Chapter 48
Exercise in the Heat

with Timothy Noakes

*This Chapter is online in its entirety. Click on the links below to browse through the whole chapter.*

Mechanisms of heat gain and loss
Clinical Perspective
Heatstroke - a temperature above 41ºC
Exercise-associated collapse
Cramps

Heat stroke - a temperature < 41 degrees C

When running, metabolic rate is a function of running speed and body mass; thus, the highest rectal temperatures are usually seen in the fastest runners competing in events from 8-21 km. In such runners, the rectal temperatures may increase to 40.5 degrees C without symptoms or evidence of heat-related illness ([4, 5]. Higher rectal temperatures are usually associated with symptoms that include dizziness, weakness, nausea, headache, confusion, disorientation and irrational behavior including aggressive combativeness, or drowsiness progressing to coma. Examination reveals the patient is hypotensive and has tachycardia. 

If, during exercise, a previously healthy athlete shows marked changes in mental functioning - for example, collapse with unconsciousness, or a reduced level of consciousness (stupor, coma) or mental stimulation (irritability, convulsions) - in association with a rectal temperature greater than 41 degrees - the diagnosis of heatstroke is confirmed and warrants immediate initiation of cooling. 

Management of heatstroke

The more rapidly the rectal temperature is reduced to 38 degrees C the better the prognosis. The patient should be placed in a bath of ice water for 5-10 minutes. The body temperature should decrease to 38 degrees C within this time [6]. Care must be taken to avoid inducing hypothermia as rectal temperature lags behind the core temperature. Shivering indicates that core temperature has decreased to 37 degrees C or below. Although there is no evidence that dehydration is the single critical factor causing heatstroke, intravenous fluids may be given to correct the expected dehydration and to assist stabilizing the hyperkinetic circulation. Thus, 1 to 1.5 L of a 0.5 or 0.9% saline solution can be given initially, in part to ensure rapid venous access, should this be required. Mortality from heatstroke should be zero in healthy athletes who are cooled promptly. Indeed, it is usual for athletes to be fully recovered and ambulatory within 30-60 minutes of collapse, providing they are correctly and expeditiously treated. 

Is hospital admission indicated 

The medical team must decide whether or not to admit the athlete to hospital for further observation after his or her temperature has been reduced to <30 degrees C. There is a tendency for rectal temperature to increase after cooling; this increase may not be noticed if the patient returns home without appropriate supervision. An increasing rectal temperature after cessation of exercise and appropriate cooling indicates ongoing heat-generating biochemical processes in muscle, unrelated to exercise that may be related to conditions like malignant hyperthermia. 

Hospital admission is always required if the patient fails to regain consciousness within 30 minutes of appropriate therapy that returns the rectal temperature to 38 degrees C. Patients who regain consciousness rapidly, whose cardiovascular system is stable, and whose rectal temperature does not increase in the first hour after active cooling ceases usually do not need hospital admission. Thus, the decision as to whether hospital admission is needed can usually be made within an hour of the patient reaching medical treatment. 

An absolute indication for hospital admission would be a failure to achieve cardiovascular stability during that time. A persisting tachycardia and hypotension in the lying position suggest that cardiogenic shock is developing. As heatstroke is an uncommon complication during exercise it should raise the possibility that other factors may be operative. These include genetic predisposition, unaccustomed drug use, or subclinical viral infection. 

Complications of heat stroke

Heatstroke may damage one or more body systems as shown in Table 48.2. It appears that there is an individual susceptibility to heatstroke. Malignant hyperthermia, which is usually activated by certain general anesthetic agents, may also be triggered by other stimuli, perhaps including exercise. The biochemical abnormality resides in skeletal muscle where it may activate uncontrolled metabolism and hyperthermia, and ultimately an extensive, and potentially fatal, rhabdomyolisis (degeneration of skeletal muscle). The process can only be reversed by a specific drug, dantrolene sodium or by rapid whole-body cooling. Patients suffering rhabdomyolysis present with brown-colored urine accompanied by muscle weakness, swelling and pain. The skin may become discolored because of hemorrhages and the muscles have a 'doughy' feel. The urine contains high levels of myoglobin, which causes the brown discoloration and granular casts. Serum creatine kinase levels are also high. Laboratory tests may reveal elevated levels of potassium and uric acid and, in severe cases, evidence of disseminated intravascular coagulation. This condition requires urgent intensive care treatment. 

Table 48.2 Complications of heatstroke

Exercise-associated collapse

Exercise-associated collapse (EAC) describes the common type of collapse that occurs in athletes who successfully complete endurance events without distress, but who suddenly develop symptoms and signs of postural hypotension when they stop exercising. This condition has been referred to as 'heat syncope' and 'heat exhaustion' but we avoid these terms as the condition is benign and the rectal temperature is generally not abnormally elevated. The largest modern study of subjects who required medical attention after long-distance events found that only a tiny proportion of participants had markedly elevated rectal temperatures and few required hospitalization [7]. 

This phenomenon of collapse after completing a sporting event in the heat occurs because the sudden cessation of exercise induces postural hypotension by causing blood to pool in the dilated capacitance veins in the lower limb when the 'second heart' action of the lower limb musculature stops. In addition, there may be abnormal perfusion of the splanchnic circulation with loss of a large fluid volume into the highly compliant splanchnic veins. The problem is a precipitous fall in the central (rather than circulating) blood volume and hence, atrial filling pressures [8-11]. The early publications referring to this condition did not find elevated rectal temperatures and used the terms 'heat exhaustion', 'heat prostration' or 'heat syncope' to describe the condition of collapse due to postural hypotension that develops in people who exercise in the heat. Unfortunately, this terminology has been misinterpreted to indicated the collapse is caused by elevated body temperature and failure of heat regulation. 

The diagnosis of EAC can be made on the basis of a typical history, findings of a postural hypotension reversed by lying supine with the pelvis and legs elevated, and the exclusion of readily identifiable medical syndromes such as diabetes, heatstroke as discussed earlier (also Chapter 39). 

Management of exercise associated collapse

As patients with EAC are conscious, they can be encouraged to ingest fluids orally during recovery. Sports drinks containing both glucose (4-8%) and electrolytes (Na 1-20mM) are appropriate. The patients should lie with their pelvis and legs elevated. Nursing patients in this head-down position is always dramatically effective, producing a more stable cardiovascular system within 30-90s and, usually, instant reversal of symptoms. The symptoms of dizziness, nausea and vomiting associated with this condition may result simply from a sudden reduction in blood pressure, especially as there is a dramatic fall from the elevated blood pressure maintained during exercise. Generally, recovery occurs within 10-20 minutes. Most athletes with EAC will be able to stand and walk unaided within 10-30 mins of appropriate treatment and can be encouraged to leave the facility at that time. 

Few, if any athletes with EAC are sufficiently dehydrated to show the usual clinical signs of dry mucous membranes, loss of skin turgor, sunken eyeballs and an inability to spit. Some clinicians advocate intravenous therapy when these signs are present but we only use intravenous therapy in athletes who continue to have increased heart rates (>100 beats/min) and hypotension (<110 mmHg) when lying supine with the legs and pelvis elevated above the level of the heart.