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In a special edition of the Journal of Science and Medicine in Sport, the following articles related to Heat Stress in Sport.

The following is a list of articles featured in this special edition and associated media releases. Click on the article title to view the aricle summary.

Media Releases

Heat stress in sport —Fact and Fiction

Heat stress in sport — some facts: How do you know when you should stop exercising?

Editorials

Heat stress—A challenge for sports science in Australia
John R. Brotherhood

Heat stress in sport—Fact and fiction
Timothy D. Noakes

Heat articles

Heat stress and strain in exercise and sport
John R. Brotherhood

A modern classification of the exercise-related heat illnesses
Timothy David Noakes

Heat-related injuries resulting in hospitalisation in Australian sport
Timothy Robert Driscoll, Raymond Cripps and John R. Brotherhood

The descriptive epidemiology of sports/leisure-related heat illness hospitalisations in New South Wales, Australia
Caroline F. Finch and Soufiane Boufous

The incidence of heat casualties in sprint triathlon: The tale of two Melbourne race events
Cameron McR. Gosling, Belinda J. Gabbe, Jeanne McGivern and Andrew B. Forbes

Reducing the risk of heat-related decrements to physical activity in young people
G.A. Naughton and J.S. Carlson

Physiological limits to exercise performance in the heat
Mark Hargreaves

Double blind carbohydrate ingestion does not improve exercise duration in warm humid conditions
Camila Nassif, Ana Paula Araujo Ferreira, Aline Regina Gomes, Luciana De Martin Silva, Emerson Silami Garcia and Frank E. Marino

Wet-bulb globe temperature (WBGT)—its history and its limitations
Grahame M. Budd

 

 

Editorials

 

Heat stress—A challenge for sports science in Australia
John R. Brotherhood

This issue of the Journal of Science and Medicine in Sport arises from the need for Sports Medicine Australia (SMA) to provide evidence-based guidelines for conducting sport in hot weather that are applicable throughout Australia.

In 2001 SMA released a national policy titled ‘Preventing Heat Illness in Sport’. The aims of the policy were to (1) alert sporting bodies and participants of the risk of heat illness from physical activity in hot weather conditions. (2) Provide a clear cancellation policy for sporting bodies conducting events in hot weather conditions. (3) Educate sporting bodies and participants on methods of minimizing the risk of heat illness and the avoidance of situations that may worsen heat illness. The policy recommended the wet bulb globe temperature (WBGT) as the best measure of heat ‘strain’ and indicated levels of risk of heat injury according to the WBGT. Specifically the policy stated that “At WBGT greater than 28 degrees Celsius there is extreme risk of heat injury to all participants”, and prescribed that “sporting events or activities requiring moderate to intense exercise should be postponed or cancelled when the WBGT exceeds 28 degrees Celsius”. The policy was based on the 1984 American College of Sports Medicine Position Stand—Prevention of Heat Injuries During Distance Running.1

The Queensland branch of SMA soon questioned this policy. They pointed out that if the direction regarding cancellation/postponement was to be followed Australia-wide no responsible sporting agency would risk scheduling any competitive sport during the summer months in Queensland. Yet a wide range of amateur and professional sport is enjoyed in Queensland on a daily basis in summer without undue restriction, and there is little evidence of catastrophic heat injuries during sporting participation.2

Queensland's concern highlights the difficulty of setting environmental limits for sports participation. Such limits must be based on good evidence that unacceptable numbers of heat casualties would occur if sport was carried on in conditions that exceed the limits; otherwise they are likely to restrict sport unnecessarily. Environmental limits might also vary between geographical regions because humans adapt to variations in climate through factors such as behaviour and acclimatisation.

