Thermoregulatory responses during road races in hot-humid conditions at the 2019 Athletics World Championships.

The purpose of this study was to characterize thermoregulatory and performance responses of elite road-race athletes, while competing in hot, humid, night-time conditions during the 2019 IAAF World Athletic Championships. Male and female athletes, competing in the 20 km racewalk (n = 20 males, 24 females), 50 km racewalk (n = 19 males, 8 females), and marathon (n = 15 males, 22 females) participated. Exposed mean skin (Tsk) and continuous core body (Tc) temperature were recorded with infrared thermography and ingestible telemetry pill, respectively. The range of ambient conditions (recorded roadside) was 29.3°C-32.7°C air temperature, 46%-81% relative humidity, 0.1-1.7 m·s-1 air velocity, and 23.5°C-30.6°C wet bulb globe temperature. Tc increased by 1.5 ± 0.1°C but mean Tsk decreased by 1.5 ± 0.4°C over the duration of the races. Tsk and Tc changed most rapidly at the start of the races and then plateaued, with Tc showing a rapid increase again at the end, in a pattern mirroring pacing. Performance times were between 3% and 20% (mean = 113 ± 6%) longer during the championships compared with the personal best (PB) of athletes. Overall mean performance relative to PB was correlated with the wet-bulb globe temperature (WBGT) of each race (R2 = 0.89), but not with thermophysiological variables (R2 ≤ 0.3). As previously reported in exercise heat stress, in this field study Tc rose with exercise duration, whereas Tsk showed a decline. The latter contradicts the commonly recorded rise and plateau in laboratory studies at similar ambient temperatures but without realistic air movement.NEW & NOTEWORTHY This paper provides a kinetic observation of both core and skin temperatures in 108 elite athletes, during various outdoor competition events, adding to the very limited data so far available in the literature taken during elite competitions. The field skin temperature findings contrast previous laboratory findings, likely due to differences in relative air velocity and its impact on the evaporation of sweat. The rapid rise in skin temperature following cessation of exercise highlights the importance of infrared thermography measurements being taken during motion, not during breaks, when being used as a measurement of skin temperature during exercise.

Heat Adaptation and Nutrition Practices: Athlete and Practitioner Knowledge and Use.

PURPOSE: To survey elite athletes and practitioners to identify (1) knowledge and application of heat acclimation/acclimatization (HA) interventions, (2) barriers to HA application, and (3) nutritional practices supporting HA. METHODS: Elite athletes (n = 55) and practitioners (n = 99) completed an online survey. Mann-Whitney U tests (effect size [ES; r]) assessed differences between ROLE (athletes vs practitioners) and CLIMATE (hot vs temperate). Logistic regression and Pearson chi-square (ES Phi [ϕ]) assessed relationships. RESULTS: Practitioners were more likely to report measuring athletes' core temperature (training: practitioners 40% [athletes 15%]; P = .001, odds ratio = 4.0, 95% CI, 2%-9%; competition: practitioners 25% [athletes 9%]; P = .020, odds ratio = 3.4, 95% CI, 1%-10%). Practitioners (55% [15% athletes]) were more likely to perceive rectal as the gold standard core temperature measurement site (P = .013, ϕ = .49, medium ES). Temperate (57% [22% hot]) CLIMATE dwellers ranked active HA effectiveness higher (P < .001, r = .30, medium ES). Practitioners commonly identified athletes' preference (48%), accessibility, and cost (both 47%) as barriers to HA. Increasing carbohydrate intake when training in the heat was more likely recommended by practitioners (49%) than adopted by athletes (26%; P = .006, 95% CI, 0.1%-1%). Practitioners (56% [28% athletes]) were more likely to plan athletes' daily fluid strategies, adopting a preplanned approach (P = .001; 95% CI, 0.1%-1%). CONCLUSIONS: Practitioners, and to a greater extent athletes, lacked self-reported key HA knowledge (eg, core temperature assessment/monitoring methods) yet demonstrated comparatively more appropriate nutritional practices (eg, hydration).

Pharmacological hypotheses: Is acetaminophen selective in its cyclooxygenase inhibition?

