and BV-regulating hormones remained unchanged for both groups. In conclusion, Hbmass was slightly increased following prolonged training in the heat and although the mechanistic link remains to be revealed, the increase could represent a compensatory response in erythropoiesis secondary to PV expansion.

Background: Within the context of the COVID-19 pandemic, the WHO endorses facemask use to limit aerosol-spreading of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, concerns have been raised regarding facemask-associated dyspnea, thermal distress and self-reported impairment of cognition. Accordingly, we tested how facemask-use affects motor-cognitive performances of relevance for occupational safety. We hypothesized that mask use would affect cognitively dominated performances and thermal discomfort, but not alter whole-body thermal balance. Methods: Eight participants completed a facemask and a barefaced (control) trial, in a counterbalanced order, in 40°C and 20% humidity conditions. Motor-cognitive performance, physiological (rectal, mean skin and local facial temperatures) and perceptual (thermal comfort and dyspnea) measures were assessed at baseline and following 45 min of light work (100 W). Results: Perceived dyspnea was aggravated with prolonged facemask use (p = 0.04), resulting in 36% greater breathlessness compared to control. However, no other differences were observed in motor-cognitive performance, physiological strain, or thermal discomfort. Conclusions: Contradicting negative self-reported impacts of facemask-use, only dyspnea was aggravated in the present study, thereby reinforcing global recommendations of mask use, even in hot environments. (Funded by: European Union's Horizon 2020 research and innovation program under the grant agreement No 668786).