Exercise Associated Collapse and Death in Thoroughbred Racehorses: A Mechanistic Argument for Heat Stroke as the Silent Killer

Abstract

Meg Brownlow

For some decades, cases of acute collapse followed by death during or shortly after racing have been attributed to ‘acute heart failure’, the premise being that an underlying cardiac abnormality becomes activated during strenuous exercise, triggering a lethal arrythmia which causes collapse and death. This has been acknowledged as a speculative diagnosis, because affected horses have not been examined at the point of collapse or during their demise, and in the majority of cases a thorough post mortem examination does not provide a definitive diagnosis of cardiac pathology.

In a recent editorial penned by a special interest group of veterinarians, the Exercise-Associated Sudden Death (EASD) condition was discussed at length, but there was no reference to the effect of adverse environmental conditions or heat shock/stroke as the possible cause or even a risk factor.

The reader may at this point be wondering how a racehorse could be affected by heat shock/stroke so quickly as to cause death in a matter of minutes during racing. The most important point to appreciate is the extreme quantity of metabolic heat produced when a racehorse performs strenuous exercise. This has been estimated at approximately 30 times the resting rate, and because only 20% is used for the exercise activity, 80% represents excess waste heat, which rapidly causes core body temperature to rise to a critical level if it is not dissipated to the environment.

It has been shown that the maximum rate of heat loss in any exercising animal is determined by three factors: (1) the capacity of heat loss mechanisms; for racehorses, a powerful sweating ability, (2) the cooling power of the environment, which dictates the degree of thermal strain and its CVS response, and finally, (3) the internal mechanisms which enable the transportation of heated blood from exercising muscles to the body surface.

Why do relatively few racehorses succumb to heat shock/stroke? The answer would appear to involve individual susceptibility; in this respect, all the horses arriving at the barriers may not be equal. A dysfunction in one of the abovementioned systems may predispose to a minor heat illness episode, but changes to all three could result in thermoregulatory failure, causing collapse and death. Another predisposing factor has recently been identified. Intestinal hypoperfusion from the exercise-associated reduction in blood supply has been shown to cause leakage of endotoxin into the central circulation. It has been demonstrated that under certain circumstances this may initiate a systemic inflammatory cascade, which perpetuates a positive feedback loop, driving continuous levels of endotoxin and cytokine production, and further activating systemic inflammation. This can become a key driver of the heat shock/stroke condition to its end stage, characterized by tissue necrosis, disseminated coagulation, and organ failure. The fact that this can be independent of hyperthermia means that an elevated temperature cannot be relied upon for its diagnosis.

This article is intended to challenge the ‘acute heart failure’ explanation in favour of another, also arguably a speculative diagnosis, in which heat shock/stroke may be responsible for many of these incidents, with circulatory failure as the mechanism of action. Such a change in diagnosis brings significant alterations to preventative strategies and a totally different clinical perspective to welfare implications for the TB racehorse.

PDF