Heat casualties do occur in Australian sport, but they affect only a small number of participants. They are not restricted to energetic sports such as running and football, but can also occur in cricket, golf and bowls,3 presumably because these sports can involve long periods of exposure to hot weather. Hot and humid conditions are usually considered to be the principal cause of heat casualties in sport, but exertional heat exhaustion also occurs in cool weather in community fun runs such as the Sydney City to surf. Over-motivation and running too hard with inadequate training appears to cause many of these cases.4 Most cases of sport-related heat illness are probably post-exercise hypotension or heat exhaustion.5 With initial aid they recover without complication and need for referral to the health system. Heat stroke seems to be rare.3

Answers to some fundamental questions are required to develop evidence-based management of heat stress in the wide range of sports enjoyed throughout Australia. These are what are the incidence, nature and severity of heat casualties, and in what sports do they occur What are the human factors, including behaviour, and what are the environmental factors, that result in heat casualties What are the impacts of environmental heat on comfort and performance What are the most appropriate methods for assessing and predicting the impact of heat stress on sports participants This issue of the journal addresses some of these questions. If it does not provide all the answers, it does aim to focus attention on relevant targets and challenges for research to develop objective strategies for managing heat stress in sport.

In 2005 Sports Medicine Australia released revised guidelines for playing and exercising safely in hot weather.6 The guidelines note that heat stress varies with exercise intensity, they warn of the dangers of over-motivation, and they point out the need to watch for potential heat casualties in vigorous activity, even in cool weather. They recommend modifying activities according to environmental conditions including the options of postponing or cancelling events. They also stress the importance of prompt assessment and first aid to minimize the impact of heat illness.

I am most grateful to all the authors who have contributed to this issue of the journal, but especially to Grahame Budd; Tim Driscoll and Ray Cripps; Caroline Finch and Soufiane Boufous; Mark Hargreaves; and Timothy Noakes for their generous responses to my invitation to contribute papers.

 

Heat stress in sport—Fact and fiction
Timothy D. Noakes

The past century has witnessed a remarkable growth in our understanding of the physiological changes that occur when humans exercise in the heat. And why there are sometimes pathological consequences.

The gold mining industry in South Africa, conducted as much as 4 km below the earth's surface where the temperature at the rock face exceeds 50 °C is but one example of an enterprise made possible by that knowledge.1 Nor would it be possible for belligerent nations to conduct war in the desert but for the studies initiated by the British military in India and Mesopotamia, now Iraq, before and during the First World War.[2], [3] and [4]

Thus, a 100 years ago it was believed that the direct effects of the sun's rays on the head and spine[4] and 5] caused the condition of “sunstroke”. Prevention required that human habitations in the sunny regions of the world should have especially thick roofs. Mad Englishmen exposed to the mid-day sun wore “thick pith topees or an efficient service helmet” and “spinal pads 9 in. wide” (p.394) to deflect these harmful rays. Then Sambon6 suggested that heatstroke was caused by an infectious agent that “may be conveyed to man with dust blown by the wind or thrown up under the tread of a marching column. It is then inhaled into the lungs, or ingested into the alimentary canal, where it produces the deadly toxin which probably… sets up the symptoms of the disease” (p.748). This theory was based on an apparently endemic distribution of heatstroke cases only in specific regions and its absence in adjacent areas with “precisely similar climatic influences” (p.745). This incorrect theory was neatly disproved by a remarkable 3-year study7 which established that cases of heatstroke in the British Army in India were “endemic” only to the hottest and most humid areas. As a result Rogers concluded that “the hyperpyrexia is caused by a failure of the cooling mechanism of the body during exposure to heat, especially if accompanied by much moisture in the air and (is) of prolonged duration” (p.32). Rogers also established that the correct treatment was to place affected patients in a cold bath. These were quite remarkable conclusions at the time.

This classic era of research left us with two other findings which may have been overlooked. First that British soldiers in Mesopotamia during the First World War developed heatstroke only after they had visibly stopped sweating.8 This conflicts with the condition of heatstroke in modern athletes all of whom, in my experience, are actively sweating at the time of collapse. The absence of sweating in classically described heatstroke would not be due to profound dehydration but is more probably related to a neural mechanism inhibiting sweating. Second that there were only two forms of illness directly caused by heat exposure: Heatstroke (heat hyperpyrexia) which occurred in those who stopped sweating and was associated with an altered level of consciousness; and Heat Exhaustion which was a form of syncopy due to postural hypotension that was easily treated by simply lying the patients down until they had recovered. It is my opinion that these are still the two primary diagnoses that should be considered in those who collapse during exercise in the heat.9

The theory that humans evolved our presently long-legged, hairless and sweaty torsos in order to hunt non-sweating antelope on the sultry African savannah was also first advanced in 1900[10] and [11] and has since achieved scientific respectability. Thus, some believe that our ability to perform feats of unequalled endurance in severe dry heat is the defining characteristic that began our evolutionary road to Homo sapiens 2–3 million years ago.12

Alongside these remarkable achievements over the past century have been some notable errors. The adoption of a false physiology produced a novel disease, exercise-associated hyponatraemia (EAH) with sometimes fatal consequences.13 The scientific process must always remain fiercely independent of external influences that desire predetermined outcomes.

