Effect Of Acute Heat Exposure Research Articles

Effect of acute heat exposure on the determination of critical power and W′ in women and men

ABSTRACT The goal of this study was to investigate to what extent acute heat exposure would affect the parameters of the power-duration relationship, i.e. CP and W′, using multiple constant workload tests to task failure, in women and men. Twenty four young physically active participants (12 men, 12 women) performed 3-5 constant load tests to determine CP and W′, both in temperate (TEMP; 18°C) and hot (HOT; 36°C) environmental conditions. A repeated-measures ANOVA was executed to find differences between TEMP and HOT, and between women and men. In HOT, CP was reduced by 6.5% (227 ± 50 vs. 212 ± 47 W), while W′ increased 12.4% (16.4 ± 4.4 vs. 18.5 ± 5.6 kJ). No significant two-way sex × temperature interactions were observed, indicating that the environmental conditions did not have a different effect in men compared with women. The intersection of the average curvatures in TEMP and HOT occurred at 137 s and 280 W in women, and 153 s and 397 W in men. Acute heat exposure had an impact on the parameters CP and W′, i.e. CP decreased whereas W′ increased. The increase in W′ might be a consequence of the mathematical modelling for the used test methodology, rather than a physiological accurate value of W′ in HOT. No differences induced by heat exposure were observed between women and men.

Effect of acute heat exposure on the pressor response to a voluntary hypoxic apnea.

The pressor response induced by a voluntary hypoxic apnea is mediated largely by increased sympathetic outflow. The neural control of blood pressure is altered in recovery from acute heat exposure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Therefore, we tested the hypothesis that prior heat exposure would attenuate the pressor response induced by a voluntary hypoxic apnea. Eleven healthy adults (five women) were exposed to whole body passive heating (water-perfused suit) sufficient to increase body core temperature by 1.2°C. Voluntary hypoxic apneas were performed at baseline and in recovery when body core temperature returned to ≤ 0.3°C of baseline. Participants breathed gas mixtures of varying [Formula: see text] (21%, 16%, and 12%; randomized) for 1 min followed by a 15-s end-expiratory apnea. The change in arterial oxygen saturation during each apnea did not differ from baseline to recovery (P = 0.6 for interaction), whereas the pressor response induced by a voluntary hypoxia apnea was reduced ([Formula: see text] 21%, baseline 17 ± 7 mmHg vs. recovery 14 ± 7 mmHg; [Formula: see text] 16%, baseline 24 ± 8 mmHg vs. recovery 18 ± 7 mmHg; [Formula: see text] 12%, baseline 28 ± 11 mmHg vs. recovery 24 ± 11 mmHg; P = 0.01 for main effect of time). These data suggest that prior heat exposure induces a cross-stressor effect such that the pressor response to a voluntary hypoxic apnea is attenuated.NEW & NOTEWORTHY The pressor response induced by a voluntary hypoxic apnea is mediated by increased sympathetic outflow. The neural control of blood pressure is altered in recovery from acute heat exposure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Our data suggest that prior heat exposure induces a cross-stressor effect such that the pressor response to a voluntary hypoxic apnea is attenuated.

The effect of acute heat exposure on the determination of exercise thresholds from ramp and step incremental exercise.

The aim of this study was to examine how respiratory (RT) and lactate thresholds (LT) are affected by acute heat exposure in the two most commonly used incremental exercise test protocols (RAMP and STEP) for functional evaluation of aerobic fitness, exercise prescription and monitoring training intensities. Eleven physically active male participants performed four incremental exercise tests, two RAMP (30W·min-1) and two STEP (40W·3min-1), both in 18°C (TEMP) and 36°C (HOT) with 40% relative humidity to determine 2 RT and 16 LT, respectively. Distinction was made within LT, taking into account the individual lactate kinetics (LTIND) and fixed value lactate concentrations (LTFIX). A decrease in mean power output (PO) was observed in HOT at LT (-6.2 ± 1.9%), more specific LTIND (-5.4 ± 1.4%) and LTFIX (-7.5 ± 2.4%), compared to TEMP, however not at RT (-1.0 ± 2.7%). The individual PO difference in HOT compared to TEMP over all threshold methods ranged from -53W to +26W. Mean heart rate (HR) did not differ in LT, while it was increased at RT in HOT (+10 ± 8bpm). This study showed that exercise thresholds were affected when ambient air temperature was increased. However, a considerable degree of variability in the sensitivity of the different threshold concepts to acute heat exposure was found and a large individual variation was noticed. Test design and procedures should be taken into account when interpreting exercise test outcomes.

