- Email: [email protected]
Symposium on special problems and management of allergic athletes
Symposium management Simon
Godfrey,
on special problems of allergic athletes M.D., Ph.D., F.R.C.P. Jerusalem, Israel
With the forthcoming Olympic Games of 1984, it was indeed opportune to hold a symposium to discuss the special problems facing athletes with asthma and upper respiratory tract allergy. It was particularly pleasing to me to be asked to prepare this preface since exactly 8 yr ago Dr. K. D. Fitch and I wrote a review entitled “Asthma and Athletic Performance” as a prelude to the 1976 Olympic Games. ’ Comparing that review with the present state of the art as expressed in the articles presented at the Palm Springs Symposium serves to emphasize just how far our knowledge of EIA has advanced in a relatively short period of time. Even so, by 1976 many of the facts about EIA had been established through the work of a number investigators, some of whom participated in the present symposium. It is perhaps worth reiterating some of the basic points since not all aspects of the problem were reviewed during the symposium. When an asthmatic exercises, he or she is likely to develop EIA, which is really postexercise bronchospasm, since the maximum fall in lung function occurs some 5 to 10 min after stopping the exercise. During exercise there is usually some mild bronchodilation that may be replaced by the onset of bronchospasm after 4 to 6 min in very sensitive subjects. The most severe EIA is produced by continuous exercise of marked intensity that lasts 6 to 8 min. After the attack of EIA, the subject is relatively refractory to another attack, the magnitude of this refractoriness diminishing during the next 3 to 4 hr.’ Any form of interrupted exercise or less severe exercise, as for example in many team sports, is much less likely to cause EIA than is the type of steady-state exercise described by Dr. Eggleston in this issue. Of considerable theoretic and practical importance was the observation that cromolyn sodium, which is known to inhibit the re-
From the Department of Pediatrics, Hadassah University Mount Scopus, Jerusalem, Israel. 630
and
Hospital,
Abbreviationsused
EIA: HIA: RHL: NCF:
Exercise-induced asthma Hyperventilation-induced asthma Respiratory heat loss Neutrophil chemotactic factor
lease of mediators from mast cells, could inhibit EIA if administered before exercise but not if given after exercise but before the onset of the attack of EIA.” Dr. Ellis points out that methyl xanthines have rather similar activity on EIA. By the mid 1970s it was widely believed that EIA was caused by the release of stored mediators through some unknown exercise-related mechanism. At that time it was not apparent why certain types of exercise such as swimming, even of severe intensity, usually failed to induce bronchospasm. In the past 8 yr we have begun to understand some of the mysteries surrounding EIA but, as with most constructive research, we have seen the appearance of new mysteries to replace them. Three articles in the symposium are directed toward the present understanding of the initiating events in EIA and isocapnic HIA. Much of this work was stimulated by the observation referred to above that different types of exercise of identical severity could result in different amounts of EIA. More or less at the same time, three groups of investigators noted that breathing humid air attenuated EIA,“6 and this could certainly explain the low asthmagenicity of swimming. This concept was taken up in a series of outstanding studies by the group working with Dr. McFadden in Boston7-’ and, although they did not present their work at this symposium, they were most certainly present “in spirit.” Essentially they were able to show a close correlation between RHL and the severity of asthma whether the heat loss was due to the hyperventilation of exercise or simply isocapnic hyperventilation without exercise. The concept that EIA is simply a form of HIA seems to have been
VOLUME NUMBER
73 5. PART 2
generally accepted by the participants in the symposium, and Dr. Rosenthal describes a simple system for performing isocapnic hyperventilation challenges with a minimum of equipment. Unfortunately, it seems that there is a danger that we shall be falling into the same trap that beset some of the earlier work on EIA in that the various protocols for HIA testing often involve intermittent or progressive tests and ignore the refractory period that normally follows HIA as well as EIA.“‘, ” While the RHL hypothesis is very attractive, certain discrepancies led us and others to question whether it could really explain the mechanism of EIA. Some studies have shown that EIA can occur even if there is no RHL, with the subject breathing air at body temperature fully saturated with water vapor”. ” and, moreover, a refractory period follows exercise in warm, humid air even in the absence of EIA, but this is not the case with HIA.