Key points• People with age over 60 years, obesity, cardiovascular disease, pulmonary disease or long-standing diabetes are at increased risk of heat-related illness during heat waves because of physiological impairments in the regulation of body core temperature in hot conditions.• A homebound lifestyle, lack of contact with other people and decreased mobility can also contribute to an increased risk of heat-related illness.• Working home air conditioners, fans, access to transportation and access to cool environments during prolonged heat events have a protective effect against heat-related illness and deaths.• Physicians should be aware of these risk factors and protective factors against heat illness, and should counsel at-risk patients accordingly.CMAJ 2009. DOI:10.1503/cmaj.081050Previously published at www.cmaj.caReview rise in body core temperature may lead to heat illness and eventually death. Exposure to the combination of external heat stress and metabolically generated heat can lead to heat-related disorders. The prevalence of heat stress symptoms increases in direct proportion to the elevation of body core temperature. The major heat-related disorders -heat cramps, heat exhaustion and heatstroke -involve various degrees of thermoregulatory failure, which occurs when a person is exposed to excessive heat or elevations in body core temperature over a prolonged period. Risk factors for heat stress AgeObservational studies have shown that people aged 60 years and older are among the worst affected by extreme heat, 3−5 with those living in institutions, confined to bed or living alone having the highest rates of illness, injury and death. 5,8,15−17 In their ecological time-series study, Fouillet and associates 2 showed that during the 2003 heat wave in Europe, mortality ratios (ratios of observed deaths to expected deaths) in France increased continuously with age, from 1.3 for people 35-74 years of age to more than 1.7 for those over the age of 75 (Figure 1). Although the greater prevalence of comorbidities and medication use in this population may be responsible for some of the heat-related deaths, laboratory-based physiological studies have indicated that the ability to sense heat 20 and to manifest appropriate behavioural (especially fluid intake) 21−26 and physiological (e.g., blood distribution, sweating) responses 27−33 during exposure to heat may be compromised in otherwise healthy older individuals.The ability to physiologically maintain body core temperature during heat stress becomes compromised with age. 27 This decrease in thermoregulatory ability can be attributed to a combination of factors, including changes in sweating, [28][29][30]34 blood flow to the skin 30,31,34,35 and cardiovascular function. 32The problem can be exacerbated by the decreases in overall physical fitness and increases in body adiposity that may accompany aging. 36 Experts have suggested that, in combination, these age-related changes in thermoregulatory and cardiovascular function can decrease the body's abilit...

Hot ambient conditions and associated heat stress can increase mortality and morbidity, as well as increase adverse pregnancy outcomes and negatively affect mental health. High heat stress can also reduce physical work capacity and motor-cognitive performances, with consequences for productivity, and increase the risk of occupational health problems. Almost half of the global population and more than 1 billion workers are exposed to high heat episodes and about a third of all exposed workers have negative health effects. However, excess deaths and many heat-related health risks are preventable, with appropriate heat action plans involving behavioural strategies and biophysical solutions. Extreme heat events are becoming permanent features of summer seasons worldwide, causing many excess deaths. Heat-related morbidity and mortality are projected to increase further as climate change progresses, with greater risk associated with higher degrees of global warming. Particularly in tropical regions, increased warming might mean that physiological limits related to heat tolerance (survival) will be reached regularly and more often in coming decades. Climate change is interacting with other trends, such as population growth and ageing, urbanisation, and socioeconomic development, that can either exacerbate or ameliorate heat-related hazards. Urban temperatures are further enhanced by anthropogenic heat from vehicular transport and heat waste from buildings. Although there is some evidence of adaptation to increasing temperatures in high-income countries, projections of a hotter future suggest that without investment in research and risk management actions, heat-related morbidity and mortality are likely to increase.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimize performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimize performance is to heat acclimatize. Heat acclimatization should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimize dehydration during exercise. Following the development of commercial cooling systems (e.g., cooling vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organizers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimizing the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events for hydration and body cooling opportunities when competitions are held in the heat.

