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PHYSIOLOGICAL EFFECTS AFTER EXPOSURE TO HEAT: 
A BRIEF LITERATURE REVIEW
Cornelis P. BOGERD 1 & Hein A. M. DAANEN 2, 3
1 University of Primorska, Science and Research Centre of Koper, Institute of Kinesiology Research, Slovenia
2 VU University Amsterdam, Faculty of Human Movement Sciences, MOVE research group, Netherlands
3 TNO Behavioural and Social Sciences, Expertise Center Human Performance, Netherlands
Corresponding author:
Cornelis P. Bogerd
University of Primorska, Science and Research Centre of Koper, 
Institute of Kinesiology Research, Garibaldijeva 1, 6000 Koper, Slovenia
e-mail: niels.bogerd@upr.si
ABSTRACT
Many employees are exposed to heat stress during their work. Although the direct 
effects of heat are well reported, the long term physiological effects occurring after 
heat exposure are hardly described. The present manuscript addresses these issues in 
the form of a brief literature review. Repeated heat exposure results in heat acclima-
tization. These physiological adaptations decay gradually afterwards, re-increasing 
the vulnerability to heat injuries. Repeated heat exposure may lead to kidney damage 
(related to dehydration) and reduced efficiency of the reproductive system. A history of 
heat stroke may increase the sensitivity to heat illness. The increased susceptibility pos-
sibly indicates an impaired thermoregulatory system resulting from a heat stroke, or a 
genetic predisposition prior to the first heat stroke.
Keywords: heat, strain, stress, physiology, health, temperature
review article                UDC: 613.6:331.47
received: 2011-06-13
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FIZIOLOŠKI UČINKI PO VROČINSKI IZPOSTAVLJENOSTI: 
KRATEK PREGLED LITERATURE
IZVLEČEK
Mnogi delavci so pri svojem delu izpostavljeni vročinskemu stresu. Čeprav so ne-
posredni učinki vročine dobro preučeni, so dolgoročne fiziološke spremembe le redko 
opisane. Članek opisuje tovrstno tematiko v obliki kratkega pregleda literature. Pona-
vljajoče se izpostavljanje vročini vodi v vročinsko aklimatizacijo, te fiziološke prilago-
ditve pa začnejo postopoma upadati ter povečujejo občutljivost za vročinske poškodbe. 
Ponavljajoča se izpostavljenost vročini lahko vodi v ledvične okvare (povezane z de-
hidracijo) in zmanjšano učinkovitostjo reproduktivnega sistema. Predhodno prebolela 
vročinska kap (toplotni udar) poveča občutljivost za vročinske obolevnosti. Večja do-
vzetnost najverjetneje nakazuje na neučinkovitost termoregulacijskega sistema, ki je 
posledica vročinske kapi ali genske predispozicije pred prvo vročinsko kapjo.
Ključne besede: vročina, napor, stres, fiziologija, zdravje, temperatura
INTRODUCTION
A core temperature in a narrow band around 37 °C is essential for optimal human 
functioning. This thermal equilibrium can be achieved if heat gain equals heat loss. In 
the absence of thermal extremes, core temperature is maintained through constriction 
and dilatation of blood vessels in the skin. In the heat, and particularly during exercise, 
sweat evaporation contributes substantially to the heat balance. If sweat evaporation 
is compromised, for instance due to wearing protective clothing, the core temperature 
increases. High core temperatures result in reduced performance, both physiological 
(Galloway & Maughan, 1997; Gonzalez-Alonso et al., 1999; Parkin, Carey, Zhao & 
Febbraio, 1999) and psychological, e.g., on vigilance and complex dual tasks (Ramsey, 
1995; Pilcher, Nadler & Busch, 2002; Hancock, Ross & Szalma, 2007). For instance, 
the physiological strain endured by fire fighters is described elsewhere (Romet & Frim, 
1987), in addition, it is established that warm environments can reduced driving perfor-
mance (Wyon, Wyon & Norin, 1996). If heat strain results in an increased core temper-
ature (hyperthermia) it can lead to mortality and morbidity under healthy, well trained 
individuals, through exertional heat stroke (Coris, Ramirez & Van Durme, 2004).