“. ‘-I. ” In the present symposium Dr. Anderson elegantly reviews the data that she and her colleagues have been accumulating to show that the initiating event in EIA (or HIA) might well be the lossof water and not the lossof heat from the airways. She points out that the temperature of the inspired air was less critical than would be expected from the RHL hypothesis and questionssome of the assumptionsused when calculating RHL. Similar observations are reported in the symposium by Dr. Sheppard. Of particular interest is the possibility that the lossof water results in hyperosmolarity in the airway mucosasince the inhalation of hypertonic solutions alsoprovokes bronchospasmin asthmaticsand this can be inhibited by pretreatment with cromolyn sodium. Thus we now have the respiratory water loss hypothesis competing with the RHL hypothesis and hyperventilation competing with exercise as the trigger for EIA. What all this meansfor the asthmatic athlete is probably that he should try to avoid exercising in cold, dry conditions andshouldchooseswimming rather than skiing as his preferred sport. In this context, the article by Dr. Fitch is interesting in that some 8% to 10% of the Australian Olympic Team were asthmaticin 1976and 1980, and of theseslightly more than half were swimmers. The role of chemical mediators in acting as messengersin EIA and HIA is now establishedalmost beyond doubt, and the subject is dealt with in some detail by Dr. Lee. He and his colleagueshave shown very clearly that NCF is liberated by asthmaticsinto the bloodstream during exercise in quantities comparable to those liberated after antigen challenge and that the rise in NCF follows a similar time course to the postexercisefall in lung function. Both the rise in NCF and the fall in lung function could be prevented
Int.i(.~3LlCtiO??
631
by pretreatment with cromolyn sodium. They made similar observa.tionswith plasmahistamine. Curiously, the rise in histamine was more marked with HIA than with EIA and they found no rise :n NCF with HIA. They suggestedthat this may be due to an easier. accessto the circuiation caused by the greater blood flow during exercise. However. it seemsto me that an increased blood how could equally well he expetted to result in a lower blood level by diluting any releasedmediator in a larger volume of blood. and it could not explain the difference in behavior of NCF and histamine. Perhaps this should also herve as a warning that EIA and HIA may not be thr samething. The appearanceof late airways obstruction after exercise akin to I:he late responseto antigen challenge was recently described by Dr. Bierman and his colleagues and he reviews this topic in the symposium. As with the late allergic response.a second rise in NCF has been shown to occur with the late response to exercise. Why this late responseshould not have been observed previously is a bit of a mystery but it certainly warrants further study. Of somerelevance to the subject of EIA and mediators is the interesting problem of exercise-induced urticaria. which i4 reviewed by Dr. Kaplan, and exercise-inducedanaphylaxis, which is reviewed by Dr. She&-. ln both of these conditions physical exercise results in the type of responseusually associatedwith allergic reactions that have beenshown to be accompaniedhy the release of histamine. NCF. and other mediators. These reactions are more easily provoked by t,xcrcise in a warm environment, but cold alone can also result in urticaria. It may not be stretching the point too far to wonder if EIA or HIA could result from these types of responsesthat occur in the bronchi rather than in the skin. This thought is supported further by the presentationsof Drs. Nadel and Middleton who discuss local mechanismsthat may be responsiblefor these reactions. The severity of EIA dependson the bronchial reactivity of the individual and this in turn can be influenced by both allergic and nonallergic factors. It is now well establishedthat a positive allergic bronchial challenge rend!ersthe subject hyperreactive to nonspecific stimuli such as the inhalation oi histamineor methacholine, especially if there is a marked late reaction.lh We have recently studied a number ot. children who exercise and found a similar increasein EIA after a positive allergic bronchial chaIlenge. Dr. Pierson reviews the importance of atmosphericpollutants such asozone andsulphur dioxide in enhancing bronchial reactivity and summatingwith exercise to cause more severe E:IA. Recent studies in our laboratory have shown that the level of ionization i.rf the air can
J.ALLERGYCLIN.IMMUNOL. MAY19&1
