Vulnerability to heat was examined for populations of 6 major cities in South Korea (Seoul, Incheon, Daejeon, Gwangju, Daegu, and Busan). Daily excess mortality and maximum temperature from 1991 to 2005 were employed in this study. The results show that the standardized mortality increase associated with a $1^{\circ}C$ increase in daily maximum temperature above the city-specific threshold explains the heat acclimatization effect better than the threshold temperature itself. The estimated increase in mortality (standardized per 10 million population) associated with a $1^{\circ}C$ increase in temperature above the threshold is 4.8 in Incheon, 4.7 in Seoul, 4.3 in Daejeon, 2.8 in Gwangju, 2.4 in Daegu, and 1.5 in Busan, well reflecting the latitudinal locations and local climates of each city. Climate models project more frequent, more intense, and longer lasting heat waves in most land areas in both hemispheres in the 21st century under increasing greenhouse gas concentrations. In order to mitigate the adverse human health impacts due to excess heat, more detailed characteristics of acclimatization to heat need to be understood and quantified.
To determine the peripheral mechanisms involved in thermal sweating during the hot summers in July before acclimatization and after acclimatization in September, we evaluated the sweating response of healthy subjects (n=10) to acetylcholine (ACh), a primary neurotransmitter involved in peripheral sudomotor sensitivity. The quantitative sudomotor axon reflex test (QSART) measures sympathetic C fiber function after iontophoresed ACh evokes a measurable reliable sweat response. The QSART, at 2 mA for 5 min with 10% ACh, was applied to determine the directly activated (DIR) and axon reflex-mediated (AXR) sweating responses during ACh iontophoresis. The AXR sweat onset-time by the axon reflex was $1.50{\pm}0.32$ min and $1.84{\pm}0.46$ min before acclimatization in July and after acclimatization in September, respectively (p<0.01). The sweat volume of the AXR(l) [during 5 min 10% iontophoresis] by the axon reflex was $1.45{\pm}0.53\;mg/cm^2$ and $0.98{\pm}0.24\;mg/cm^2$ before acclimatization in July and after acclimatization in September, respectively (p<0.001). The sweat volume of the AXR(2) [during 5 min post-iontophoresis] by the axon reflex was $2.06{\pm}0.24\;mg/cm^2$ and $1.39{\pm}0.32\;mg/cm^2$ before and after acclimatization in July and September, respectively (p<0.001). The sweat volume of the DIR was $5.88{\pm}1.33\;mg/cm^2$ and $4.98{\pm}0.94\;mg/cm^2$ before and after acclimatization in July and September, respectively (p<0.01). These findings suggest that lower peripheral sudomotor responses of the ACh receptors are indicative of a blunted sympathetic nerve response to ACh during exposure to hot summer weather conditions.
Laying hens kept in different light and dark periods of the day at high ambient temperature of maximum $35^{\circ}C$ were challenged to $38.5{\pm}0.5^{\circ}C$ acute heat 3 hours daily for 7 consecutive days. They were found to have a significant (p<0.01) acclimatization response (rectal temperature) to heat stress during the dark period compared to those exposed to the same temperature during the light period. The blood pH was not significantly different. The partial pressure of carbon dioxide ($PCO_2$) was significantly high (p<0.01) except in day 4. Similarly the blood bicarbonate ($HCO_3$) concentration was significantly high (p<0.05) except day three and day four. Acute heat exposure in the first day increased the body temperature in both groups (Light and Dark) reaching $44^{\circ}C$, followed by gradual reduction in body temperature. The dark treated birds showed rapid reduction in body temperature ($42.88^{\circ}C$) and adaptation to high temperature during days 2-4 but that this was lost to some extent in days 6-8. However this was not obvious in the light treated birds. It is concluded that darkness reduce hyperthermia and enhance acclimatization responses during acute heat stress.