Heat strain is common in many occupations as recognized by the American Na-
tional Institute for Occupational Safety and Health (NIOSH). Due to the rising environ-
mental temperature the occurrence of heat strain is likely to increase in at least some 
occupations. In fact, the Intergovernmental Panel on Climate Change (IPCC, 2007) 
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predicts a global temperature rise of 1.1 °C to 6.4 °C within this century, mainly due 
to the greenhouse effect. Besides global warming can also urbanization play a role in 
increases in temperature to which people are exposed. For instance, people working in 
urban environments are exposed to higher levels of heat stress compared to workers in 
rural areas. This phenomenon is caused by so called urban heat islands, and can account 
for an increased ambient temperature as large as 8 °C for a city size of about half a mil-
lion inhabitants compared to a rural area (Roodenburg, 1983).
Most research is conducted in the area of direct effects of heat on health and 
performance. However, less is known about the long term effect on heat exposure 
on health. This is relevant since many employees are exposed to heat for prolonged 
periods in their life, such as workers in the metal melting industry, road construction 
workers, and military personnel serving in jungle and desert climates for several 
months. On a national level, governments are introducing new laws making employ-
ers more responsible for the health of their employees, in order to minimize the nega-
tive effect of work on the general health. The goal of these changes is to reduce sick-
leave and thereby increasing productivity. However, the stimulus of governments did 
not result in increased research activity in the field of health effects after exposure to 
heat stress; this manuscript will focuses on these effects. Physiological effects dur-
ing exposure to heat stress are covered elsewhere (see e.g., Sawka & Young, 2005; 
Cheung, 2010).
PHYSIOLOGICAL EFFECTS AFTER EXPOSURE TO HEAT
Decay of acclimatization
Exposure to heat for a sufficient period results in physiological adaptations known 
as acclimatization (Nielsen, 1994). Moreover, Nielsen and co-workers conducted a se-
ries of extensive studies (Nielsen et al., 1993; Nielsen, Strange, Christensen, Warberg 
& Saltin, 1997) in which they monitored the acclimation effects to dry and humid heat. 
In these studies respectively 8 and 12 participants exercised till exhaustion at 50% of 
the maximum oxygen uptake (VO2max), in a laboratory kept at 41 °C, 12% relative hu-
midity (RH) and 35 °C, 87% RH. Both studies find an increased sweat rate, increased 
plasma volume, decreased heart rate and increased time to exhaustion, as a result of 
acclimation. Understanding the decay of acclimatization will allow for improved rein-
tegration schemes or prescribed heat strain exposure for employees irregularly exposed 
to warm environments.
It is often thought that most of these physiological adaptations will disappear in the 
course of one to three weeks (Armstrong & Maresh, 1991; Pandolf, 1998; Astrand, Ro-
dahl, Dahl & Stromme, 2003). However, recently 16 participants underwent a 10 days 
acclimatization protocol during the UK winter months. The participants were divided 
into two even groups who carried out an exercise protocol in a warm environment after 
12 and 26, for each group separate (Weller, Linnane, Jonkman & Daanen, 2007). The 
results indicate that many of the advantageous of the adaptation remained after 12 and 
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even 26 day after completing the acclimatization protocol. Thus, contrary to general be-
lief, heat acclimation decay may take more than a month (Weller et al., 2007; Daanen, 
Jonkman, Linnane & Weller, in press). Although acclimatization effects are similar for 
conditions with comparable levels of heat stress (Griefahn, 1997), some studies indi-
cate that acclimatization to dry heat in athletes will persist longer than acclimatization 
to humid heat (Pandolf, 1998). Acclimatization will also persist longer in physically 
active individuals (Pandolf, 1998). The latter being intuitive because physical activity 
is likely to coincide with elevated levels of the core temperature. Since hyperthermia 
is the trigger for the acclimatization process (Nielsen, 1998) the acclimatization decay 
will be slower when high levels of physical activity are maintained.
