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Aging and heat tolerance at rest or during work.

Collectively, the literature on heat tolerance suggests that middle-aged (45-64 year old) men and women are more work-heat intolerant, and suffer more physiological strain during heat acclimation, than do younger individuals. However, it is unclear whether the age differences in work-heat intolerance and physiological strain during heat acclimation are related to age per se or associated with other factors such as certain disease states, decreased physical activity, and/or lowered aerobic fitness. In contrast, the work-heat tolerance and physiological responses during heat acclimation of habitually active or aerobically trained middle-aged men are the same or better than younger individuals. The reviewed studies emphasize the importance of aerobic fitness and pertinent morphological factors, such as body fat, body weight, and surface area in maintaining work-heat tolerance with aging. Recent studies suggest that middle-aged and older men and women may be more susceptible to greater heat strain at physiologically significant levels of dehydration than those younger. However, additional research appears necessary to support this hypothesis. When the effects of chronic debilitating diseases in the elderly (greater than 64 years old) are minimized, their heat tolerance and thermoregulatory responses are comparable to those younger. In fact, healthy and well-acclimated elderly men and women appear to perform as well as those younger during desert walks in dry heat. This review shall discuss experimental observations from previously published studies concerning aging and heat tolerance or the physiological heat strain during heat acclimation at rest or during work; and, will suggest future research efforts needed to advance the area.

Acclimatization↗

Effect of changes in dietary energy intake and environmental temperature on heat tolerance in the fowl.

The improvement in heat tolerance acquired during the acclimatization of laying hens to intermittent heat stress was lost or considerably reduced when energy intake increased following the addition of maize oil to the diet. The oxygen consumption (VO2) of acclimatised hens increased after the addition of maize oil to the diet. Reducing the environmental temperature (Ta) from 30 degrees to 10 degrees C prevented the development of acclimatization if the heat stress commenced soon after the change of Ta; if the heat stress commenced 5 weeks after the change of Ta acclimatization took place normally. Reducing the Ta from 30 degrees to 10 degrees C resulted in an increased VO2 and food intake. The administration of triiodothyronine increased VO2 and reduced the heat tolerance of acclimatised hens. It is concluded that heat tolerance, despite being reinforced by regular exposure to heat stress, remains susceptible to changes in energy metabolism brought about by dietary or environmental means.

Acclimatization↗

A role for gastrointestinal endotoxins in enhancement of heat tolerance by physical fitness.

To further elucidate mechanisms underlying the higher heat tolerance of physically fit compared with sedentary people, we have investigated the possibility that endotoxins (of gastrointestinal origin) act, as in the normal development of fever, to raise body temperature and therefore reduce heat tolerance. In an initial series of experiments, five physically fit and four sedentary sheep were exposed twice at rest to an environment of 42/35 degrees C (dry/wet bulb temperature). When animals were given normal saline i.v., rectal temperature (Tre) rose at a significantly higher rate in sedentary than in fit animals; this confirms that heat tolerance is improved by physical fitness. Treatment with i.v. indomethacin did not affect the rate of rise of Tre in fit animals. In sedentary animals, however, Tre was lowered to approximate that of fit animals. Because indomethacin blocks prostaglandin pathways involved in endotoxin-induced fever, the indomethacin-induced improvement of heat tolerance of sedentary but not fit animals supports the contention that endotoxins play a role in determining that difference in heat tolerance. In a second series of experiments, quantitative cardiovascular measurements were made by using radioactive microspheres. Under normothermic conditions, blood flows in the brain, ileum, and diaphragm were higher in fit than in sedentary animals. During hyperthermia up to Tre of 42 degrees C (in a 42/39 degrees C environment), fit compared with sedentary animals exhibited 1) a greater increase in cardiac output, 2) an increase in blood flow through arteriovenous anastomoses to higher and better maintained levels, 3) less reduction in blood flow to the ileum, and 4) greater increase in blood flows to the myocardium, turbinates, nasal mucosa, and respiratory muscles. Endotoxins are likely to come from the gut lumen, because reduction of gut blood flow forms part of the normal response to heat stress. We suggest that improvement of heat tolerance by physical fitness is caused by a greater cardiovascular capacity that permits not only greater perfusion of heat-loss tissues but the maintenance of a better gastrointestinal tract blood supply, thereby better maintaining the normal barrier to movement of endotoxins from gut lumen to plasma. Sedentary people, with their lower cardiovascular capacity, redistribute more blood flow away from the gut during environmentally induced hyperthermia, thus allowing endotoxin-induced fever to aggravate hyperthermia.