The precise mechanistic action of acetaminophen (ACT; paracetamol) remains debated. ACT's analgesic and antipyretic actions are attributed to cyclooxygenase (COX) inhibition preventing prostaglandin (PG) synthesis. Two COX isoforms (COX1/2) share 60% sequence structure, yet their functions vary. COX variants have been sequenced among various mammalian species including humans. A COX1 splice variant (often termed COX3) is purported by some as the elusive target of ACT's mechanism of action. Yet a physiologically functional COX3 isoform has not been sequenced in humans, refuting these claims. ACT may selectively inhibit COX2, with evidence of a 4.4-fold greater COX2 inhibition than COX1. However, this is markedly lower than other available selective COX2 inhibitors (up to 433-fold) and tempered by proof of potent COX1 inhibition within intact cells when peroxide tone is low. COX isoform inhibition by ACT may depend on subtle in vivo physiological variations specific to ACT. In vivo ACT efficacy is reliant on intact cells and low peroxide tone while the arachidonic acid concentration state can dictate the COX isoform preferred for PG synthesis. ACT is an effective antipyretic (COX2 preference for PG synthesis) and can reduce afebrile core temperature (likely COX1 preference for PG synthesis). Thus, we suggest with specificity to human in vivo physiology that ACT: (i) does not act on a third COX isoform; (ii) is not selective in its COX inhibition; and (iii) inhibition of COX isoforms are determined by subtle and nuanced physiological variations. Robust research designs are required in humans to objectively confirm these hypotheses.

The influence of environmental and core temperature on cyclooxygenase and PGE2 in healthy humans.

Whether cyclooxygenase (COX)/prostaglandin E2 (PGE2) thermoregulatory pathways, observed in rodents, present in humans? Participants (n = 9) were exposed to three environments; cold (20 °C), thermoneutral (30 °C) and hot (40 °C) for 120 min. Core (Tc)/skin temperature and thermal perception were recorded every 15 min, with COX/PGE2 concentrations determined at baseline, 60 and 120 min. Linear mixed models identified differences between and within subjects/conditions. Random coefficient models determined relationships between Tc and COX/PGE2. Tc [mean (range)] increased in hot [+ 0.8 (0.4-1.2) °C; p < 0.0001; effect size (ES): 2.9], decreased in cold [- 0.5 (- 0.8 to - 0.2) °C; p < 0.0001; ES 2.6] and was unchanged in thermoneutral [+ 0.1 (- 0.2 to 0.4) °C; p = 0.3502]. A relationship between COX2/PGE2 in cold (p = 0.0012) and cold/thermoneutral [collapsed, condition and time (p = 0.0243)] was seen, with higher PGE2 associated with higher Tc. A within condition relationship between Tc/PGE2 was observed in thermoneutral (p = 0.0202) and cold/thermoneutral [collapsed, condition and time (p = 0.0079)] but not cold (p = 0.0631). The data suggests a thermogenic response of the COX/PGE2 pathway insufficient to defend Tc in cold. Further human in vivo research which manipulates COX/PGE2 bioavailability and participant acclimation/acclimatization are warranted to elucidate the influence of COX/PGE2 on Tc.

Long-Haul Northeast Travel Disrupts Sleep and Induces Perceived Fatigue in Endurance Athletes.

Introduction: Long-haul transmeridian travel is known to cause disruptions to sleep and immune status, which may increase the risk of illness. Aim: This study aimed to determine the effects of long-haul northeast travel for competition on sleep, illness and preparedness in endurance athletes. Methods: Twelve trained (13.8 ± 3.2 training h/week) masters (age: 48 ± 14 years) triathletes were monitored for sleep (quantity via actigraphy and quality via self-report), mucosal immunity (salivary immunoglobulin-A) and stress (salivary cortisol) as well as self-reported illness, fatigue, recovery and preparedness. Baseline measures were recorded for 2 weeks prior to travel for all variables except for the saliva samples, which were collected on three separate days upon waking. Participants completed normal training during the baseline period. Measures were subsequently recorded before, during and after long-haul northeast travel from the Australian winter to the Hawaiian summer, and in the lead up to an Ironman 70.3 triathlon. Results: All comparisons are to baseline. There was a most likely decrease in sleep duration on the over-night flight (-4.8 ± 1.2 h; effect size; ±90% confidence limits = 3.06; ±1.26) and a very likely increase in sleep duration on the first night after arrival (0.7 ± 1.0 h; 1.15; ±0.92). After this time, sleep duration returned to baseline for several days until it was very likely decreased on the night prior to competition (-1.2 ± 1.0 h; 1.18; ±0.93). Nap duration was likely increased on the first day after arrival (36 ± 65 min; 3.90; ±3.70). There was also a likely increase in self-reported fatigue upon waking after the first night in the new destination (1.1 ± 1.6 AU; 0.54; ±0.41) and there were three athletes (25%) who developed symptoms of illness 3-5 days after arrival. There were no changes in sleep quality or mucosal measures across study. Discussion: Long-haul northeast travel from a cool to a hot environment had substantial influences on sleep and self-reported fatigue, but these alterations had returned to pre-departure baseline 48 h after arrival. Endurance athletes undertaking similar journeys may benefit from optimizing sleep hygiene, especially on the first 2 days after arrival, or until sleep duration and fatigue levels return to normal.