This special issue of the journal contains articles that review current ideas relating to exercise in the heat. In the great tradition of Australian medical and scientific research, these articles address practical issues and contain fresh ideas that challenge some hardy dogmas.

Brotherhood14 challenges the concept that environmental heat indices alone can be used to determine when it is safe to exercise. He makes the telling point that it is the metabolic rate that determines the risk that heat injury will occur during exercise, regardless of the environmental conditions. Thus, there are environmental conditions in which for example, it is perfectly safe (albeit uncomfortable) to play a championship tennis match but in which it would be extremely hazardous to attempt to break the world record in a 5–10 km running race. This is not a novel idea but seems somehow to have been forgotten by many modern thermal physiologists.

He proposes the use of a Heat Stress Index (HSI) that compares the heat load acting on the athlete from exercise and the environment that must be dissipated by sweat evaporation (Ereq) with the maximum capacity of the environment to evaporate sweat (Emax). Provided Emax exceeds Ereq so that the HSI is less than 100% body temperature can be controlled and exercise can be safely performed. Brotherhood also argues that the human body is not designed for a catastrophe failure; it has fail-safe mechanisms that almost always terminate exercise before disaster strikes. Thus, almost all athletes will alter their behaviours and so reduce their rates of heat production before they develop heatstroke. Had humans been designed for failure, our ancestors would not have survived their antelope hunts in mid-day African heat. In which case some other species would have produced this journal.

Budd's article15 reinforces some of the points made by Brotherhood. He thoroughly reviews the development of the Wet Bulb Globe Temperature (WBGT) index and confirms that humans cope in extreme environments, for example fighting Australian bushfires, by modifying their behaviours. He concludes that the WBGT works well when used in defined populations and circumstances such as recruit training in the United States Marine Corp, for which it was developed. He points out that the WBGT underestimates the stress imposed by high humidity and low wind movement, both of which restrict heat loss by evaporation. He also warns that equations for estimating the WBGT that exclude the Natural Wet Bulb and Globe Temperatures are invalid. He concludes that the WBGT can provide “only a general guide to the likelihood of adverse effects of heat” so that measuring the individual elements of the thermal environment provides a better assessment. This is achieved by the techniques proposed by John Brotherhood.

Driscoll et al.16 have determined the number of persons hospitalized for the treatment of exercise-related “heat” illnesses in Australia whereas Finch and Boufous17 have performed the same analysis for the state of New South Wales. The relatively large number of cases occurring in activities of low intensity in both studies suggests that not all can be due to a failure of heat loss leading to excessive heat accumulation. Perhaps many cases occurring in activities like walking, lawn bowls, golf, fishing, cricket and softball and even swimming might be due to exercise-associated postural hypotension9 in which there is no abnormal heat retention. Finch and Boufous suggest that perhaps the diagnostic categories for hospital admissions for “heat” illness should be reviewed both in Australia and elsewhere. Interestingly the term “sunstroke” is still used as are the terms heat syncope and heat exhaustion that in my opinion are the same condition and are more usefully considered as exercise-associated postural hypotension.9

Gosling et al.18 show that many more cases of “heat illness” occurred in the first of two Melbourne triathlon races held in similar environmental conditions 2 months apart. Thus, whereas 15 such cases, three of heatstroke, occurred in the first race held in unseasonably hot weather at the start of summer, in the second race there were none. The authors concluded that the absence of cases in the second race was probably the result of superior heat acclimatization achieved by the competitors training in the summer heat. Interestingly the three cases of (probable) heat stroke occurred in the shorter distance (sprint) triathlon that was completed in times ranging from 23 to 52 min and before significant “dehydration” could have occurred.

