It has frequently been reported that attacks of polio have occurred after moderate to severe exertion. Football players, marathon runners, and other athletes have contracted polio so soon after drills, contests, and the like, as to suggest a causal relationship between the exertion and the onset of the disease. Medical journals contain such reports. Drs. Voss, Bremer, de Rudder, Petersen, Nase have made such reports. (5) Voss’ case was that of a 17 year old girl who contracted polio after a strenuous tennis match. Bremer’s case was that of a student who contracted polio after a difficult mountain climb. Petersen and de Rudder observed two small epidemics following athletic contests. The athletes, who were between 13 and 19 years of age, were reported as being in good health and trained in athletics at the time of the contests. Eleven boys became ill with polio within a week after the contest. Another group of six boys became ill a few days after a second contest. Nase reports the case of a 26 year old soldier who participated in a cross-country run. At the end of the run he was completely exhausted, began to vomit, and had a high temperature. He was admitted to the hospital the next morning. At this time he was unable to sit up in bed, was unable to move his legs. He died nine hours after admission with paralysis of the respiratory muscles. An autopsy revealed polio.

Football players in this country have contracted polio after games and after arduous drills. One southern team in 1948 had three players who developed polio during the same week. One of them died. The college authorities canceled the games scheduled for the rest of the season. I have questioned young polio patients during epidemics and have found that many of them took sick the day after an all day outing or picnic during which they played games, swam long and hard, and ate a good deal of sweets, ice cream, and soda pop

How does exertion bring on or predispose one to polio? I attribute this increased susceptibility to polio after exertion to low blood sugar. Physical exertion, when immoderate, is accompanied by strong and prolonged muscular contractions which are performed at the expense of the blood sugar and result in a severe drain on liver glycogen stores. The depletion of liver glycogen results in a reduced output of glucose into the blood and the blood sugar concentration falls. Drs Levine, Gordon, and Derick of Boston found low blood sugar in six of nine marathon runners at the end of a long race. The blood sugar values of the six were 45, 47, 49, 50, 65, and 65 mg per 100 cc. All six finished the race in poor general condition and one of them was on the verge of collapse. Three who finished in good condition had normal blood sugar values, viz, 82, 82, and 89 mg (6)

Physical exertion, especially in summer, is accompanied by much sweating, thirst, and fatigue. The desire for cool sweet drinks is great and thirst is most pleasantly quenched by sweet drinks and ice cream. This ingestion of sugar may cause a fall in blood sugar. Thus the combined effect of physical exertion and the ingestion of sweets may greatly depress the blood sugar and thereby favor the onset of polio. Under such circumstances polio may have its onset within 24 hours.

This rapid onset may be explained by stating that the individual was in apparent good health at the beginning of the exertion and was a carrier of the virus, i.e., harbored the virus in the nose, throat, or gastrointestinal tract, like many other healthy individuals during an epidemic (It has been stated that for every frank case of polio during an epidemic there are about 200 healthy carriers of the virus). During the period of low blood sugar following the exertion, the virus crossed tissue barriers that harbored it, invaded the nervous system and attacked the nerve cells, with eventual paralysis. That polio may develop in such a short time after exertion is further suggested by the fact that I was able to infect rabbits after 8 to 10 hours when the rabbits’ blood sugar was experimentally lowered with insulin.

Dr. W. J. McCormick of Toronto has also implicated sugar and starch as dietary factors responsible for polio (7). He believes that the ingestion of refined sugar and starch eventually cause a metabolic disturbance in the tissues of the nervous system with development of the disease. Dr. McCormick took careful dietary histories on many patients during polio epidemics. The following case report is an example:

Case 1). I. C., a boy eleven years of age, onset of illness at a beach resort on July 29. Prior to illness the patient had been in the habit of bicycling 18 miles daily to and from the beach, where, in addition to swimming, he played eight holes of golf daily. On the evening before the onset he went on a raft which he propelled by "poling" for half a mile, after which he was "very tired."

Usual diet prior to illness: Breakfast: cornflakes, or other toasted cereal, bacon, eggs, white bread toast, two or three slices with jam or marmalade, milk or cocoa, canned fruit juice. Lunch: white bread sandwiches, milk, cake, white buns. Dinner: boiled potatoes and meat, white bread and butter, cabbage salad, watermelon. Bedtime: white bread, jam, chocolate milk. On the day before the onset the weather was very hot, and he had five drinks of pop, several chocolate bars, and a popsicle.