Animals↗

Habituation of Salmonella spp. at reduced water activity and its effect on heat tolerance.

The effect of habituation at reduced water activity (a(w)) on heat tolerance of Salmonella spp. was investigated. Stationary-phase cells were exposed to a(w) 0.95 in broths containing glucose-fructose, sodium chloride, or glycerol at 21 degrees C for up to a week prior to heat challenge at 54 degrees C. In addition, the effects of different a(w)s and heat challenge temperatures were investigated. Habituation at a(w) 0.95 resulted in increased heat tolerance at 54 degrees C with all solutes tested. The extent of the increase and the optimal habituation time depended on the solute used. Exposure to broths containing glucose-fructose (a(w) 0.95) for 12 h resulted in maximal heat tolerance, with more than a fourfold increase in D(54) values. Cells held for more than 72 h in these conditions, however, became as heat sensitive as nonhabituated populations. Habituation in the presence of sodium chloride or glycerol gave rise to less pronounced but still significant increases in heat tolerance at 54 degrees C, and a shorter incubation time was required to maximize tolerance. The increase in heat tolerance following habituation in broths containing glucose-fructose (a(w) 0.95) was RpoS independent. The presence of chloramphenicol or rifampin during habituation and inactivation did not affect the extent of heat tolerance achieved, suggesting that de novo protein synthesis was probably not necessary. These data highlight the importance of cell prehistory prior to heat inactivation and may have implications for food manufacturers using low-a(w) ingredients.

Adaptation, Physiological↗

Individual differences in self-reported heat tolerance. Is there a link to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat?

AIM: Tolerance to exercise in heat exhibits great interindividual variability. We questioned whether individual differences in self-reported heat tolerance within a group of endurance trained athletes are linked to the cardiocirculatory, thermoregulatory and hormonal response to endurance exercise in heat. METHODS: Using a rating scale to assess the individual degree of tolerance to exercise in heat we allocated 12 non-heat-acclimated trained runners into two groups of 5 highly heat tolerant (HHT) and 7 less heat tolerant (LHT) athletes. Both groups performed a 60-min treadmill run (velocity 90% of individual anaerobic threshold, room temperature and humidity 28 inverted exclamation mark C and 50%, respectively). RESULTS: Sweating rate did not differ between HHT (mean +/- SEM: 0.44+/-0.02) and LHT (0.40+/-0.02 ml x kg(-1) x min(-1)). Compared to LHT, exercise-induced rises in core temperature (39.3+/-0.2/40.0+/-0.2 inverted exclamation mark C), heart rate, plasma norepinephrine and cortisol were significantly lower in HHT, while epinephrine did not exhibit differences between the groups. In contrast, response of human growth hormone (hGH) was significantly more pronounced in HHT. CONCLUSION: Our initial results, obtained in a small group of endurance-trained runners, show that self-reported tolerance to exercise in heat is associated with an attenuated rise in body core temperature during prolonged exercise under elevated ambient temperatures. This finding in heat tolerant athletes is paralleled by a lower stress response as reflected by lower rises in heart rate and stress hormones such as norepinephrine and cortisol. The functional significance (i.e. with respect to sweating function) of the more pronounced response of hGH in heat tolerant athletes warrants further research.

Body Temperature↗

Heat sensitivity in a bentgrass variant. Failure to accumulate a chloroplast heat shock protein isoform implicated in heat tolerance.

Two variants of creeping bentgrass (Agrostis stolonifera cv palustris), developed using tissue culture, have been used to determine the roles of chloroplast-localized small heat shock proteins (CP-sHSPs) in heat tolerance. Results from previous research indicate that the heat-tolerant variant expressed two additional CP-sHSP isoforms not expressed in the heat-sensitive variant, that accumulation of the additional CP-sHSP isoforms was genetically linked to thermotolerance, and that the presence of the additional isoforms in the heat-tolerant variant provided greater protection to photosystem II during heat stress. To determine the basis of the differential expression, we isolated the genes encoding the CP-sHSPs from both variants and characterized their structure and expression. Two genes, ApHsp26.2 and ApHsp26.7a, were isolated from the heat-tolerant variant, and three genes, ApHsp26.2m, ApHsp26.8, and ApHsp26.7b, were isolated from the heat-sensitive variant. The sequence of ApHsp26.2m from the heat-sensitive variant was identical to ApHsp26.2, except for a point mutation that generated a premature stop codon. Therefore, the protein product of ApHsp26.2m did not accumulate in the heat-sensitive line. Mass spectrometry analysis confirmed that ApHsp26.2 encoded for the CP-sHSP isoforms unique to the heat-tolerant variant. An identical mutation was detected in one of the three parental lines used to develop the creeping bentgrass variants. This suggests that ApHsp26.2m was inherited from this parent and did not arise from a mutation that occurred during tissue culture. The presence of two isoforms encoded by the same gene might be due to differential processing of the N-terminal amino acids during or after import into the chloroplast.