History of heat stroke and thermal physiological function
An elevated core temperature might lead to heat illness (Wexler, 2002), of which 
heat stroke is the most severe. Heat stroke is life-threatening and trained medical per-
sonal should supervise treatment (Wexler, 2002). For health individuals, a core temper-
ature around 40 °C is usually associated with an increased risk for heat stroke (Wexler, 
22; Coris et al., 2004). Two types of heat stroke can be differentiated: (i) classic (or 
non exertional) heat stroke resulting from a high environmental temperatures; (ii) exer-
tional heat stroke which is the result of excessive heat produced due to high metabolic 
demands. The mechanisms of heat stroke are described elsewhere (Gisolfi & Mora, 
2000). Understanding the relationship between the history of heat stroke and the ther-
mal physiological functioning, allows for improved screening of suitable individuals 
for jobs were heat exposure is inevitable.
Several studies have focused on the effect of a history of exertional heat stroke on 
the thermal physiological response to heat. One study found such effect (Shapiro et al., 
1979), whereas other studies do not confirm these results (Armstrong, De Luca & Hub-
bard, 1990; Royburt, Epstein, Solomon & Shemer, 1993). Shapiro et al. (1979) exam-
ined 9 young men whom suffered from heat stroke 2–5 years earlier and 10 young men 
without a history of heat illness. They found significant differences in heart rate and 
rectal temperature between the two groups during exercise (40 and 80 W for 45 and 20 
min, respectively) at room temperature (23 °C, 50% RH) and high ambient temperature 
(40 °C, 50% RH). However, VO2 was significantly lower in patients who had a history 
of heat stroke during exercise in a warm environment, this was left unexplained. In ad-
dition, no significant difference was found for sweat rate. It was concluded that since 
the former heat stroke patients generated the same amount of external power (and even 
had a lower VO2), their significantly higher body core temperature might indicated an 
impaired transport of heat from the core to periphery.
Other studies were carried out under comparable conditions (Armstrong et al., 
1990; Royburt et al., 1993), and did not find a difference between former heat stroke 
patients and matched control participants in hear rate and body core temperature dur-
ing exercise. It is difficult to indicate the basis for this discrepancy; it could be due 
to differences in anthropometrics, or response time and treatments to which the heat 
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stroke patients were exposed. The latter are indicated as relevant for the efficiency of 
recovery (Lew, Lee, Date & Melnik, 2002). It therefore remains unclear if former heat 
stroke patients are more sensitive to heat after some recovery time. However, the for-
mer heat stroke patients used in the above mentioned studies suffered from exertional 
heat stroke. Interestingly, history of heat stroke is often indicated as a risk factor for 
heat illness (Gisolfi & Mora, 2000; Coris et al., 2004). Thus, it is unclear if heat stroke 
causes a degradation of the thermoregulatory system, it is equally likely that former 
heat stroke patients had a degraded thermoregulatory system beforehand.
Exertional heat stroke is more relevant to a working population than classical heat 
stroke. However, the latter is not irrelevant due to trend of increasing the retirement 
age as a response to the recent reduction in economic prosperity combined with the 
increasing life expectancy. From research done during the 1995 heat wave in Chicago, 
which resulted in 600 excess deaths, only 52% of the former classic heat stroke patients 
survived the first year (Dematte et al., 1998). None of these surviving patients (n = 
58) recovered completely within a year. The authors concluded that near fatal classic 
heat stroke is associated with multi-organ dysfunction. However, it is difficult to com-
pare patients suffering from exertional and classic heat stroke, since the former affects 
healthy exercising individuals and the latter affects the young, the elderly and the sick. 
Thus, patients suffering from classic heat stroke are less favoured, they have a 50% 
change not to survive the year following their stroke, and will most likely not recover 
completely within a year.
Reduced efficiency of the reproductive system
Different organs in the human body exhibit different sensitivities towards heat. 
For instance, whole body effects of muscle impairment at a given high temperature 
are likely less severe than brain tissue impairment at the same temperature (Gisolfi & 
Mora, 2000). Although increased temperature of the reproductive system is unlikely 
life threatening to the exposed individual, it is likely to affect new life due to its effect 
on spermatogenesis. In fact, long term difficulties with desired and successful repro-
duction are likely to be an important factor for mental wellbeing.