Effects of acute heat exposure on oxidative stress and antioxidant defenses in overwintering frogs, Nanorana parkeri

Climate warming is intensifying on the Tibetan Plateau and poses a serious threat to amphibians that live there. Although hibernation physiology and ecology of Nanorana parkeri, a frog species native to the Tibetan plateau, has been well studied, little information is available about the physiological and biochemical responses to acute rising temperature. Here, we conducted an acute warming experiment comparing hibernating N. parkeri (acclimated at 4 °C) and frogs acutely warmed to 10 °C for 12 h, comparing indicators of oxidative stress and antioxidant defense between the two groups. Acute warming led to a significant increase in the content of oxidized glutathione and the ratio of oxidized:reduced glutathione in liver and muscle, indicating that rapid warming causing oxidative stress could be a negative factor for frogs inhabiting the Tibetan plateau. Malondialdehyde content increased by 57% only in muscle but decreased significantly in three tissues. Protein carbonyl groups rose by 15% in brain, 28% in liver, and 21% in muscle after heat exposure but vitamin C content in heart decreased by 44%. Acute heat exposure also induced tissue-specific upregulation of antioxidant enzyme activities. Catalase activity increased by 27% in heat-exposed frogs, as compared to controls, and glutathione peroxidase activity rose by 12% in brain, 30% in liver, and 12% in muscle. Glutathione-S-transferase activity was also enhanced in heart and muscle of heat-exposed frogs. Acute warming also resulted in a rise in total antioxidant capacity in all tissues examined except kidney, relative to controls. In summary, our findings show that acute heat exposure to hibernating N. parkeri causes a tissue-specific increase in oxidative damage and antioxidant defenses, with skeletal muscle being the most affected tissue. These results reveal the physiological responses to acute temperature change in overwintering N. parkeri.

Effect of Acute Heat Exposure on the Pressor Response to a Voluntary Hypoxic Apnea: A Cross‐Tolerance Study

The pressor response induced by a voluntary hypoxic apnea is exaggerated in individuals with obstructive sleep apnea and is strongly correlated to sympathetic overactivity. Acute heat exposure alters neural control of blood pressure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Therefore, we tested the hypothesis that acute heat exposure would attenuate the pressor response to a voluntary hypoxic apnea, and thereby manifest as a form of physiological cross‐tolerance. Six young adults (2 females, 25 ± 1 yrs) were exposed to passive heat stress (water‐perfused suit) sufficient to increase body core temperature by 1.2 °C. Voluntary hypoxic apneas were performed in duplicate before acute heat exposure (pre‐heat) and in recovery when body core temperature returned to ≤ 0.3 °C of baseline. Participants breathed gas mixtures of varying FiO2 (21%, 16%, and 12%; randomized) for 1 min followed immediately by a 15 s end‐expiratory apnea. Beat‐by‐beat arterial blood pressure (Finometer) and arterial oxygen saturation (finger pulse oximetry) were measured throughout. The pressor response was calculated as the difference between baseline mean arterial pressure and the peak response following each apnea. The change in arterial oxygen saturation during each apnea did not differ from pre‐heat to recovery (FiO2 21%: pre‐heat, Δ0 ± 1 % vs. recovery, Δ1 ± 2 %; FiO2 16%: pre‐heat, Δ‐4 ± 1 % vs. recovery, Δ‐3 ± 1 %; FiO2 12%: pre‐heat, Δ‐9 ± 3 % vs. recovery, Δ‐10 ± 4 %; P = 0.6 for interaction). The pressor response to a voluntary apnea was attenuated in recovery from acute heat exposure across all gas mixtures (FiO2 21%: pre‐heat, Δ14 ± 11 mmHg vs. recovery, Δ10 ± 7 mmHg; FiO2 16%: pre‐heat, Δ22 ± 15 mmHg vs. recovery, Δ15 ± 11 mmHg; FiO2 12%: pre‐heat, Δ28 ± 15 mmHg vs. recovery, Δ21 ± 16 mmHg; P < 0.01 for main effect of time). These data suggest that acute heat exposure induces a cross‐tolerance effect such that the pressor response to a voluntary hypoxic apnea is reduced. Acute heat exposure could improve hypertension in adults with obstructive sleep apnea, secondary to altered chemoreflex function and sympathetic neural control, and provide additional therapeutic options for this population to improve cardiovascular health.