Adaptation, Physiological↗

Heat-Shock Response in Heat-Tolerant and Nontolerant Variants of Agrostis palustris Huds.

The heat-shock response in heat-tolerant variants (SB) and non-tolerant variants (NSB) of creeping bentgrass (Agrostis palustris Huds.) was investigated. Both variants were derived from callus initiated from a single seed of the cultivar Penncross. SB and NSB synthesized heat-shock proteins (HSPs) of 97, 83, 70, 40, 25, and 18 kD. There were no major differences between SB and NSB in the time or temperature required to induce the heat-shock response. When the HSPs synthesized by SB and NSB were analyzed by two-dimensional gel electrophoresis, it was apparent that SB synthesized two to three additional members of the HSP27 family, which were smaller (25 kD) and more basic than those synthesized by NSB. Analysis of F1 progeny of NSB x SB indicated that 7 of the 20 progeny did not synthesize the additional HSP25 polypeptides. These progeny were significantly less heat tolerant than progeny that did synthesize the additional HSP25 polypeptides. The X2 test of independence (X2 = 22.45, P < 0.001) indicated that heat tolerance and the presence of the additional HSP25 polypeptides are linked traits.

Journal Article↗

Heat tolerance and aging.

Work-heat tolerance has been reported to be generally lower in middle-aged and elderly men and women than in younger men and women. Some authors have suggested that physically fit older men have fewer decrements in performance during work-heat stress than do less fit men of the same age. However, none of the studies matched older and younger individuals on any pertinent physiological or morphological variables. Recently, four different researchers have reported results of studies in which men or women differed in average age by 25 to 36 years but were matched for body weight, surface area, surface area: body weight ratio, percentage of body fat, and maximal aerobic power. Evidence from three of these studies indicated little impairment of the thermoregulatory system during acute work-heat stress or heat acclimation in these men and women, at least through the seventh decade of life. One of the four studies did indicate higher core temperatures and lower sweating rates in middle-aged women than in younger women after heat acclimation; however, the length of time the heat could be tolerated did not differ between these matched groups. These observations generally support the importance of aerobic fitness and other morphological factors to middle-aged and elderly individuals working or performing recreational activities in hot environments.

Adolescent↗

Effects of a heat shock protein inhibitor KNK437 on heat sensitivity and heat tolerance in human squamous cell carcinoma cell lines differing in p53 status.

PURPOSE: The effects of a heat shock protein (hsp) inhibitor KNK437 (N-formyl-3,4-methylenedioxy-benzylidene-gamma-butyrolactam) were examined on the heat sensitivity and heat tolerance of human cancer cells with special reference to p53 status. MATERIALS AND METHODS: Human squamous cell carcinoma (SAS) and glioblastoma cell lines (A-172) transfected with mutant p53 (mp53) or control neo genes were used. KNK437 was added in culture medium at a final concentration of 50, 100 or 300 microM 1 h before heating (42 degrees C). Surviving fractions of cells were measured by use of a clonogenic assay. Effects of KNK437 on the accumulation of heat shock proteins and DNA binding activity of heat shock factor 1 were examined with Western blot analysis and gel mobility-shift assay, respectively. Heat-induced apoptotic bodies were detected by Hoechst 33342 staining. RESULTS: The mp53-transfected SAS (SAS/mp53) and A-172 (A-172/mp53) cells were more resistant to heat than the neomycin (neo)-transfected SAS (SAS/neo) and A-172 (A-172/neo) cells. The constitutive amount of hsp27 was larger in SAS/mp53 than in SAS/neo cells. Clear differences in the constitutive amounts of hsp40, hsp72 and hsp90 were not observed between SAS/mp53 and SAS/neo cells. KNK437 enhanced the heat sensitivity in SAS/mp53 and A-172/mp53 cells more effectively than in neo control cells. Heat tolerance was suppressed by KNK437 in SAS/mp53 and SAS/neo cells and also in A-172/mp53 and A-172/neo cells. Along with suppression of heat tolerance, KNK437 suppressed heat-induced accumulation of both hsp27 and hsp72. Heat-induced apoptotic bodies were enhanced by KNK437 in SAS/mp53 and SAS/neo cells. CONCLUSION: The results suggest a possible mechanism for the heat sensitivity of SAS cells. Heat sensitivity depends on p53 status regulating the amount of hsp27. Heat tolerance is suppressed by KNK437 through the suppression of heat-induced accumulations of hsp27 and hsp72 and the induction of p53-independent apoptosis.