Rachootin and Olsen (1983) found that exposure to heat was associated with an 
increased risk of delayed conception, with a factor 1.8. It was further found that sper-
matozoa have a greater likelihood for morphological abnormalities. This finding was 
explained through a deviation away from the optimum testicular temperature ranging 
from 34–35 °C. Intuitively, these authors identified that warm environment to which 
the workers were exposed as the cause for the increased testicular temperature. Also 
other studies confirm this (Baird & Wilcox, 1986; Figa-Talamanca et al., 1992; Mur, 
Wild, Rapp, Vautrin & Coulon, 1998). However, if assessed, no effect on the female 
reproductive system was found in the before mentioned studies.
The effects on the reproductive system are mainly exhibited during exposure, with 
parameters such as spermatozoa quantity, morphology, and function, returning to nor-
mal levels soon after exposure. In fact, almost all human populations exhibit seasonal 
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variation in births (Bronson, 1995; Sharpe, 2000). This is partly explained by seasonal 
variation in the frequency of conception. Bronson (1995) also recognizes temperature 
as an important factor for these variations. In fact, 9 months after the summer birth 
rates are lower compared to 9 months after the winter season, this tends to indicate a 
recovery of from heat exposure.
Nephrolithiasis
While exposed to heat stress, the human body can produce excessive amounts of 
sweat, in an attempt to lose heat through sweat evaporation. In fact, sweat rates of 7 
l per working day have been reported (Leithead & Lind, 1964). Sweat is produced 
from intercellular fluid but excreted with a reduced osmolarity. Thus, work in a warm 
environment intensifies the kidney function aimed at maintaining a stable blood osmo-
larity. Ingestion of fluids, which is essential for compensating for water loss through 
sweating, further affects the osmolarity of blood. This mechanism forms the basis for 
the relationship between exposure to heat and nephrolithiasis (the development of 
kidney stones) (Vander, Sherman & Luciano, 2001). Understanding the relationship 
between warm environments and nephrolithiasis is likely to contribute to the reduction 
of its occurrence.
Borghi et al. (1993) studied 236 employers of a glass plant in Italy exposed to heat 
(30 °C WBGT) and 165 employers of the same factory not exposed to heat (25 °C 
WBGT). Urine analysis revealed an increased uric acid (722 vs. 482 mg/l), decreased 
pH (5.3 vs. 5.6), increased specific gravity (1026 vs. 1021 kg/m) and higher incidence 
of nephrolithiasis (8.5 vs. 2.4%) for the workers exposed to heat. They concluded that 
the increased incidence for nephrolithiasis was caused by an insufficient fluid intake 
(dehydration). This is supported by an epidemiological survey that demonstrated a 
higher prevalence of nephrolithiasis in populations of hot climates (Parry & Lister, 
1975). Another group studied workers exposed to heat and intense sunlight for at least 
6 months per year and confirmed a higher incidence of kidney stones (Better, Mel-
amud, Shabtai, Berenheim & Chaimowitz, 1978). A sufficient fluid and salt intake was 
suggested as a solution to this problem. However, from athletes it is known, that usu-
ally voluntarily insufficient fluids are consumed while exercising in a hot environment 
(Nielsen & Krog, 1994; Murray, 1995). This is likely also the case for employees work-
ing in hot environments.
There might also be a link between sunshine and nephrolithiasis. This link is formed 
through vitamin D, which is generated due to ultraviolet B radiation from sunlight 
and stimulates the absorption of calcium from the intestines (Holick, 2003). An in-
creased vitamin D production can lead to an increased calcium concentration in the 
blood and thus to an increased calcium flux through the kidneys. An increased calcium 
flux through the kidneys coexists with an increased risk of nephrolithiasis (Shekarriz 
& Stoller, 2002). This hypothesis is postulated by Parry and Lister (1975). However, if 
vitamin D plays a substantial role in nephrolithiasis, it can easily be prevented by using 
sunscreen (Holick, 2003).
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CONCLUSIONS
This brief literature review focused on physiological effects after exposure to heat. 
