These techniques were very effective. The runners on the “carbohydrate trial” completed the race in excellent physical condition; their postrace blood glucose levels were elevated, and their performances were improved. This study had such an effect that for the next 56 years, most authorities virtually dismissed the possibility that hypoglycemia could be a factor in fatigue during marathon running (Felig et al, 1982). .
My personal interest in this problem arose during the 1980 Comrades Marathon, a race for which I had not prepared properly. After 60 km I started to have difficulty concentrating. My mind would clear for 5 to 10 minutes every time I drank 100 ml of cola. By 65 km my pace began to fall, and by 80 km I was forced to sit on the side of the road lest I fall over. After about 5 minutes I recovered sufficiently to return to the road to walk the remaining 10 km to the finish. On the road I met two other runners who had suffered the same fate. Like me, they had started to feel faint and giddy and could simply not continue running. We all had intense hunger and cravings for sweets.
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Subsequently, two famous incidences of what was almost certainly hypoglycemia in elite Comrades Marathon runners came to my attention. In the 1979 race, his first attempt at a race longer than 56 km, Johnny Halberstadt led the race convincingly from the start and established a record time at the halfway mark. On the morning of the race he did not eat breakfast and during the race he drank an electrolyte-containing ‘ ‘athletic drink’ ’ that had a very low carbohydrate content. He dominated most of the race, but 14 km from the finish he became disoriented, was unable to concentrate, and had to.lie down to prevent himself from falling over. He also had an intense craving for something sweet. Shortly after drinking 1 L of Coke, which contains about 100 g of carbohydrate, Halberstadt took off with renewed vigor, just failing to win the race.
This remarkable recovery is identical to those reported by pioneering Scandinavian exercise physiologists who showed that exhausted, hypoglycemic subjects were able to exercise without distress after consuming drinks with a high-carbo-hydrate content (Boje, 1936; E.H. Christensen & Hansen, 1939).
In the same 1979 Comrades Marathon, a young and unknown runner, Bruce Fordyce (see post 8), also went through a “bad patch” at about the same point as Halberstadt20 km from the finish. Fordyce recalls that quite suddenly he was unable to maintain his running pace. His father forced him to drink a high-carbohydrate solution (cola with added sugar). The results were quite dramaticBruce finished strongly in third place, and the career of one of the greatest ultradistance racers had begun.
Why should hypoglycemia occur specifically in elite ultramarathon runners but be apparently uncommon in standard marathon runners (Noakes et al, 1988b)? The answer would appear to lie in Exercises 3.4. If we assume that total muscle glycogen stores are about 460 g and liver glycogen stores are about 135 g, an athlete running at standard marathon pace (85% V02max) will use up muscle glycogen stores at a rate of 3.8 g/min (with total stores lasting about 120 minutes) and will use up liver glycogen stores at 1.1 g/min (with stores lasting 122 minutes). In addition, the liver has the ability to produce new glucose (glycogen) at a rate of about 10 g/hr. Thus, after 122 minutes of exercise, the liver will still have sufficient glycogen for another 25 minutes of exercise.
However, an athlete running at ultramarathon pace (70 to 75 % V02max) will use muscle glycogen at a rate of only 1.5 g/min (with stores lasting 310 minutes). The study of C.T.M. Davies and Thompson (1986) supported this finding; they showed that complete muscle glycogen depletion did not occur in a group of ultramarathon runners who ran for 4 hours at 67 to 73 % of V02max. The authors’ data therefore fit the prediction of Exercises 3.4 quite accurately.
The rate at which liver glycogen is used at this pace drops to 0.8 g/min, and stores will last 220 minutes. So liver glycogen stores will be depleted long before muscle glycogen stores during an ultramarathon race, and hypoglycemia will develop unless something is done to boost liver glycogen levels.
An athlete who drank 250 ml of Coke (which has a carbohydrate content of 100 g/L) for every hour of running would extend the time to hypoglycemia, so that he or she would become hypoglycemic after about 5 hours and 10 minutes. This is remarkably close to the time it took both Johnny Halberstadt and Bruce Fordyce to become hypoglycemic during the 1979 Comrades Marathon.
Arthur Newton (see post 5) made a striking observation:
When you have gone some thirty-five miles something in connection with digestion or assimilation of food is apt to make you think that you are getting badly tired. I haven’t yet solved this to my complete satisfaction though I seem to be getting near a likely cause. It may be that you have utilized all the immediately available energy from your last meal and on top of that used all your extra and ordinary reserves. (1935, pp. 191-192)
Newton seems to be describing the ineviExercises hypoglycemia that occurs after 4 or so hours of running if the athlete has ingested inadequate carbohydrate during the race. Because Newton never really learned to take in sufficient carbohydrate during his races lasting less than 24 hours, it is possible that he never completely found the answer to this problem, which almost certainly was a detriment to his performance. This is particularly surprising, because Newton clearly appreciated the critical importance of a high-sugar intake during multiday events, in particular the Transcontinental Races of 1928 and 1929, about which he wrote: “It was sugar that sustained practically every one of us: sugar and a liquid to dissolve it inlemonade or tea or, in a few cases, wine” (1940, p. 118).
As discussed subsequently, present evidence suggests that the optimum carbohydrate source to prevent hypoglycemia during ultramarathon running is a glucose or glucose polymer solution.
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