Apoptosis↗

Heat tolerance of vancomycin resistant Enterococcus faecium.

The heat tolerance of 27 Enterococcus faecium isolates in water was studied. Stationary phase cultures including vancomycin resistant and sensitive clinical and food isolates were exposed to heat at 60 degrees, 65 degrees, 71 degrees, and 80 degrees C for one, three, 10, and 30 minutes and the log10 reductions in bacterial counts were determined. Exposure at 71 degrees and 80 degrees C resulted in > 6 log10 reduction in viable counts for all isolates. Seven (24%) isolates survived (< 5 log10 reduction) heat at 65 degrees C for 10 minutes. The E faecium isolates were more resistant to heat than the two E faecalis reference strains. No differences in heat tolerance were observed between vancomycin sensitive and resistant strains or between isolates of human or food origin.

Drug Resistance, Microbial↗

Effects of physical training and cardiorespiratory physical fitness on exercise-heat tolerance: recent observations.

Most authors agree that physical training in a cool environment improves tolerance to exercise in the heat and the rate of heat acclimatization, but the extent or degree of improvement remains controversial. The best improvement in heat tolerance for men is associated with intensive interval or continuous training at a training intensity greater than 50% of maximal oxygen uptake (Vo2max) for 8-12 weeks; the Vo2max should be increased 15-20%. Far less is known about the appropriate type, intensity and duration of endurance training associated with improved exercise-heat tolerance in women. The major benefits of physical training appear to apply to both short term (less than 2 hrs) or long term (greater than 2 hrs) exercise-heat exposures for men. Generally, individuals with high Vo2max values (previously trained and endurance athletes) are at an advantage in the heat. Utilization of proper physical training appears to produce about 50% of the total adjustment resulting from heat acclimatization, while increased fitness is associated with greater retention of acclimatization in cool environments. Female athletes appear somewhat better able to tolerate exercise in hot environments than nonathletic females while differences between highly trained females and males do not appear as dramatic as once thought.

Acclimatization↗

Human heat tolerance in simulated environment.

The heat tolerance of 11 male volunteers were examined under seven climatic conditions in a climatic chamber. The conditions were 38 to 49 degrees C dry bulb temperature and 45 to 80 per cent relative humidity, i.e., 32.3 to 40 degrees C effective temperature-basic [ET(B)]. The ET(B) values were equated to other heat stress indices, e.g., WBGT (Wet-bulb Globe Temperature Index) and Oxford Index. The subjects did ergometric work at an intensity of 60 per cent VO2max. The exposure durations were decided by the cardiorespiratory, body temperature and sweating responses. Of the climatic conditions studied, at 35.4, 38, 39 and 40 degrees C ET(B), the body core temperature (Tcr) reached over 39 degrees C and heart rates attained 172 to 182 beats/min, which were taken as the tolerance limit. The total oxygen demand significantly varied with the increase in environmental warmth, i.e., increase or decrease of one litre of oxygen demand was equivalent to one minute change in tolerance time. The volunteers were not susceptible to heat; only in extreme hot situations beyond 35.4 degrees C ET(B), were unacceptable levels of physiological and psychophysical reactions seen. The study suggests the acceptable and tolerable limits for human exposure in heat: (i) acceptable at 38 to 38.2 degrees C Tcr for a tolerance time of 80 to 85 min; and (ii) the tolerable limit of short duration (40-45 min) at 39 degrees C Tcr that corresponded to 31.5 and 36.5 degrees C ET(B).

Adolescent↗

Correlation between heat tolerance during exercise and maximum aerobic work capacity.

