Making sense of why runners collapse

Why Runners Collapse

Why would anyone expect the symptom of thirst to be present in collapsed runners? Thirst is such a powerful urge that any thirsty marathon runner suffering from dehydration during a race will simply stop at the next refreshment station and drink until her thirst is slaked. Simple.

The basis for the belief that collapsed runners were suffering from dehydration began with the explosive growth in the number of marathon runners after 1976 (figure 2a, page xv). This produced a massive increase in the number of runners requiring medical care at the finish of those races. Logically, the collapse of an athlete after rather than during a sporting event cannot be due to dehydration, since dehydration, which allegedly impairs circulation, must cause the athlete to collapse during the race when the strain on the heart and circulation is the greatest. This cannot happen immediately after the exercise terminates when any stress on the heart and circulation is falling. But this simple logic was ignored. Instead, it was concluded that all these collapsed athletes were suffering from dehydration, and their symptoms were caused by that dreaded disease.

But the truth is that athletes who collapsed after endurance events develop very low blood pressure only when standing (exercise-associated postural hypertension, or EAPH). This is caused by physiological changes that begin the moment the athlete stops running or walking after exercise and to which dehydration does not contribute. We know this because the moment these collapsed athletes lie flat, or better, with their legs and pelvis elevated above the level of the heart (“head down”), their symptoms instantly disappear.4 Thus, if the symptoms occur in athletes who are not thirsty and can be reversed instantly without fluid ingestion, the condition cannot be due to dehydration. Rather, EAPH must be due to the relocation of a large volume of blood from the veins in the chest and neck (which fill the heart and ensure its proper functioning) to the veins of the lower legs (which lie below the level of the heart) and therefore fill whenever an athlete stands.

One of the physiological costs of bipedalism is that it made it more difficult for exercising humans to regulate blood pressure when standing, because more than 60% of the blood in circulation is contained in large veins that are situated below the level of the heart. If this volume increases abruptly at any time, especially on cessation of exercise, it will cause EAPH to develop. Two factors cause this translocation immediately after the exercise terminates. First, the muscles in the calf, the contraction of which empties blood from the leg veins pumping it toward the heart, stop working. As a result, the action of this “second heart” is lost, causing blood to pool in the legs. Second, exercise impairs the bodily responses to any sudden reduction in blood pressure. This response requires the rapid activation of the sympathetic nervous system, which raises the blood pressure by increasing the resistance to blood flow in many organs, including the muscles of the legs. But endurance training reduces the sensitivity of the sympathetic nervous system to respond to such sudden stresses.

Those athletes who do not develop EAPH are able to prevent this relocation of blood volume from the center of the body to the legs, which begins the moment exercise terminates, in part because they activate an appropriate response of their sympathetic nervous system the moment they stop exercising.

The symptoms of EAPH are caused by this sudden onset of a falling blood pressure, which results in an inadequate blood supply to the brain (cerebral ischemia). The symptoms of cerebral ischemia are dizziness, nausea leading perhaps to vomiting, and a transient loss of consciousness (fainting). These symptoms persist until the blood flow to the brain is restored by an increase in blood pressure. Usually this occurs when the athlete falls to the ground and lies flat, thereby relocating a large volume of blood from the legs (and intestine) back to the center of the body. This sudden return of blood to the heart rapidly improves heart function and restores blood pressure to the appropriate postexercise value
(100 to 120/60 to 80 mmHg), which is usually slightly lower than the accepted normal
(110 to 140/60 to 90 mmHg) for resting humans who have not recently exercised.

The point is that dizziness, fainting, and nausea are the symptoms not of dehydration but of an inadequate blood supply to the brain. People who die from profound fluid loss when they are lost in the desert for three or more days without water also become confused. But this is not because of an inadequate blood supply to the brain—one of the body's most protected physiological functions—but because they develop multiple organ failure, including heart, kidney, and liver failure. The heart failure reduces blood flow to the brain, while kidney failure and liver failure cause the accumulation of certain toxic chemicals in the body that interfere with brain functioning, causing confusion and ultimately coma and death.

Experienced sport physicians are unable to determine the extent of dehydration (or volume of depletion) on the basis of the methods taught in medical school, that is, by examining the turgor of the skin, the state of hydration of the mucous membranes in the mouth, the presence of “sunken eyes,” the ability to spit, and the sensations of thirst (McGarvey, Thompson, et al., 2010). The only way accurately to determine the level of an athlete's state of hydration after prolonged exercise is to measure the body weight before and after exercise and, better, to measure the change in body water. The use of urine color, much promoted by some scientists, is of no value (Cheuvront, Ely, et al., 2010), because it is a measure of the brain and kidneys' response to changes in blood osmolality. It does not tell us exactly what the blood osmolality is and whether it is raised, lowered, or normal. As we will show, athletes with EAH typically excrete a dark urine even though they are severely overhydrated with blood osmolalities that are greatly reduced.

While serving as medical consultant at the 1998 Ironman Hawaii Triathlon, I attempted to introduce the concept of elevating the base of the bed to treat the low blood pressure (postural hypotension) that, in my opinion, is by far the most common cause of postrace collapse in athletes. Lifting the base of the bed cures the symptoms of postural hypotension and reduces the need to give intravenous fluids (inappropriately) for this condition.

This I showed at least to my own satisfaction in one elderly (>70-year-old) finisher whom I was called to see because he was deathly pale. The attending doctor could not detect a measurable pulse or blood pressure. I immediately lifted the base of the bed. Within seconds the patient's pulse became palpable, color returned to his face, and he was miraculously “cured.”

Years later, scientific papers written by some of the doctors I had interacted with showed that some lessons had been learned. Dr. Robert Sallis, who had been my close companion in the medical tent in 1998, wrote an article on the GSSI website acknowledging the value of this simple intervention. In that article he wrote, “The most common benign cause of collapse is low blood pressure due to blood pooling in the legs after cessation of exercise (as in postural hypotension, heat exhaustion, or syncope). This condition is treated by elevating the feet and pelvis until symptoms improve” (Sallis, 2004, p. 1). In the article, Dr. Sallis lists dehydration as a “non-serious” cause of collapse in athletes, which seems to conflict with the message of both the ACSM and the GSSI.

SHOP

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