Naughton and Carlson19 review the literature pertaining to children exercising in the heat. They correctly conclude that children should not be precluded from physical activity simply because the external environment is hot and humid. In fact, it is my impression that there are few if any reports of heatstroke occurring in children during exercise. Thus, if children are indeed less able than adults to lose heat during exercise in hot, humid conditions, as is usually argued, then some other factor must protect them from developing heatstroke during exercise. Perhaps it is because unlike adults they “listen to their bodies” so that they rest when they perceive they are becoming too hot. There is a saying that no horse ever ran itself to death without a jockey on its back. Perhaps the same applies to children exercising in the heat.

Hargreaves2 reviews the evidence that performance during exercise in the heat is impaired by a “complex regulation and integration of thermoregulatory and motor control systems”, the understanding of which “is a significant challenge for the future”. He proposes that the only ways to modify this control is through effective pre-acclimatization to heat, pre-cooling prior to exercise and appropriate fluid ingestion during exercise.

Indeed the complexity of this control is thoroughly tested by Nassif et al.21 They evaluated the effect on exercise performance of the belief that carbohydrate is being ingested during exercise. They found that compared to placebo ingestion, time to exhaustion was not increased by carbohydrate ingestion if (i) subjects did not know for certain that they were ingesting carbohydrate and (ii) if the carbohydrate was ingested in the form of a capsule that prevented the detection of its ingestion by postulated pharyngeal (carbohydrate) receptors. In contrast, when subjects knew for certain that they were ingesting carbohydrate, even when contained in a capsule, their time to exhaustion increased by 24% compared to placebo ingestion. They concluded that this effect “could have been solely the result of suggestion” and that coaches and trainers of endurance athletes need to be aware of the potential value of this placebo effect.

These papers make an important contribution further to advance our admiration of the remarkable human capacity safely to exercise in uncomfortably hot conditions and of the complexity of the controls that allow this to happen.

 

Heat articles

 

Heat stress and strain in exercise and sport
John R. Brotherhood

Heat stress arising from the thermal environment is of concern to sports medicine and to sports administration because of the perceived risk of heat casualties, in particular heat stroke. Many sports organizations recommend environmental indices such as the WBGT for assessing risk and setting environmental limits for training and competition. But the limits are not justified by evidence. This article describes the nature of heat stress in sport and how it may be assessed objectively. Heat stress and the principal human responses to exercise heat stress are reviewed briefly. Metabolic heat production and the thermal environment provoke separate and largely independent physiological strains. Metabolic heat production drives body core temperature, and the thermal environment drives skin temperature; the combined stresses are integrated to drive sweat rate. Control of core temperature depends on adequate sweat production and the capacity of the environment to evaporate the sweat. The nature of exercise heat stress is demonstrated by rational analysis of the physical heat exchanges between the body and the environment. The principles of this analysis are applied to critical review of current practice in the assessment of heat stress in sport. The article concludes with discussion of research to establish methods for objective sport-specific assessment of heat stress.

 

A modern classification of the exercise-related heat illnesses
Timothy David Noakes

This article proposes a novel framework classification for the heat illnesses. It argues that heat stroke is the only described condition that is truly a “heat illness” since it is the only condition in which there is clear evidence for a pathological elevation of the core body temperature. If this is correct the non-descript terms such as heat fatigue, heat exhaustion and heat syncopy should be removed from the modern lexicon. Since the evidence is that most cases of post-exercise collapse are due to the development of postural hypotension immediately on the cessation of exercise, it is further proposed that more specific terms such as exercise-associated postural hypotension should be used, when appropriate, to replace the non-descript terms such as heat exhaustion, heat fatigue or heat syncopy. Furthermore this novel classification acknowledges that heat stroke may occur in some as a result of accelerated rates of endogenous heat production (thermogenesis). It also suggests that the elevated body temperature alone may not be the sole cause of fatal outcomes in heat stroke but that toxic chemicals released from damaged muscles by the processes causing this accelerated thermogenesis may also be involved.

