Cardiopulmonary values and organ blood flows before and during heat stress: data in nine subjects at rest in the upright position.

Physiological changes associated with thermoregulation can influence the kinetics of chemicals in the human body such as alveolar ventilation (VA) and redistribution of blood flow to organs. In this study, the influence of heat stress on various physiological parameters was evaluated in nine male volunteers during sessions of exposure to wet-bulb globe temperatures (WBGT) of 21, 25, and 30 °C for 4 h. Skin and core temperatures and more than 20 cardiopulmonary parameters were measured. Liver, kidneys, brain, skin, and muscles blood flows were also determined based on published measurements. Results show that most subjects (eight out of nine) have been affected by the inhalation of hot and dry air at the WBGT of 30 °C. High respiratory rates, superficial tidal volumes, and low VA values were notably observed. The skin blood flow increased by 2.16-fold, whereas the renal blood flow and liver blood flow decreased by about by 11% and 18%, respectively. A complete set of key cardiopulmonary parameters in healthy male adults before and during heat stress was generated for use in physiologically based pharmacokinetic modeling. A toxicokinetic studies are ongoing to evaluate the impact of heat stress on the absorption, biotransformation and excretion rates of volatile xenobiotics.

Involvement of endogenous central hydrogen sulfide (H2S) in hypoxia-induced hypothermia in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) display autonomic imbalance and abnormal body temperature (Tb) adjustments. Hydrogen sulfide (H2S) modulates hypoxia-induced hypothermia, but its role in SHR thermoregulation is unknown. We tested the hypothesis that SHR display peculiar thermoregulatory response to hypoxia and that endogenous H2S overproduced in the caudal nucleus of the solitary tract (NTS) of SHR modulates this response. SHR and Wistar rats were microinjected into the fourth ventricle with aminooxyacetate (AOA, H2S-synthezing enzyme inhibitor) or sodium sulfide (Na2S, H2S donor) and exposed to normoxia (21% inspired O2) or hypoxia (10% inspired O2, 30 min). Tb was continuously measured, and H2S production rate was assessed in caudal NTS homogenates. In both groups, AOA, Na2S, or saline (i.e., control; 1 µL) did not affect euthermia. Hypoxia caused similar decreases in Tb in both groups. AOA presented a longer latency to potentiate hypoxic hypothermia in SHR. Caudal NTS H2S production rate was higher in SHR. We suggest that increased bioavailability of H2S in the caudal NTS of SHR enables the adequate modulation of excitability of peripheral chemoreceptor-activated NTS neurons that ultimately induce suppression of brown adipose tissue thermogenesis, thus accounting for the normal hypoxic hypothermia.

Effect of food intake on the ventilatory response to increasing core temperature during exercise.

Food intake increases metabolism and body temperature, which may in turn influence ventilatory responses. Our aim was to assess the effect of food intake on ventilatory sensitivity to rising core temperature during exercise. Nine healthy male subjects exercised on a cycle ergometer at 50% of peak oxygen uptake in sessions with and without prior food intake. Ventilatory sensitivity to rising core temperature was defined by the slopes of regression lines relating ventilatory parameters to core temperature. Mean skin temperature, mean body temperature (calculated from esophageal temperature and mean skin temperature), oxygen uptake, carbon dioxide elimination, minute ventilation, alveolar ventilation, and tidal volume (VT) were all significantly higher at baseline in sessions with food intake than without food intake. During exercise, esophageal temperature, mean skin temperature, mean body temperature, carbon dioxide elimination, and end-tidal CO2 pressure were all significantly higher in sessions with food intake than without it. By contrast, ventilatory parameters did not differ between sessions with and without food intake, with the exception of VT during the first 5 min of exercise. The ventilatory sensitivities to rising core temperature also did not differ, with the exception of an early transient effect on VT. Food intake increases body temperature before and during exercise. Other than during the first 5 min of exercise, food intake does not affect ventilatory parameters during exercise, despite elevation of both body temperature and metabolism. Thus, with the exception of an early transient effect on VT, ventilatory sensitivity to rising core temperature is not affected by food intake.

On the use of wearable physiological monitors to assess heat strain during occupational heat stress.