632 Godfrey also affect EIA, although we had to use ion concentrations greater than those normally recorded from the atmosphere. “, ” It is encouraging that there may be some temporary adaptation to atmospheric pollutants so that the allergic athletes coming to Los Angeles for the games may have a fighting chance despite the famous local climatic conditions. Dr. Shapiro provides a clear and concise account of the use of methacholine challenge to assess the level of bronchial reactivity and makes the point that this is a relatively simple, reliable, and useful diagnostic clinical tool. Personal experience supports her conclusions, and I must admit that for practical purposes this type of challenge is easier for both the patient and the staff than either exercise or isocapnic hyperventilation tests. The management of the athlete with asthma is considered in several of the articles. Dr. Sly reviews the use of B-sympathomimetic agonists that are generally agreed to be the most effective agents for the prevention of EIA. Obviously the more recent selective &agents are to be preferred, especially for the athlete, because of their more prolonged action and freedom from cardiac side effects, and only this class is permitted by the sports authorities. Most researchers suggest that the inhaled route is the most practical and effective. Although Dr. Sly describes the use of combinations of these drugs with other agents, our own experience and that of many other investigators suggests that it is rare indeed that a good dose of inhaled albuterol or similar preparation does not totally prevent EIA. Those severe asthmatics for whom the effect is less than perfect are hardly likely to be participating in the Olympic Games. Cromolyn sodium is theoretically an ideal agent for the prevention of EIA in view of its almost total lack of side effects, and its use is reviewed by Dr. Konig. Unfortunately, as the work Dr. Konig and I undertook together some time ago shows, its effect is less than that of albuterol and, although it has interesting theoretic advantages, I do not believe it is the drug of choice solely for the prevention of EIA. For the patient regularly being treated by cromolyn sodium, it is worth taking an extra dose or a dose of albuterol immediately before strenuous exercise that is known from experience to result in EIA. The need for a dose of albuterol would also apply to patients under regular treatment with theophylline, which seems to have a similar efficacy to cromolyn sodium in the prevention of EIA. In a recent study of EIA and HIA we found that the efficacy of cromolyn sodium in the prevention of EIA was directly correlated with baseline lung function, while the efficacy in the prevention of HIA was negatively correlated with baseline lung function in most subjects.i9
If confirmed, this observation also casts some doubt on the identity of EIA and HIA. The question of upper respiratory tract allergy leading to rhinitis and sinusitis and the problems these can pose for the allergic athlete are lucidly reviewed by Drs. Slavin and Katz. Besides being a nuisance that may impede the athlete’s chances of winning, the sport itself may contribute to the problem by the introduction of infection into the sinuses in swimmers. As with EIA, there seems to be an increased sensitivity to allergic rhinitis in the presence of atmospheric pollution. The treatment of these conditions may be very important for the athlete, but sporting regulations permit only topical cromolyn and steroids. The regulations governing the use of drugs for the treatment of allergies and asthma in athletes are usefully described by Drs. Fitch and Clarke. Nutritional considerations that may have a direct effect on athletic performance are summarized by Ms. Mahan. In conclusion, I believe the organizers of this symposium are to be congratulated on putting together an excellent, informative, and highly relevant program. I am sure they and the participants in the symposium join me in wishing all the athletes, allergic or otherwise, the very best of luck in the 1984 Olympics. REFERENCES I. Fitch KD, Godfrey S: Asthma and athletic performance. JAMA 236:152-7, 1976 2. Edmunds AT, Tooley M, Godfrey S: The refractory period after exercise induced asthma, its duration and relation to severity of exercise. Am Rev Respir Dis 117:247-54, 1978 3. Silverman M, Andrea T: Time course of effect of disodium cromoglycate on exercise-induced asthma. Arch Dis Child 47:419-22, 1972 4. Weinstein RE, Anderson JA, Kvale P, Sweet LC: Effects of humidification on exercise-induced asthma (EIA). J ALLERGY CLIN IMM~NOL 57:250-I, 1976 5. Chen WY. Horton DJ: Heat and water loss from the airways and exercise-induced asthma. Respiration 34:305- 13, 1977 6. Bar-Or 0, Neuman I, Dotan R: Effects of dry and humid climates on exercise-induced asthma in children and adolescents. J ALLERGY CLIN IUMUNOL 60:163-8, 1977 7. Deal EC, McFadden ER, Ingram RH, Strauss RH, Jeager JJ: Role of respiratory heat exchange in production of exercise induced asthma. J Appl Physiol 46:467-75, 1979 8. Deal EC, McFadden ER, Ingram RH, Jeager JJ: Hyperpnea and heat flux: Initial reaction sequence in exercise-induced asthma. J Appl Physiol 46:476-83, 1979 9. Deal EC, McFadden ER, Ingram RH, Jeager JJ: Esophageal temperature during exercise in asthmatic and non-asthmatic subjects. J Appl Physiol 46:484-90, 1979 10. Wilson NM, Barnes PJ. Vickers H, Silverman M: Hyperventilation-induced asthma: Evidence for two mechanisms. Thorax 371657-62. 1982 11. Bar-Yishay E, Ben-Dov I, Godfrey S: Refractory period following hyperventilation-induced asthma. Am Rev Respir Dis 127:572-4, 1983 12. Anderson SD, Schoeffel RE, Follet R, Perry CP, Daviskas E,
VOLUME NUMBER
73 5 PART 2
Intrs2tiuction
Kendall
M: Sensitivity
to heat
exercise
in asthmatic
patients.