 

Heat-related injuries resulting in hospitalisation in Australian sport
Timothy Robert Driscoll, Raymond Cripps and John R. Brotherhood

The aim of this study was to summarise the extent and characteristics of cases of illness due to environmental heat, significant enough to result in hospitalisation, and arising during sporting activity in Australia. Cases were identified from the hospital separations database compiled by the Australian Institute of Health and Welfare, using the allocated external cause and diagnosis codes and the activity code “While engaged in sports”. Hospital separations for the 2 years 2002–2003 and 2003–2004 were used. One hundred and forty eight cases were identified (68% male). Cases were fairly evenly distributed across 10-year age groups starting from age 15 years, apart from fewer cases between 55 and 64 years. Nearly two thirds of the cases occurred in the summer months (December to February inclusive). The most commonly involved individual sports were lawn bowls, cricket, softball, golf, marathon running and walking, and the rate was highest for triathlons, lawn bowls, cricket, and running. Rates for persons aged 65 years or older were more than twice the rates at younger ages. Heat-related disorders are an uncommon cause of significant morbidity in Australians participating in sporting activity. However, particular sports have a relatively high rate of occurrence and these sports would provide an appropriate focus for prevention activity. The availability of a specific code in the International Classification of Diseases and Injuries to cover excessive endogenous production of heat would assist future analyses of the role of thermoregulatory disturbance in leading to morbidity in persons participating in sporting activity.

 

The descriptive epidemiology of sports/leisure-related heat illness hospitalisations in New South Wales, Australia
Caroline F. Finch and Soufiane Boufous

Sport-related heat illness has not been commonly studied from an epidemiological perspective. This study presents the descriptive epidemiology of sports/leisure-related heat illness hospitalisations in New South Wales, Australia. All in-patient separations from all acute hospitals in NSW during 2001–2004, with an International Classification of Diseases external cause of injury code indicating “exposure to excessive natural heat (X30)” or any ICD-10 diagnosis code in the range: “effects of heat and light (T67.0–T67.9)”, were analysed. The sport/leisure relatedness of cases was defined by ICD-10-AM activity codes indicating involvement in sport/leisure activities. Cases of exposure to heat while engaged in sport/leisure were described by gender, year, age, principal diagnosis, type of activity/sport and length of stay. There were 109 hospital separations for exposure to heat while engaging in sport/leisure activity, with the majority occurring during the hottest months. The number of male cases significantly increased over the 4-year period and 45+-year olds had the largest number of cases. Heat exhaustion was the leading cause of hospital separation (40% of cases). Marathon running, cricket and golf were the activities most commonly associated with heat-related hospitalisation. Ongoing development and refinement of expert position statements regarding heat illnesses need to draw on both epidemiological and physiological evidence to ensure their relevance to all levels of risk from the real world sport training and competition contexts.

 

The incidence of heat casualties in sprint triathlon: The tale of two Melbourne race events
Cameron McR. Gosling, Belinda J. Gabbe, Jeanne McGivern and Andrew B. Forbes

Triathlon is a popular participation sport combining swimming, cycling and running into a single event. The Triathlon Australia medical policy advocates the use of wet bulb globe temperature as the criterion for altering race distance and an ambient temperature of 35 °C as a criterion for consideration of cancellation of an event, but there is little empirical evidence detailing the effectiveness of this policy. Nor has the impact of environmental thermal stress on triathletes in shorter duration events been determined. During an injury surveillance investigation of a triathlon race series over the 2006/2007 seasons, two events with similar environmental conditions were completed. One thousand eight hundred and eighty-four participants competed in event 1 (December 2006) and 2000 competed in event 2 (February 2007). Maximum dry bulb (DBT), minimum vapour pressure (VP) and minimum relative humidity (RH) for event 1 were 37 °C DBT, 0.56 kPa VP and 9% RH measured by the Bureau of Meteorology. Fifty-three participants presented for medical aid, 15 due to heat-related collapse. The conditions measured for event 2 were 33 °C DBT, 1.16 kPa VP and 24% RH and there were no heat illness presentations despite 38 individuals presenting for medical aid. These observations suggest that the risk of heat-related collapse is greatest when high-environmental temperatures occur early in the competitive season when participants may be inadequately prepared and have not yet acquired natural acclimatisation to heat. Any Triathlon Australia policy revision could place stronger emphasis on the use of ambient temperature as a limiting criterion for race organisers.

