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Abstract
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.
Highlights
IntroductionWith uncompromised thermoregulation (i.e. without illness or pharmacological compromise) the human body will initiate heat gain/loss mechanisms (including behavioural) in an orderly manner in response to differing environments[16]
With uncompromised thermoregulation the human body will initiate heat gain/loss mechanisms in an orderly manner in response to differing environments[16]
Similar acetaminophen [paracetamol (ACT) mediated Tc responses have been observed in humans when exposed to conditions below their TNZ [10 and 20 °C 40% relative humidity (RH)22,23], they were not supplemented by biochemical analysis of COX and prostaglandin E2 (PGE2), this pathways implication remains unclear in h umans[31]
Summary
With uncompromised thermoregulation (i.e. without illness or pharmacological compromise) the human body will initiate heat gain/loss mechanisms (including behavioural) in an orderly manner in response to differing environments[16]. Similar ACT mediated (dose: 20 mg kg−1 lean body mass−1) Tc responses have been observed in humans (reduced Tc by up to 0.57 °C; a response absent without ACT ingestion) when exposed to conditions below their TNZ [10 and 20 °C 40% relative humidity (RH)22,23], they were not supplemented by biochemical analysis of COX and PGE2, this pathways implication remains unclear in h umans[31]. This study will explore the COX/ PGE2 pathway (COX1, COX2 and PGE2 concentrations) in response to acute exposure to different environmental conditions (cold, hot and thermoneutral) that challenge or maintain Tc. deductive research designs have been called for[35] and are required to elucidate the influence of COX/PGE2 on human Tc regulation. Concentrations of COX and PGE2 will be implicated in Tc changes, : (iv) COX1 concentrations will decrease (i.e. catalyzed) in the cold environment (where Trec will be challenged yet defended and remain stable) and remain stable in the thermoneutral (where Trec will remain stable) and hot (where Trec will increase); (v) COX2 will remain stable across all conditions in the absence of a febrile stimulus; (vi) PGE2 concentration will increase in the cold but remain stable in the thermoneutral and hot environment
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