Although limited literature is available on this topic, there is scientific basis for the fol-
lowing events to occur after a multi-day exposure to heat: (i) decay of acclimatization 
acquired during heat exposure, (ii) reduction in the efficiency of the reproductive sys-
tem (iii) increased risk for nephrolithiasis. It is undetermined if repeated heat exposure 
affects the risk for heat stroke.
OUTLOOK
More knowledge is needed to improve our understanding, allowing a better protec-
tion of employees. Such future work should not only focus on extending the knowledge 
on mechanisms that increase health risks, which was the focus in this brief review, but 
should also consider positive health effects of exposure to heat. For instance, from re-
search on chickens it is known that exposure to heat at a young age increases resistance 
against heat injuries later in life (Arjona, Denbow & Weaver, 1990; Yahav et al., 1997; 
Zulkifli, Liew, Israf, Omar & Hair-Bejo, 2003). At present it is unclear if such mecha-
nisms also exist in humans.
ACKNOWLEDGEMENT
The authors are grateful to Ronald Heus for his contribution to an earlier version of 
this manuscript.
REFERENCES
Arjona, A. A., Denbow, D. M., & Weaver, W. D., Jr. (1990). Neonatally-induced 
thermotolerance: physiological responses. Comparative Biochemistry and Physiol-
ogy - Part A: Molecular & Integrative Physiology, 95(3), 93–399.
Armstrong, L. E., De Luca, J. P., & Hubbard, R. W. (1990). Time course of recovery 
and heat acclimation ability of prior exertional heatstroke patients. Medicine & Sci-
ence in Sports & Exercise, 22(1) 36–48.
Armstrong, L. E., & Maresh, C. M. (1991). The induction and decay of heat acclima-
tisation in trained athletes. Sports Medicine, 12(5) 302–312.
Astrand, P. O., Rodahl, K., Dahl, H. A., & Stromme, S. B. (2003). Temperature regu-
lation. In P. O. Astrand, K. Rodahl, H. A. Dahl, & S. B. Stromme (Eds.), Textbook 
of work physiology (395–431). Champaign, USA: Human Kinetics.
Baird, D., & Wilcox, A. (1986). Effects of occupational exposures on the fertility of 
couples. Occupational medicine, 1(3), 361–374.
Better, O. S., Melamud, A., Shabtai, M., Berenheim, J., & Chaimowitz, C. (1978). 
Studies on the pathogenesis of increased incidence of nephrolithiasis in lifeguards 
in Isreal. Clinical research, 26(126A).
Cornelis P. BOGERD, Hein A.M. DAANEN: PHYSIOLOGICAL EFFECTS AFTER EXPOSURE ..., 14–23
ANNALES KINESIOLOGIAE • 2 • 2011 • 1
21
Borghi, L., Meschi, T., Amato, F., Novarini, A., Romanelli, A., & Cigala, F. (1993). 
Hot occupation and nephrolithiasis. The Journal of Urology, 1506), 1757–1760.
Bronson, F. H. (1995). Seasonal Variation in Human Reproduction: Environmental 
Factors. The Quarterly Review of Biology, 0(2), 141–164.
Cheung, S. S. (2010). Advanced environmental exercise physiology. Champaign, 
USA: Human Kinetics.
Coris, E. E., Ramirez, A. M., & Van Durme, D. J. (2004). Heat illness in athletes: the 
dangerous combination of heat, humidity and exercise. Sports Medicie, 34(1), 9–16.
Daanen, H. A. M., Jonkman, A. G., Linnane, D. M., & Weller, A. S. (in press). 
Induction and decay of heat acclimation. International Journal of Sports Medicine.
Dematte, J. E., O’Mara, K., Buescher, J., Whitney, C. G., Forsythe, S., McNamee, 
T., et al. (1998). Near-Fatal Heat Stroke during the 1995 Heat Wave in Chicago. 
Annals of Internal Medicin, 129(3), 173–181.
Figa-Talamanca, I., Dell’Orco, V., Pupi, A., Dondero, F., Gandini, L., Lenzi, A., et 
al. (1992). Fertility and semen quality of workers exposed to high temperatures in 
the ceramics industry. Reproductive Toxicoogy, 6(6), 517–523.
