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, 4
Thus, a 100 years ago it was believed that the direct effects of the sun's rays on the head and spine4, 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 190010, 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 5–10km 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 52min 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.
Hargreaves20 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.
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