and water
I. Bar-Yishai
E, Godfrey
Eur
loss at rest and during
J Respir
Dis
17.
63:459-71.
Godfrey
1982 13.
Den-Dov
14.
wIthour Henriksen humidny
15.
constriction. Ben-Dov
the
Cockcroft gen-induced Allergy
S: Exercise-induced
asthma
respiratory heat loss. Thorax 37:730-l. 1982 JM. Dahl R. Lundquist CR: Influence of relative and repeated exercise on exercise-induced bronchoAllergy I. Bar-Yishay
36:463-70, 1981 E. Godfrey S: Refractory
lowing exercise induced heat loss. Am Rev Respir 16.
Ben-Dov
asthma unexplained by Dis 125:530-4, 1982
DW. Ruffin RE, Dolovich increase in non-allergic 7:503-13,
1977
period
fol-
respiratory
J. Hargreave FE: Allerbronchial reactivity. Clin
I, Amlrav
response
challenge.
I. Shochina
S: The effect
csf asthmatic Thorax
M.
of negative
38:584-g.
children
Xmirai
iomzatiun to cxer(
633
I. B&r-\r‘i,hai 01 In+)!&
E. air on
L:X: irr histanune
1982
18.
Lipin I. Cur I. Amitai Y. Amirav I. God&y S. ‘The rtfccr ot positive ionizalion of inspired air on the rebpc,nse ot acthntatlc children to exercise. Thorax (in press)
19.
Ben Dov I. Bar-Yishay E. Godfrey S: Relation between effiLacy of sodium cromoglycate and baseline iung function in exercise and h,vperventilation induced a.>thmi. IV J Mrd Sci I in press)
Godfrey,
on special problems of allergic athletes M.D., Ph.D., F.R.C.P. Jerusalem, Israel
With the forthcoming Olympic Games of 1984, it was indeed opportune to hold a symposium to discuss the special problems facing athletes with asthma and upper respiratory tract allergy. It was particularly pleasing to me to be asked to prepare this preface since exactly 8 yr ago Dr. K. D. Fitch and I wrote a review entitled “Asthma and Athletic Performance” as a prelude to the 1976 Olympic Games. ’ Comparing that review with the present state of the art as expressed in the articles presented at the Palm Springs Symposium serves to emphasize just how far our knowledge of EIA has advanced in a relatively short period of time. Even so, by 1976 many of the facts about EIA had been established through the work of a number investigators, some of whom participated in the present symposium. It is perhaps worth reiterating some of the basic points since not all aspects of the problem were reviewed during the symposium. When an asthmatic exercises, he or she is likely to develop EIA, which is really postexercise bronchospasm, since the maximum fall in lung function occurs some 5 to 10 min after stopping the exercise. During exercise there is usually some mild bronchodilation that may be replaced by the onset of bronchospasm after 4 to 6 min in very sensitive subjects. The most severe EIA is produced by continuous exercise of marked intensity that lasts 6 to 8 min. After the attack of EIA, the subject is relatively refractory to another attack, the magnitude of this refractoriness diminishing during the next 3 to 4 hr.’ Any form of interrupted exercise or less severe exercise, as for example in many team sports, is much less likely to cause EIA than is the type of steady-state exercise described by Dr. Eggleston in this issue. Of considerable theoretic and practical importance was the observation that cromolyn sodium, which is known to inhibit the re-
From the Department of Pediatrics, Hadassah University Mount Scopus, Jerusalem, Israel. 630
and
Hospital,
Abbreviationsused
EIA: HIA: RHL: NCF:
Exercise-induced asthma Hyperventilation-induced asthma Respiratory heat loss Neutrophil chemotactic factor