Galloway, S. D., & Maughan, R. J. (1997). Effects of ambient temperature on the 
capacity to perform prolonged cycle exercise in man. Medicine & Science in Sports 
& Exercse, 29(9), 1240–1249.
Gisolfi, C. V., & Mora, F. (2000). The hot brain: survival, temperature, and the human 
body. Cambridge, USA: The MIT Press.
Gonzalez-Alonso, J., Teller, C., Andersen, S. L., Jensen, F. B., Hyldig, T., & Nielsen, 
B. (1999). Influence of body temperature on the development of fatigue during pro-
longed exercise in the heat. Journal of Applied Physilogy, 86(3), 1032–1039.
Griefahn, B. (1997). Acclimation to three different hot climates with equivalent wet 
bulb globe temperatures. Ergnomics, 40(2), 223–234.
Hancock, P. A., Ross, J. M., & Szalma, J. L. (2007). A meta-analysis of performance 
response under thermal stressors. Human Factors: The Journal of the Human Fac-
tors and Ergonomics Society, 49(5), 851–877.
Holick, M. F. (2003). Vitamin D: A Millenium Perspective. Journal of Cellular Biohe-
mistry, 88(2), 296–307.
IPCC (2007). Summary for Policymakers. In S. Solomon, D. Qin, M. Manning, Z. 
Chen, M. Marquis, K. B. Averyt, M. Tignor, & H. L. Miller (Eds.), Climate Change 
2007: The Physical Science Basis Contribution of Working Group I to the Fourth 
Assessment Report of the Intergovernmental Panel o Climate Change (p. 1–18). 
Cambridge, UK: Cambridge University Press.
Leithead, C. S., & Lind, A. R. (1964). Heat stress and heat disorders. London, UK: 
Cassell & Company LTD.
Lew, H. L., Lee, E. H., Date, E. S., & Melnik, I. (2002). Rehabilitation of a patient 
with heat stroke: a case report. American Journal of Physical Medicine & Reabilita-
tion, 81(8), 629–632.
Mur, J. M., Wild, P., Rapp, R., Vautrin, J. P., & Coulon, J. P. (1998). Demographic 
evaluation of the fertility of aluminium industry workers: influence of exposure to 
heat and static magnetic fields. Human eporduction, 13(7), 2016–2019.
Cornelis P. BOGERD, Hein A.M. DAANEN: PHYSIOLOGICAL EFFECTS AFTER EXPOSURE ..., 14–23
ANNALES KINESIOLOGIAE • 2 • 2011 • 1
22
Murray, R. (1995). Fluid needs in hot and cold environments. International Journal of 
Sprt Nutrition, 5 Suppl(S62–73).
Nielsen, B. (1994). Heat stress and acclimaion. Ergonomics, 37(1), 49–58.
Nielsen, B. (1998). Heat acclimation – mechanisms of adaptation to exercise in the heat. 
International Journal of Sports Medicine, 19(Suppl 2), S154–156.
Nielsen, B., Hales, J. R., Strange, S., Christensen, N. J., Warberg, J., & Saltin, B. 
(1993). Human circulatory and thermoregulatory adaptations with heat acclimation 
and exercise in a hot, dry environment. Jornal of Physiology, 460, 467–485.
Nielsen, B., & Krog, P. (1994). Optimal fluid replacement during long-lasting exercise 
in 18°C and 32 °C ambient temperature. Scandinavian Journal of Medicine Science 
in Sports, 4(3), 173–180.
Nielsen, B., Strange, S., Christensen, N.J., Warberg, J., & Saltin, B. (1997). Acute 
and adaptive responses in humans to exercise in a warm, humid environment. Euro-
pean Jornal of Physiology, 434(1), 49–56.
Pandolf, K. B. (1998). Time course of heat acclimation and its decay. International 
Journal of Sports Medicine, 19(Suppl 2), S157–160.