The effect of acute heat exposure on rat pituitary corticotroph activation: the role of vasopressin.

The increased ambient temperature affects the function of hypothalamic-pituitary-adrenal (HPA) axis. Since the correlation among vasopressin (VP), adrenocorticotropic hormone (ACTH) and corticosterone (CORT) responses to various stressors have been long recognized, the aim of this study was to reveal the aforementioned hormones production and morphology of the pituitary gland after exposure to acute heat. Rats were exposed to high ambient temperature (38 °C) for 20 or 60 minutes. The circulating hormones were determined by an ELISA test or chemiluminescence's method. The results obtained show the elevation in ACTH and CORT secretion depending on the duration of heat exposure. The VP concentration increased only after prolonged exposure to heat (60 min). The pituitary morphology was examined by routine and fluorescent immunohistochemistry as well as electron microscopy. Observed changes in the anterior and posterior pituitary well corresponded to circulating hormones, regarding the volume density of ACTH-immunopositive cells, percentage of ACTH immunopositive area v. total area and number of VP-immunopositive containing varicose fibers per total area. Acute heat exposure also induced changes in shapes of ACTH-immunopositive cells. Cells appeared stellate with numerous slender cytoplasmic processes and degranulated, which is the most obvious after 20 min. In addition, immunopositivity of endothelial and anterior pituitary cells for VP suggests its influence on ACTH secretion.

Effects of acute heat exposure on prosencephalic c-Fos expression in normohydrated, water-deprived and salt-loaded rats

In the present study, the distribution pattern of c-Fos protein immunoreactivity (Fos-IR) in prosencephalic areas of the brain involved in thermoregulatory and osmoregulatory responses was investigated, in rats exposed or not exposed to a hyperthermic environment, under three different conditions: normohydration, dehydration induced by water deprivation and hyperosmolarity induced by an acute intragastric salt load. Normohydrated, water-deprived or salt-loaded male Wistar rats (270 ± 30 g) were submitted or not to acute heat exposure (33 °C for 45 min). A separate group of animals was submitted to the same experimental protocol and had blood samples collected before and after the heating period to measure serum osmolarity and sodium. The brains were processed for c-Fos immunohistochemistry using the avidin–biotin peroxidase method. After analyzing Fos-IR in the brains of animals in the present study, three different types of prosencephalic areas were identified: (1) those that respond to hydrational and to heat conditions, with an interaction between these two factors (PaMP and SON); (2) those that respond to hydrational and to heat conditions, but with no interaction between these factors (MnPO, LSV and OVLT); and (3) those that respond only to hydrational status (SFO and PaLM).

Acute heat exposure increases high-intensity performance during sprint cycle exercise

The purpose of this study was to investigate the effects of acute heat exposure at thermal balance on high-intensity performance during sprint cycle exercise. Nine healthy male subjects were tested in three different, well-controlled environments in an environmental chamber: T (22 degrees C, 65% RH), H1 (30 degrees C, 55% RH) and H2 (35 degrees C, 62% RH), each test being carried out on a different day following a randomized sequence. After 30 min of exposure to the set environment, subjects performed the 30-s sprint cycle exercise. Heart rate, rectal and skin temperatures were measured prior to exercise, at rest, before and after environmental exposure, and after exercise. There were no differences in subjects' core temperature or heart rate prior to exercise. However, skin temperature was significantly higher in hot trials compared with the control throughout the experimental session (P < 0.05). Peak power was significantly higher in the hot environments compared with the control. Mean power was higher only in H2 compared with T (P < 0.05). This difference in power output was the consequence of a faster pedaling cadence in the hot trials (P < 0.05). Plasma ammonia was higher in the hot trials versus control at 4 min post-sprint. No differences in blood lactate levels at 3 min post-sprint were observed between tests. The results of this study suggest that the exposure to hot environment caused an improvement in power output for a single 30-s sprint. This increase in power output was associated with an elevation in plasma ammonia suggestive of an increase in adenine nucleotide loss.