lease of mediators from mast cells, could inhibit EIA if administered before exercise but not if given after exercise but before the onset of the attack of EIA.” Dr. Ellis points out that methyl xanthines have rather similar activity on EIA. By the mid 1970s it was widely believed that EIA was caused by the release of stored mediators through some unknown exercise-related mechanism. At that time it was not apparent why certain types of exercise such as swimming, even of severe intensity, usually failed to induce bronchospasm. In the past 8 yr we have begun to understand some of the mysteries surrounding EIA but, as with most constructive research, we have seen the appearance of new mysteries to replace them. Three articles in the symposium are directed toward the present understanding of the initiating events in EIA and isocapnic HIA. Much of this work was stimulated by the observation referred to above that different types of exercise of identical severity could result in different amounts of EIA. More or less at the same time, three groups of investigators noted that breathing humid air attenuated EIA,“6 and this could certainly explain the low asthmagenicity of swimming. This concept was taken up in a series of outstanding studies by the group working with Dr. McFadden in Boston7-’ and, although they did not present their work at this symposium, they were most certainly present “in spirit.” Essentially they were able to show a close correlation between RHL and the severity of asthma whether the heat loss was due to the hyperventilation of exercise or simply isocapnic hyperventilation without exercise. The concept that EIA is simply a form of HIA seems to have been
VOLUME NUMBER
73 5. PART 2
generally accepted by the participants in the symposium, and Dr. Rosenthal describes a simple system for performing isocapnic hyperventilation challenges with a minimum of equipment. Unfortunately, it seems that there is a danger that we shall be falling into the same trap that beset some of the earlier work on EIA in that the various protocols for HIA testing often involve intermittent or progressive tests and ignore the refractory period that normally follows HIA as well as EIA.“‘, ” While the RHL hypothesis is very attractive, certain discrepancies led us and others to question whether it could really explain the mechanism of EIA. Some studies have shown that EIA can occur even if there is no RHL, with the subject breathing air at body temperature fully saturated with water vapor”. ” and, moreover, a refractory period follows exercise in warm, humid air even in the absence of EIA, but this is not the case with HIA.“. ‘-I. ” In the present symposium Dr. Anderson elegantly reviews the data that she and her colleagues have been accumulating to show that the initiating event in EIA (or HIA) might well be the lossof water and not the lossof heat from the airways. She points out that the temperature of the inspired air was less critical than would be expected from the RHL hypothesis and questionssome of the assumptionsused when calculating RHL. Similar observations are reported in the symposium by Dr. Sheppard. Of particular interest is the possibility that the lossof water results in hyperosmolarity in the airway mucosasince the inhalation of hypertonic solutions alsoprovokes bronchospasmin asthmaticsand this can be inhibited by pretreatment with cromolyn sodium. Thus we now have the respiratory water loss hypothesis competing with the RHL hypothesis and hyperventilation competing with exercise as the trigger for EIA. What all this meansfor the asthmatic athlete is probably that he should try to avoid exercising in cold, dry conditions andshouldchooseswimming rather than skiing as his preferred sport. In this context, the article by Dr. Fitch is interesting in that some 8% to 10% of the Australian Olympic Team were asthmaticin 1976and 1980, and of theseslightly more than half were swimmers. The role of chemical mediators in acting as messengersin EIA and HIA is now establishedalmost beyond doubt, and the subject is dealt with in some detail by Dr. Lee. He and his colleagueshave shown very clearly that NCF is liberated by asthmaticsinto the bloodstream during exercise in quantities comparable to those liberated after antigen challenge and that the rise in NCF follows a similar time course to the postexercisefall in lung function. Both the rise in NCF and the fall in lung function could be prevented
Int.i(.~3LlCtiO??