Journal of the Korean Society of Clothing and Textiles
/
v.21
no.4
/
pp.669-676
/
1997
The purpose of this study is to examine the effect of the improved cold tolerance resulting from cool clothing in winter on heat tolerance in summer. Ten healthy women were divided into two groups, cold group(C group) (n=5) and warm group(W group) (n=5) . In the previous study, C group was proved that their cold acclimatization was achieved through wearing cool clothing from September to February of the following year, while Wgroup was not proved because of wearing warm clothing during same period. After February, no more clothing training was continued in two groups. To determine the heat tolerance, both groups were exposed from a thermoneutral environment(25$\pm$1$^{\circ}C$, 50$\pm$5% R.H.) to a hot environment (35$\pm$1$^{\circ}C$, 50$\pm$5% R.H.) before and after clothing training, respectively September in 1994 and truly in 1995. Rectal temperature, skin temperatures, thermal sensation and comfort were measured every 10 min., and Os uptake was measured at 10, 45, 85 min. after entering the chamber for 5 min. Body weight was measured before and after the experiment and amount of local sweat was measured during the 90 min long experiment. The results are as follows: Rectal temperatures in 35'c environment of C group were increased after training when compared with before clothing, while those of W group were not changed. But the changes of rectal temperature and heat production during 90 min in hot environment were almost the same in two groups after training. And mean skin temperatures, the changes of mean skin temperatures during 90 min in hot environment, total sweat amount and local sweat amount after training were also the same in two groups. From these results, it might be supposed that the heat loss of two groups were the same but the heat production, especially heat production during rest in C group was higher than in Wgroup. This fact suggests that the increase of rest heat production from cold acclimatization in winter is maintained to summer of the following year. And mild cold acclimatization coming from westing cool clothing does not have a negative effect on heat tolerance.
Journal of the Korean Society of Clothing and Textiles
/
v.35
no.7
/
pp.713-720
/
2011
This study investigated the effect of cold acclimatization training on body composition including weight, fat mass, and muscle mass with 10 subjects (5 males and 5 females). During the 3-week acclimatization training program, they visited an artificial climate chamber ($15^{\circ}C$) 15 times and were exposed to cold environment with light clothing for 2 hours. Body composition was measured before and after cold training using bioelectric impedance analysis that was later compared by a paired t-test. In the process of thermoregulation, muscle contraction was accompanied by increased substrate metabolism for rising heat production. After cold training, the muscle mass increased and fat mass decreased significantly (p<.1, p<.05), subsequently the body composition changed. It was found that cold acclimatization training could be used as a treatment for obesity. It was suggested that further investigation on the long term effects of mild cold exposure using clothing and its potential applicability as an obesity treatment.
This experiment was conducted to evaluate the effect of feed withdrawal (F) and heat acclimatization (A) on malebroiler and -layer chickens responses to acute heat stress (AHS) at four weeks of age. Totals of ninety male chicks of broiler or layer type were randomly allocated into 30 pens of grower batteries with raised wire floors. Chicks were subjected to F and A three times a week through the first three weeks of age. At each time, feed withdrawal and heat acclimatization (T = $35^{\circ}C$) lasted for six and four hours, respectively. Feed consumption (FC), body weight (BW), and feed conversion ratio (FCR) were recorded weekly for broiler type chickens only. At four weeks of age, all groups of chickens were exposed to AHS (T = $39{\pm}1^{\circ}C$) for three hours. Before and after AHS challenge, body temperature (Tb), heterophil (H), and lymphocyte (L) counts were recorded, and H/L ratio was calculated. Antibody (Ab) response to sheep red blood cells (SRBC) was assessed from all treatments without being exposed to AHS. Group F of broiler-type chickens weighed less (p<0.05) compared to control group. Also, both A and F groups of broiler-type chickens consumed less (p<0.05) feed when compared to control group. Acute heat stress elevated Tb of all treatment groups, however the increase was more profound (p<0.001) in broiler chicks. Broiler chicks of both A and F groups showed a tendency to have higher (p = 0.08) Tb when compared to control group. Acute heat stress elevated (p<0.001) H/L ratio in both types of chickens. Broiler chicks maintained higher (p<0.001) H/L ratio. Both F and A groups reduced (p<0.01) the level of elevation in H/L ratio compared to control groups of both types of chickens. Neither A nor F group affected the Ab production in response to SRBC. However, there was a tendency towards higher Ab responses in F group when compared to other groups in both types of chickens. Results of the present study demonstrate that previous history of feed withdrawal or episodes of heat exposures improved chicks'physiological withstanding of AHS and a tendency to improved humoral immune response.