Observation of the physiological responses during exercise in a hot environment and measurement of maximal work capacity were made on eight young male subjects, ages 20--22. Exercise was performed on a bicycle ergometer at a constant work load of 450 kg . m/min at a cycling rate of 50 rpm for 30 min in a climatic chamber at 30 degree C with 70% relative humidity. The maximum work capacity was measured by bicycle ergometer exercise. Heat tolerance during exercise was assessed by the magnitude of physiological strain expressed by the combination of relative rise in rectal temperature, relative water loss and relative salt loss. Heat load during exercise was calculated using metabolic rates at rest and during exercise, assuming heat loss through the respiratory tract to be 10 percent of metabolic rate. Fairly good correlations were found between the ratio of work done to maximum work capacity and rise in rectal temperature, ratio of body weight loss to body weight and heat tolerance during exercise. Close correlations were found among relative heat load during exercise and rise in rectal temperature, relative body weight loss and heat tolerance. Heat tolerance during exercise in a hot environment correlated well to capacity of heat dissipation and maximum work capacity.

Adult↗

Heat-stress induced synthesis of chloroplast protein synthesis elongation factor (EF-Tu) in a heat-tolerant maize line.

A heat-tolerant maize (Zea mays L.) line, ZPBL 1304, synthesizes a unique set of five heat-shock polypeptides of 45 kDa. Previous studies suggested that these polypeptides might play a role in the development of thermotolerance in maize (Ristic et al., 1996, J. Plant Physiol. 149:424-432; Ristic et al., 1998, J. Plant Physiol. 153:497-505). In the present study, we isolated these polypeptides, sequenced them, and investigated their subcellular distribution and origin. Of the five polypeptides of 45 kDa, three polypeptides, including the two most abundant ones, yielded amino acid sequences similar to the chloroplast and bacterial protein synthesis elongation factor (EF-Tu). This was further confirmed using an antibody raised against maize EF-Tu, which showed a very strong reaction with the 45-kDa heatshock protein(s). Studies on subcellular distribution and origin revealed that the 45-kDa polypeptides were localized to the chloroplasts, and were likely of nuclear origin. A full-length maize EF-Tu cDNA (Zmeftu1), previously isolated from the B73 line of maize, was used as a probe for northern blot analysis of RNA extracted from the ZPBL 1304 maize line (the nucleotide and deduced amino acid sequences of Zmeftu1 are 88% identical to the rice EF-Tu sequence). Northern blots showed a 1.85-fold increase in steady-state levels of EF-Tu mRNA during heat stress. An increase in EF-Tu transcript levels during heat stress was accompanied by increased levels of the EF-Tu protein. Isolated chloroplasts from heat-stressed plants also had higher levels of EF-Tu as compared to control chloroplasts. The maize EF-Tu polypeptides showed > 80% sequence similarity with the bacterial EF-Tu, which has recently been shown to function as a molecular chaperone and to play a role in the protection of other proteins from thermal denaturation (Caldas et al., 1998, J. Biol. Chem. 273:11478-11482). It is hypothesized that chloroplast EF-Tu of the ZPBL 1304 maize line plays an important role in the development of thermotolerance.

Amino Acid Sequence↗

Human ACE I/D polymorphism is associated with individual differences in exercise heat tolerance.

We hypothesized that there is an association between the angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism with the variability in exercise heat tolerance in humans. Fifty-eight Caucasian men were exposed to a 2-h exercise heat-tolerance test. We analyzed the association between their heat-tolerance levels with the ACE DD (n = 25) and I+ (n = 33) genotypes and with various anthropometrical parameters and aerobic fitness. It was found that the relative changes in body core temperature, heat storage, and heart rate during the 120-min exposure to exercise heat stress was consistently lower in the I+ genotype group compared with the DD genotype group (0.8 +/- 0.2 vs. 1 +/- 0.1 degrees C, P < 0.05; 17.7 +/- 1.8 vs. 19.8 +/- 1.3 W/M(2), P < 0.05; and 33 +/- 7 vs. 44 +/- 5 beats/min, respectively, P = 0.06). No significant association was found between heat strain response and the anthropometrical measurements or aerobic fitness in the various genotype groups. We suggest that the ACE I+ polymorphism may be considered as a possible candidate marker for increased heat tolerance.

Adult↗

[Itch and the heat tolerance scale: effects of thermographic biofeedback].