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Heat balance in humans is maintained at near constant levels through the adjustment of physiological mechanisms that attain a balance between the heat produced within the body and the heat lost to the environment. Heat balance is easily disturbed during changes in metabolic heat production due to physical activity and/or exposure to a warmer environment. Under such conditions, elevations of skin blood flow and sweating occur via a hypothalamic negative feedback loop to maintain an enhanced rate of dry and evaporative heat loss. Body heat storage and changes in core temperature are a direct result of a thermal imbalance between the rate of heat production and the rate of total heat dissipation to the surrounding environment. The derivation of the change in body heat content is of fundamental importance to the physiologist assessing the exposure of the human body to environmental conditions that result in thermal imbalance. It is generally accepted that the concurrent measurement of the total heat generated by the body and the total heat dissipated to the ambient environment is the most accurate means whereby the change in body heat content can be attained. However, in the absence of calorimetric methods, thermometry is often used to estimate the change in body heat content. This review examines heat exchange during challenges to heat balance associated with progressive elevations in environmental heat load and metabolic rate during exercise. Further, we evaluate the physiological responses associated with heat stress and discuss the thermal and nonthermal influences on the body's ability to dissipate heat from a heat balance perspective.

Age-associated functional declines and the accompanying risk of work-related injury can be prevented or at least delayed by the practice of regular physical activity. Older workers could optimally pursue their careers until retirement if they continuously maintain their physical training.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimise performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimise performance is to heat acclimatise. Heat acclimatisation should comprise repeated exercise-heat exposures over 1–2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimise dehydration during exercise. Following the development of commercial cooling systems (eg, cooling-vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organisers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimising the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events, for hydration and body cooling opportunities, when competitions are held in the heat.

We assessed whether comparisons of thermoregulatory responses between groups unmatched for body mass and surface area (BSA) should be performed using a metabolic heat production (prod) in Watts or Watts per kilogram for changes in rectal temperature (ΔTre), and an evaporative heat balance requirement (Ereq) in Watts or Watts per square meter for local sweat rates (LSR). Two groups with vastly different mass and BSA [large (LG): 91.5 ± 6.8 kg, 2.12 ± 0.09 m(2), n = 8; small (SM): 67.6 ± 5.6 kg, 1.80 ± 0.09 m(2), n = 8; P < 0.001], but matched for heat acclimation status, sex, age, and with the same onset threshold esophageal temperatures (LG: +0.37 ± 0.12°C; SM: +0.41 ± 0.17°C; P = 0.364) and thermosensitivities (LG: 1.02 ± 0.54, SM: 1.00 ± 0.38 mg·cm(-2)·min(-1)·°C(-1); P = 0.918) for sweating, cycled for 60 min in 25°C at different levels of prod (500 W, 600 W, 6.5 W/kg, 9.0 W/kg) and Ereq (340 W, 400 W, 165 W/m(2), 190 W/m(2)). ΔTre was different between groups at a prod of 500 W (LG: 0.52 ± 0.15°C, SM: 0.92 ± 0.24°C; P < 0.001) and 600 W (LG: 0.78 ± 0.19°C, SM: 1.14 ± 0.24°C; P = 0.007), but similar at 6.5 W/kg (LG: 0.79 ± 0.21°C, SM: 0.85 ± 0.14°C; P = 0.433) and 9.0 W/kg (LG: 1.02 ± 0.22°C, SM: 1.14 ± 0.24°C; P = 0.303). Furthermore, ΔTre was the same at 9.0 W/kg in a 35°C environment (LG: 1.12 ± 0.30°C, SM: 1.14 ± 0.25°C) as at 25°C (P > 0.230). End-exercise LSR was different at Ereq of 400 W (LG: 0.41 ± 0.18, SM: 0.57 ± 0.13 mg·cm(-2)·min(-1); P = 0.043) with a trend toward higher LSR in SM at 340 W (LG: 0.28 ± 0.06, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.057), but similar at 165 W/m(2) (LG: 0.28 ± 0.06, SM: 0.28 ± 0.12 mg·cm(-2)·min(-1); P = 0.988) and 190 W/m(2) (LG: 0.41 ± 0.18, SM: 0.37 ± 0.15 mg·cm(-2)·min(-1); P = 0.902). In conclusion, when comparing groups unmatched for mass and BSA, future experiments can avoid systematic differences in ΔTre and LSR by using a fixed prod in Watts per kilogram and Ereq in Watts per square meter, respectively.