631
by pretreatment with cromolyn sodium. They made similar observa.tionswith plasmahistamine. Curiously, the rise in histamine was more marked with HIA than with EIA and they found no rise :n NCF with HIA. They suggestedthat this may be due to an easier. accessto the circuiation caused by the greater blood flow during exercise. However. it seemsto me that an increased blood how could equally well he expetted to result in a lower blood level by diluting any releasedmediator in a larger volume of blood. and it could not explain the difference in behavior of NCF and histamine. Perhaps this should also herve as a warning that EIA and HIA may not be thr samething. The appearanceof late airways obstruction after exercise akin to I:he late responseto antigen challenge was recently described by Dr. Bierman and his colleagues and he reviews this topic in the symposium. As with the late allergic response.a second rise in NCF has been shown to occur with the late response to exercise. Why this late responseshould not have been observed previously is a bit of a mystery but it certainly warrants further study. Of somerelevance to the subject of EIA and mediators is the interesting problem of exercise-induced urticaria. which i4 reviewed by Dr. Kaplan, and exercise-inducedanaphylaxis, which is reviewed by Dr. She&-. ln both of these conditions physical exercise results in the type of responseusually associatedwith allergic reactions that have beenshown to be accompaniedhy the release of histamine. NCF. and other mediators. These reactions are more easily provoked by t,xcrcise in a warm environment, but cold alone can also result in urticaria. It may not be stretching the point too far to wonder if EIA or HIA could result from these types of responsesthat occur in the bronchi rather than in the skin. This thought is supported further by the presentationsof Drs. Nadel and Middleton who discuss local mechanismsthat may be responsiblefor these reactions. The severity of EIA dependson the bronchial reactivity of the individual and this in turn can be influenced by both allergic and nonallergic factors. It is now well establishedthat a positive allergic bronchial challenge rend!ersthe subject hyperreactive to nonspecific stimuli such as the inhalation oi histamineor methacholine, especially if there is a marked late reaction.lh We have recently studied a number ot. children who exercise and found a similar increasein EIA after a positive allergic bronchial chaIlenge. Dr. Pierson reviews the importance of atmosphericpollutants such asozone andsulphur dioxide in enhancing bronchial reactivity and summatingwith exercise to cause more severe E:IA. Recent studies in our laboratory have shown that the level of ionization i.rf the air can
J.ALLERGYCLIN.IMMUNOL. MAY19&1
632 Godfrey also affect EIA, although we had to use ion concentrations greater than those normally recorded from the atmosphere. “, ” It is encouraging that there may be some temporary adaptation to atmospheric pollutants so that the allergic athletes coming to Los Angeles for the games may have a fighting chance despite the famous local climatic conditions. Dr. Shapiro provides a clear and concise account of the use of methacholine challenge to assess the level of bronchial reactivity and makes the point that this is a relatively simple, reliable, and useful diagnostic clinical tool. Personal experience supports her conclusions, and I must admit that for practical purposes this type of challenge is easier for both the patient and the staff than either exercise or isocapnic hyperventilation tests. The management of the athlete with asthma is considered in several of the articles. Dr. Sly reviews the use of B-sympathomimetic agonists that are generally agreed to be the most effective agents for the prevention of EIA. Obviously the more recent selective &agents are to be preferred, especially for the athlete, because of their more prolonged action and freedom from cardiac side effects, and only this class is permitted by the sports authorities. Most researchers suggest that the inhaled route is the most practical and effective. Although Dr. Sly describes the use of combinations of these drugs with other agents, our own experience and that of many other investigators suggests that it is rare indeed that a good dose of inhaled albuterol