Effects of heat tolerance (HT) relating with individual emotionality, and of thermal biofeedback on itching were examined. Fourteen high HT subjects and 12 low HT subjects were selected by the Cold and Heat Tolerance Scales (Dienstbier, LaGuardia, & Wilcox, 1987). The experiment was divided into three phases: rating of itch, eight thermal biofeedback (increase or decrease) training sessions, and rating of itch with biofeedback. Itching was produced by a glue made from Japanese yam powder. Yam glue was applied on the subjects' dorsal forearm. The biofeedback information was given by the thermographics on the CRT, where its color was changed according to the changes in temperature of the dorsal forearm skin. Results showed that (a) subjects who were instructed to decrease their skin temperature reported comparatively lower intensities of itching, although their actual temperature controls were unsuccessful, and (b) the biofeedback performance reduced the intensity of itching for the low HT subjects, but raised it for the high HT subjects who were instructed to increase their skin temperature. The results suggested that the biofeedback performance could have different central effects on itching among the HT groups.

Adult↗

Heat tolerance of Boran and Tuli crossbred steers.

Experiments were conducted to evaluate the heat tolerance of the following breeds: Hereford (H), Brahman (B), H x B, H x Boran (H x Bo), and H x Tuli (H x T). Heat tolerance was evaluated in a climatically controlled room (Exp. 1) and under summer environmental conditions (Exp. 2) by comparing rectal temperatures (RT), respiration rates (RR), and sweating rates (SW). In Exp. 1, under extremely hot conditions (mean temperature-humidity index [THI] > 90), purebred B had significantly (P < .05) lower RT and RR than other genotypes, which may be indicative of greater surface area per mass to dissipate heat and a lower metabolic rate than other genotypes. Boran and Tuli crosses had RT (39.5 degrees C) that were intermediate to those of B (39.0 degrees C) and H x B (40.0 degrees C). The H genotype had the greatest RT at 40.3 degrees C. Among the breeds, trends in RR were similar to RR observed at THI < 77; B had the lowest RR, and H x B were intermediate. However, in these extreme conditions, RR did not differ among the purebred H and the Boran and Tuli crossbred steers, but H x B steers had lower RR than the other H crossbred steers. Sweating rates were significantly greater for the Bos indicus x Bos taurus crosses (H x B and H x Bo) than for the purebred genotypes (H and B) and the Bos taurus cross (H x T). In Exp. 2, mean RT for B, H x B, H x Bo, and H x T were very similar to those recorded under the moderate heat stress conditions found in Exp. 1. There were no differences in RT among B, H x Bo, and H x T genotypes. The RR increased over time for H only, and RR for other genotypes tended to be elevated only slightly over time. Among genotypes, SW was significantly greater for the H x Bo steers. The ability of the Bos indicus crosses to dissipate heat through enhanced SW and associated evaporative cooling was evident. However, the heat-tolerant nature of the Bos taurus cross (H x T) was not evident through enhanced RR or SW in either experiment. Compared with other genotypes, the lower RR of B steers was clearly evident and is assumed to be due to greater surface area and other skin characteristics that allow them to dissipate heat to maintain lower RT. These data suggest that the H x Bo and H x T are similar to H x B and intermediate to H and B genotypes in maintaining homeostasis when exposed to a high heat load.

Adaptation, Physiological↗

Heat tolerance, thermoregulation and ageing.

Older individuals, regardless of how one classifies 'old', are the most rapidly growing portion of the population. Statistics from heat waves and other morbidity-mortality data strongly suggest that older persons are at greater risk of developing life-threatening manifestations of heat stress such as heat stroke. Most laboratory studies have found that ageing is associated with decreased heat tolerance and alterations in thermoregulatory effector responses. What is not so clear is the role of ageing per se in this decreased heat tolerance (as opposed to some concomitant functional decline, e.g. decreasing VO2max, which accompanies ageing across a population). Studies have shown decrements in resting heat tolerance and responses to thermal transients in older adults. With exercise in warm environments, most research has focused on the sweating response and it appears that whether or not sweating rate declines in the elderly is dependent upon the environment studied. In hot dry environments, older persons (of both sexes) consistently secrete sweat at a lower rate than their younger counterparts. However, as humidity of the environment increases, this difference tends to disappear. A key issue which deserves further attention is that of hydration in the elderly, both in terms of body water content and compartmentalisation, and of skin water content. Finally, ageing is often accompanied by other conditions (e.g. hypertension, diabetes, cardiovascular insufficiencies, long term therapeutic drug modalities) which further affect heat tolerance and thermoregulation.

Adult↗