The Effects of Acute Heat Exposure on Muscular Strength, Muscular Endurance, and Muscular Power in the Euhydrated Athlete

The Effects of Acute Heat Exposure on Muscular Strength, Muscular Endurance, and Muscular Power in the Euhydrated Athlete

The Effects of Acute Heat Exposure on Muscular Strength, Muscular Endurance, and Muscular Power in the Euhydrated Athlete

The purpose of this study was to determine the effects of acute heat exposure upon muscular strength, muscular endurance, and muscular power in euhydrated athletes. Ten healthy, weight-trained men (average age = 23.0 +/- 4.0 years) volunteered for this investigation. Subjects were randomized to normothermic (22.5 degrees C, 65% relative humidity [RH]) or hyperthermic (65-75 degrees C, 15% RH) condition for 30 minutes. Results indicated that all subjects experienced significant (p < 0.05) hemodynamic stress because of the 30 minutes of heat exposure (blood pressure [BP](rest) 124/78 mm Hg to BP(postsauna) 148/60 mm Hg, heart rate [HR](rest) 64 b.min(-1) to HR(postsauna) 122 b.min(-1)). Oral and tympanic temperature measurements correlated strongly (r(2) = 0.904) and increased by 2.48 and 2.71 degrees C, respectively, during sauna exposure. One repetition maximum (1RM) bench press strength did not differ between the 2 conditions, whereas 1RM leg press strength was significantly decreased (p < 0.05) after the hyperthermic protocol. Subjects' muscular endurance decreased significantly (p < 0.05) in both the leg press (29.2%) and bench press (15.8%) after the sauna exposure. In contrast, muscular power (vertical jump) increased significantly (3.1%, p < 0.5) after acute heat exposure. In agreement with previous studies, we concluded that acute heat exposure is detrimental to muscular endurance; however, the areas of strength and power are far less unequivocal.

Effect of acute heat exposure on blood flow and its distribution in the unrestrained laying fowl (Gallus domesticus)

Abstract 1. The effect of heat exposure (air temperature 35–45°C) for 1.5 h on blood flow distribution between the abdominal viscera and the muscles of abdominal wall and hind leg was investigated in unanaesthetised, unrestrained laying fowl. 2. Heat stressed fowl showed a significant hyperthermia (+ 1.3°C), rapid shallow breathing (229 breaths/min) and significant hypocapnia ( − 8 Torr). 3. Significant increases in absolute blood flow (ml/g per min) were measured in the kidneys, spleen, liver and duodenum during hyperthermia, but there was no change in the absolute blood flow to the reproductive tract or the relative perfusion of the reproductive tract compared with the other tissues sampled. 4. We conclude that in these acute conditions of heat exposure, blood flow to the reproductive tract of the laying fowl is not compromised by any simultaneous thermoregulatory needs.

Effect of acute heat exposure on triglyceride transfer to the preovulatory follicles of the laying fowl (Gallus Domesticus)

1. The effect of acute heat exposure on triglyceride (TG) transfer to preovulatory follicles was studied in the laying fowl. 2. Heat exposure of laying fowl resulted in a 1.1 degree C rise in body temperature, a 10-fold increase in respiration frequency and mild hypocapnia and hypoxaemia. 3. Plasma and follicular tissue TG concentrations were not significantly affected by heat exposure, but plasma TG specific radioactivity decreased significantly and was negatively correlated with body temperature. 4. The transfer rate of TG to the preovulatory follicles was not affected significantly by hyperthermia. 5. We conclude that nutrient supply to the developing follicles is not compromised in acutely heat-exposed laying fowl.

Effects of acute heat exposure on respiratory metabolism and blood glucose in freshwater fishes, Prochilodus scrofa (curimbatá) and Cyprinus carpio (carp) acclimatized to tropical winter

1. 1. Routine oxygen consumption and blood glucose were determined from freshwater fishes, Prochilodus scrofa and Cyprinus carpio, exposed at high temperatures for 1 hr. 2. 2. Prochilodus scrofa had a significantly higher rate of oxygen consumption at 30°C than at 25°C, and carp higher at 25°C than at 30°C. 3. 3. Blood glucose was significantly higher for Cyprinus carpio than for Prochilodus scrofa at 25 and 30°C; however, after exposure to these temperatures for 1 hr blood glucose did not change significantly for both species. 4. 4. The results suggest that these interspecific variations may be linked to the differences between native and foreign fishes and their way of life.