Workers in many industries are required to perform arduous work in high heat-stress conditions, which can lead to rapid increases in body temperature that elevate the risk of heat-related illness and even death. Traditionally, effort to mitigate work-related heat injury has been directed toward the assessment of environmental heat stress (e.g., wet-bulb globe temperature), rather than toward the associated physiological strain responses (e.g., heart rate and skin and core temperatures). However, because a worker's physiological response to a given heat stress is modified independently by inter-individual factors (e.g., age, sex, chronic disease, others) and intra-individual factors both within (e.g., medication use, fitness, acclimation and hydration state, others) and beyond (e.g., shift duration, illness, others) the worker's control, it becomes challenging to protect workers on an individual basis from heat-related injury without assessing those physiological responses. Recent advancements in wearable technology have made it possible to monitor one or more physiological indices of heat strain. Nonetheless, information on the utility of the wearable systems available for assessing occupational heat strain is unavailable. This communication is therefore directed toward identifying the physiological indices of heat strain that may be quantified in the workplace and evaluating the wearable monitoring systems available for assessing those responses. Finally, emphasis is placed on the barriers associated with implementing these devices to assist in mitigating work-related heat injury. This information is fundamental for protecting worker health and could also be utilized to prevent heat illnesses in vulnerable people during leisure or athletic activities.

Local versus whole-body sweating adaptations following 14 days of traditional heat acclimation.

The purpose of this study was to examine if local changes in sweat rate following 14 days of heat acclimation reflect those that occur at the whole-body level. Both prior to and following a 14-day traditional heat acclimation protocol, 10 males exercised in the heat (35 °C, ∼20% relative humidity) at increasing rates of heat production equal to 300 (Ex1), 350 (Ex2), and 400 (Ex3) W·m(-2). A 10-min recovery period followed Ex1, while a 20-min recovery period separated Ex2 and Ex3. The exercise protocol was performed in a direct calorimeter to measure whole-body sweat rate and, on a separate day, in a thermal chamber to measure local sweat rate (LSR), sweat gland activation (SGA), and sweat gland output (SGO) on the upper back, chest, and mid-anterior forearm. Post-acclimation, whole-body sweat rate was greater during each exercise bout (Ex1: 14.3 ± 0.9; Ex2: 17.3 ± 1.2; Ex3: 19.4 ± 1.3 g·min(-1), all p ≤ 0.05) relative to pre-acclimation (Ex1: 13.1 ± 0.6; Ex2: 15.4 ± 0.8; Ex3: 16.5 ± 1.3 g·min(-1)). In contrast, only LSR on the forearm increased with acclimation, and this increase was only observed during Ex2 (Post: 1.32 ± 0.33 vs. Pre: 1.06 ± 0.22 mg·min(-1)·cm(-2), p = 0.03) and Ex3 (Post: 1.47 ± 0.41 vs. Pre: 1.17 ± 0.23 mg·min(-1)·cm(-2), p = 0.05). The greater forearm LSR post-acclimation was due to an increase in SGO, as no changes in SGA were observed. Overall, these data demonstrate marked regional variability in the effect of heat acclimation on LSR, such that not all local measurements of sweat rate reflect the improvements observed at the whole-body level.

Effect of postprandial thermogenesis on the cutaneous vasodilatory response during exercise.

To examine the effect of postprandial thermogenesis on the cutaneous vasodilatory response, 10 healthy male subjects exercised for 30 min on a cycle ergometer at 50% of peak oxygen uptake, with and without food intake. Mean skin temperature, mean body temperature (Tb), heart rate, oxygen uptake, carbon dioxide elimination, and respiratory quotient were all significantly higher at baseline in the session with food intake than in the session without food intake. To evaluate the cutaneous vasodilatory response, relative laser Doppler flowmetry values were plotted against esophageal temperature (Tes) and Tb. Regression analysis revealed that the [Formula: see text] threshold for cutaneous vasodilation tended to be higher with food intake than without it, but there were no significant differences in the sensitivity. To clarify the effect of postprandial thermogenesis on the threshold for cutaneous vasodilation, the between-session difference in the Tes threshold and the Tb threshold were plotted against the between-session difference in baseline Tes and baseline Tb, respectively. Linear regression analysis of the resultant plot showed significant positive linear relationships (Tes: r = 0.85, P < 0.01; Tb: r = 0.67, P < 0.05). These results suggest that postprandial thermogenesis increases baseline body temperature, which raises the body temperature threshold for cutaneous vasodilation during exercise.