My interpretation of the sequence of events in this case is as follows: After a long day of excessive physical exertion, i.e., bicycling, swimming, golfing, and poling a raft, the boy felt very tired at night. This tired feeling no doubt reflected a state of low blood sugar. Since the day was very hot he consumed much sugar in the form of soda-pop, ice cream, and candy — all this in addition to the sugar and starch contained in his three regular meals. The combined effects of the physical exertion and the heavy consumption of sugar could have produced a state of very low blood sugar lasting for several hours. During this state any polio virus present on the surface of the membranes of the nose, or gastrointestinal tract could readily cross tissue barriers, invade the nervous system and cause the disease within 24 hours.

Thus, during epidemics of polio and even during non-epidemic periods, severe physical exertion should be avoided. This means complete avoidance of, or reduced participation in, such sports as long distance running, distance running, tennis, and the like. Short periods of exercise are permissible. Swimming in very cold water should be avoided. Cold water chills the body, and brings about an increased oxidation of sugar to provide heat in order to maintain normal body temperature. This extra combustion of sugar occurs at the expense of the blood sugar and liver glycogen. Marked shivering after cold water bathing is due to involuntary muscular contractions, the purpose of which is to produce extra heat.

Dr. Levinson found that monkeys forced to swim to the point of exhaustion in cold water developed more severe paralysis than did either those that remained in cages or those that were immersed in water at body temperature and protected from exercise and chilling (8).

The incidence of polio in any town or city during an epidemic is usually spotty. Cases occur here and there and it is usually impossible to establish that a polio victim had been in previous contact with another polio victim. In this respect, polio does not behave like measles and scarlet fever which are highly contagious. Some researchers state that during an epidemic the virus is universally distributed in the epidemic area and that many healthy individuals harbor the virus on surface membranes of the nose, throat, and gastrointestinal tract. Such individuals are called carriers.

Most researchers also believe that there must be some inherent factor of susceptibility present in the bodies of those who fall victims of the disease, a factor which lowers the resistance of the body for a period of time and permits the virus to penetrate the surface membranes and invade the central nervous tissues. I maintain that the presence of low blood sugar is this factor of susceptibility. The lowering of the blood sugar lowers the gates and permits the virus to enter.

When I injected the polio virus into rabbits whose blood sugar had been lowered by insulin, some of the rabbits showed signs of infection after only eight hours. This is an unusually short incubation period (The length of time between injection of the virus and the appearance of symptoms is called the incubation period). In monkeys, the incubation period is from 5 to 10 days, sometimes longer. Its exact duration in humans is not known and has been variously given as from 5 to 20 days. From my rabbit experiments I have concluded that, in the presence of low blood sugar, the virus is able to travel from surface membranes to the central nervous tissues in a matter of hours. The speed with which the virus travels will depend on the degree to which the blood sugar is lowered and on the duration of the low blood sugar. The lower the blood sugar and the longer it persists the greater the speed of invasion, the greater the multiplication of the virus, and the more severe the infection.

Those cases of polio that progress rapidly to extensive paralysis and death are cases that had prolonged low blood sugar at the time of invasion. Abortive polio cases are those which exhibit signs and symptoms of infection without developing gross signs of paralysis and which recover without evidence of paralysis. I would say that such cases had short periods of moderately low blood sugar and so only a small amount of virus reached the central nervous system, caused some inflammation but no paralysis.

In line with what has been previously stated about protective adrenal-sympathetic system, I would say abortive cases were able to recover from low blood quickly enough to prevent extensive invasion of the virus and subsequent injury to the cells of the nervous system. Between the two extremes of extensive paralytic and abortive cases, there are many degrees of involvement depending on: (1) how low the blood sugar falls, (2) how long the period of low sugar lasts, (3) the amount of glycogen stored in the liver, and (4) the effectiveness of the adrenal sympathetic response.

There are other physiological and immunological factors concerned with resistance to infection but I believe that they play a minor role at the onset of the infection. Potent immunological factors do not come into play until the infection is well established I regard the above listed factors as the most important, by far, since they play a leading role in prevention.