Parkin, J. M., Carey, M. F., Zhao, S., & Febbraio, M. A. (1999). Effect of ambient 
temperature on human skeletal muscle metabolism during fatiguing submaximal 
exercise. Journal of Applied Physiology, 86(3), 902–908.
Parry, E. S., & Lister, I. S. (1975). Sunlight and hyprcalciuria. Lancet, 1(7915), 1063–
1065.
Pilcher, J. J., Nadler, E., & Busch, C. (2002). Effects of hot and cold temperature 
exposure on performance: a meta-analyic review. Ergonomics, 45(10), 682–698.
Rachootin, P., & Olsen, J. (1983). The risk of infertility and delayed conception as-
sociated with exposures in the Danish workplace. Journal f Occupational Medicine, 
25(5), 394–402.
Ramsey, J. D. (1995). Task-performance in het - A review. Ergonomics, 38(1), 154–
165.
Romet, T., & Frim, J. (1987). Physiological responses to fire fighting activities. Euro-
pean Journal of Applied Physiology ad Occupational Physiology, 56(6), 633–638.
Roodenburg, J. (1983). Adaptation of rural minimum temperature forecasts to an ur-
ban environment. Theoretial and Applied Climatology, 32(4), 395–401.
Royburt, M., Epstein, Y., Solomon, Z., & Shemer, J. (1993). Long-term psychologi-
cal and physiological effects of heat sroke. Physiology & Behavior, 54(2), 265–267.
Sawka, M. N., & Young, A. J. (2005). Physiological systems and their responses to 
conditions of heat and cold. In C. M. Tipton, M. N. Sawka, C. A. Tate, & R. L. Ter-
jung (Eds.), ACM′s Advanced Exercise Physiology (p. 535–563). Baltimore, USA: 
Lippincott Williams & Wilkins.
Shapiro, Y., Magazanik, A., Udassin, R., Ben-Baruch, G., Shvartz, E., & Shoen-
feld, Y. (1979). Heat intolerance in former heatstroke patient. Annals of Internal 
Medicine, 90(6), 913–916.
Sharpe, R. M. (2000). Lifestyle and environmental contribution to male infertlity. Brit-
ish Medical Bulletin, 56(3), 630–642.
Cornelis P. BOGERD, Hein A.M. DAANEN: PHYSIOLOGICAL EFFECTS AFTER EXPOSURE ..., 14–23
ANNALES KINESIOLOGIAE • 2 • 2011 • 1
23
Shekarriz, B., & Stoller, M.L. (2002). Uric acid nephrolithiasis: current concepts and 
controversie. The Journal of Urology, 168(4 Pt 1), 1307–1314.
Vander, A., Sherman, J., & Luciano, D. (2001). Human physiology: The mechanisms 
of body function. Boston, USA: McGraw Hill.
Weller, A., Linnane, D., Jonkman, A., & Daanen, H. (2007). Quantification of the 
decay and re-induction of heat acclimation in dry-heat following 12 and 26 days 
without exposure to heat stress. Euroean Journal of Applied Physiology, 102(1), 
57–66.
Wexler, R. K. (2002). Evaluation and treatment of heat-related illesses. American Fam-
ily Physician, 65(11), 2307–2314.
Wyon, D. P., Wyon, I., & Norin, F. (1996). Effects of moderate heat stress on driver 
vigiance in a moving vehicle. Ergonomics, 39(1), 61–75.
Yahav, S., Shamai, A., Haberfeld, A., Horev, G., Hurwitz, S., & Einat, M. (1997). 
Induction of thermotolerance in chickens by temperature conditioning: Heat shock 
protein expressiona. Annalsof the New York Academy of Sciences, 813(1), 628–
636.
Zulkifli, I., Liew, P. K., Israf, D. A., Omar, A. R., & Hair-Bejo, M. (2003). Effects 
of early age feed restriction and heat conditioning on heterophil/lymphocyte ra-
tios, heat shock protein 70 expression and body temperature of heat-stressed broile 
chickens. Journal of Thermal Biology, 28(3), 217–222.
Cornelis P. BOGERD, Hein A.M. DAANEN: PHYSIOLOGICAL EFFECTS AFTER EXPOSURE ..., 14–23