 

Reducing the risk of heat-related decrements to physical activity in young people
G.A. Naughton and J.S. Carlson

The purpose of this review is to highlight differences in thermoregulatory responses during activity of children and adolescents compared with adults. Some differences are due to movement inefficiency and physical size such as body surface area to body mass ratio, and body composition. Identified physiological differences in sweat rates appear to alter with maturation, at least in boys, but the research remains incomplete. A number of findings from hydration studies with young people exercising in the heat are also discussed. The research on clothing is adult-based, but key concepts from this research also apply to children. The final section addresses the limited research on acclimatization of children to hot conditions. Specific recommendations for children who are active in the heat conclude this review.

 

Physiological limits to exercise performance in the heat
Mark Hargreaves

Exercise in the heat results in major alterations in cardiovascular, thermoregulatory, metabolic and neuromuscular function. Hyperthermia appears to be the key determinant of exercise performance in the heat. Thus, strategies that attenuate the rise in core temperature contribute to enhanced exercise performance. These include heat acclimatization, pre-exercise cooling and fluid ingestion which have all been shown to result in reduced physiological and psychophysical strain during exercise in the heat and improved performance.

 

Double blind carbohydrate ingestion does not improve exercise duration in warm humid conditions
Camila Nassif, Ana Paula Araujo Ferreira, Aline Regina Gomes, Luciana De Martin Silva, Emerson Silami Garcia and Frank E. Marino

The positive effects of carbohydrate (CHO) supplementation on endurance exercise are well documented but the placebo (PLAc) effect can make the ergogenic qualities of substances more difficult to determine. Therefore, this study tested the effect of double blind ingestion of PLAc and CHOc in capsules versus known capsule (CHOk) ingestion on prolonged exercise heat stress. Nine well trained male volunteers (mean ± S.D.: 23 ± 3 years; 62.4 ± 6.5 kg and 65.8 ± 5.2 mL kg−1 min−1 peak oxygen consumption) exercised at 60% of maximum power output until volitional exhaustion (TTE) in the three different conditions. Capsules were ingested with 252 ± 39 mL of water. Blood glucose in CHOc and CHOk was similar but higher (p < 0.05) than PLAc from 45 min to end of exercise. There were no differences in TTE between PLAc (125.2 ± 37.1 min) or CHOc (138.8 ± 47.0 min) or between CHOc and CHOk (155.8 ± 54.2 min). Time to volitional exhaustion was different between PLAc and CHOk (p < 0.05). Increased TTE resulted when participants and researchers knew the capsule content, but not in the double blind condition. The difference could be related to a combined effect of CHO ingestion and knowledge of what was ingested possibly acting as a potent psychological motivator.

 

Wet-bulb globe temperature (WBGT)—its history and its limitations
Grahame M. Budd

Wet-bulb globe temperature (WBGT) is nowadays the most widely used index of heat stress, yet many users appear to be unaware of its history and its limitations.

History of WBGT: WBGT was invented and first used during the 1950s as one element in a successful campaign to control serious outbreaks of heat illness in training camps of the United States Army and Marine Corps. Control measures based on air temperature and humidity, and applied to all trainees alike, had proved effective but had entailed excessive compliance costs in the form of lost training time. New control measures introduced in 1956 further reduced heat illness and also lost fewer training hours. Crucial innovations were (1) replacing the temperature and humidity measurements with WBGT, which additionally responds to sun and wind, (2) using epidemiologic analyses of casualty records to identify hazardous levels of WBGT and vulnerable trainees, and (3) protecting the most vulnerable trainees by suspending drill at lower levels of WBGT, and by improving their heat tolerance in special conditioning platoons. This campaign has considerable relevance to the prevention of heat illness in sport.

Limitations of WBGT: WBGT's most serious limitation is that environments at a given level of the index are more stressful when the evaporation of sweat is restricted (by high humidity or low air movement) than when evaporation is free. As with all indices that integrate elements of the thermal environment, interpretation of the observed levels of WBGT requires careful evaluation of people's activity, clothing, and many other factors, all of which can introduce large errors into any predictions of adverse effects. Moreover, the accuracy of WBGT is being eroded by measurement errors associated with the omission of the globe temperature, with non-standard instrumentation, and with unsatisfactory calibration procedures. Because of the above limitations WBGT can provide only a general guide to the likelihood of adverse effects of heat. A much clearer assessment can be obtained by measuring the individual elements of the thermal environment, and using those measurements to estimate the requirement for evaporative cooling, the likelihood of achieving it, and more accurate and comprehensive indices of heat stress.

 

 

 


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