Journal of the Korean Society of Clothing and Textiles
/
v.21
no.3
/
pp.536-543
/
1997
The subjects wearing cool clothing (C group) or warm clothing (W stoup) in daily life from September to February of the following year were tested to examine whether cold acclimatization takes place by clothing habits. Subjects rested at 25$\pm$1$^{\circ}C$, then were exposed to 15$\pm$1$^{\circ}C$, 50$\pm$5% R.H. for 90 min in September, November, December, and February. Rectal temperature (Tre) of C group after 90 min cold exposure did not drop below the Tre in $25^{\circ}C$ throughout the study. W group's Tre, however, dropped below the temperature in 25t from December. Shivering stopped after December in C group while W group continued to show it for the whole study. In resting, C group showed higher heat production than W group in February, and the rate of increase in heat production during cold exposure was smaller in C group than W group in February. C group showed less cold sensation than W group in the same coldness. These results suggest that the level of cold acclimatization may be improved by the habits wearing less clothes in daily life.
Journal of the Korean Society of Clothing and Textiles
/
v.21
no.6
/
pp.1003-1009
/
1997
To study the time course of increased cold tolerance, the physiological responses were measured during the course of a 2-yr study (Feb. 1995~Feb. 1996) of four female college students, whose cold tolerance was proved to be increased through wearing cool clothing in daily life from Sep. 1994 to Feb. 1995. To determine their cold tolerance, subjects rested at 25$\pm$1$^{\circ}C$, then were exposed to 15$\pm$1$^{\circ}C$, 50$\pm$5% R.H. for 90min in Feb. 1995 and Feb. 1996. Subjects' rectal temperatures, mean skin temperatures, heat production, shivering onset, thermal sensations, and comfort showed no significant changes, when they were measured in 1995 and 1996. Based on these results, we can safely assume that mild cold acclimatization coming from wearing cool clothing lasts at least oneyear, that is until the following year. One of the possible explanations for this is that the subjects did not increase their clothing thermalresistances after the cold acclimatization.
Tropical inhabitants are able to tolerate heat through permanent residence in hot and often humid tropical climates. The goal of this study was to clarify the peripheral mechanisms involved in thermal sweating pre and post exposure (heat-acclimatization over 10 days) by studying the sweating responses to acetylcholine (ACh), a primary neurotransmitter of sudomotor activity, in healthy subjects (n=12). Ten percent ACh was administered on the inner forearm skin for iontophoresis. Quantitative sudomotor axon reflex testing, after iontophoresis (2 mA for 5 min) with ACH, was performed to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, as well as oral and skin temperature changes were measured. The post exposure activity had a short onset time (p<0.01), higher active sweat rate [(AXR (p<0.001) and DIR (p<0.001)], higher sweat output per gland (p<0.001) and higher transepidermal water loss (p<0.001) compared to the pre-exposure measurements. The activated sweat rate in the sudomotor activity increased the output for post-exposure compared to the pre-exposure measurements. The results suggested that post-exposure activity showed a higher active sweat gland output due to the combination of a higher AXR (DIR) sweat rate and a shorter onset time. Therefore, higher sudomotor responses to ACh receptors indicate accelerated sympathetic nerve responsiveness to ACh sensitivity by exposure to environmental conditions.
Background: Increases in the average global temperature cause heat stress-induced disorders by disrupting homeostasis. Excessive heat stress triggers an imbalance in the immune system; thus protection against heat stress is important to maintain immune homeostasis. Korean ginseng (Panax ginseng Meyer) has been used as a herbal medicine and displays beneficial biological properties. Methods: We investigated the protective effects of Korean ginseng extracts (KGEs) against heat stress in a rat model. Following acclimatization for 1 week, rats were housed at room temperature for 2 weeks and then exposed to heat stress ($40^{\circ}C$/2 h/day) for 4 weeks. Rats were treated with three KGEs from the beginning of the second week to the end of the experiment. Results: Heat stress dramatically increased secretion of inflammatory factors, and this was significantly reduced in the KGE-treated groups. Levels of inflammatory factors such as heat shock protein 70, interleukin 6, inducible nitric oxide synthase, and tumor necrosis factor-alpha were increased in the spleen and muscle upon heat stress. KGEs inhibited these increases by down-regulating heat shock protein 70 and the associated nuclear $factor-{\kappa}B$ and mitogen-activated protein kinase signaling pathways. Consequently, KGEs suppressed activation of T-cells and B-cells. Conclusion: KGEs suppress the immune response upon heat stress and decrease the production of inflammatory cytokines in muscle and spleen. We suggest that KGEs protect against heat stress by inhibiting inflammation and maintaining immune homeostasis.
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