or similar preparation does not totally prevent EIA. Those severe asthmatics for whom the effect is less than perfect are hardly likely to be participating in the Olympic Games. Cromolyn sodium is theoretically an ideal agent for the prevention of EIA in view of its almost total lack of side effects, and its use is reviewed by Dr. Konig. Unfortunately, as the work Dr. Konig and I undertook together some time ago shows, its effect is less than that of albuterol and, although it has interesting theoretic advantages, I do not believe it is the drug of choice solely for the prevention of EIA. For the patient regularly being treated by cromolyn sodium, it is worth taking an extra dose or a dose of albuterol immediately before strenuous exercise that is known from experience to result in EIA. The need for a dose of albuterol would also apply to patients under regular treatment with theophylline, which seems to have a similar efficacy to cromolyn sodium in the prevention of EIA. In a recent study of EIA and HIA we found that the efficacy of cromolyn sodium in the prevention of EIA was directly correlated with baseline lung function, while the efficacy in the prevention of HIA was negatively correlated with baseline lung function in most subjects.i9
If confirmed, this observation also casts some doubt on the identity of EIA and HIA. The question of upper respiratory tract allergy leading to rhinitis and sinusitis and the problems these can pose for the allergic athlete are lucidly reviewed by Drs. Slavin and Katz. Besides being a nuisance that may impede the athlete’s chances of winning, the sport itself may contribute to the problem by the introduction of infection into the sinuses in swimmers. As with EIA, there seems to be an increased sensitivity to allergic rhinitis in the presence of atmospheric pollution. The treatment of these conditions may be very important for the athlete, but sporting regulations permit only topical cromolyn and steroids. The regulations governing the use of drugs for the treatment of allergies and asthma in athletes are usefully described by Drs. Fitch and Clarke. Nutritional considerations that may have a direct effect on athletic performance are summarized by Ms. Mahan. In conclusion, I believe the organizers of this symposium are to be congratulated on putting together an excellent, informative, and highly relevant program. I am sure they and the participants in the symposium join me in wishing all the athletes, allergic or otherwise, the very best of luck in the 1984 Olympics. REFERENCES I. Fitch KD, Godfrey S: Asthma and athletic performance. JAMA 236:152-7, 1976 2. Edmunds AT, Tooley M, Godfrey S: The refractory period after exercise induced asthma, its duration and relation to severity of exercise. Am Rev Respir Dis 117:247-54, 1978 3. Silverman M, Andrea T: Time course of effect of disodium cromoglycate on exercise-induced asthma. Arch Dis Child 47:419-22, 1972 4. Weinstein RE, Anderson JA, Kvale P, Sweet LC: Effects of humidification on exercise-induced asthma (EIA). J ALLERGY CLIN IMM~NOL 57:250-I, 1976 5. Chen WY. Horton DJ: Heat and water loss from the airways and exercise-induced asthma. Respiration 34:305- 13, 1977 6. Bar-Or 0, Neuman I, Dotan R: Effects of dry and humid climates on exercise-induced asthma in children and adolescents. J ALLERGY CLIN IUMUNOL 60:163-8, 1977 7. Deal EC, McFadden ER, Ingram RH, Strauss RH, Jeager JJ: Role of respiratory heat exchange in production of exercise induced asthma. J Appl Physiol 46:467-75, 1979 8. Deal EC, McFadden ER, Ingram RH, Jeager JJ: Hyperpnea and heat flux: Initial reaction sequence in exercise-induced asthma. J Appl Physiol 46:476-83, 1979 9. Deal EC, McFadden ER, Ingram RH, Jeager JJ: Esophageal temperature during exercise in asthmatic and non-asthmatic subjects. J Appl Physiol 46:484-90, 1979 10. Wilson NM, Barnes PJ. Vickers H, Silverman M: Hyperventilation-induced asthma: Evidence for two mechanisms. Thorax 371657-62. 1982 11. Bar-Yishay E, Ben-Dov I, Godfrey S: Refractory period following hyperventilation-induced asthma. Am Rev Respir Dis 127:572-4, 1983 12. Anderson SD, Schoeffel RE, Follet R, Perry CP, Daviskas E,
VOLUME NUMBER
73 5 PART 2
Intrs2tiuction
Kendall
M: Sensitivity
to heat
exercise
in asthmatic
patients.
and water
I. Bar-Yishai
E, Godfrey
Eur
loss at rest and during
J Respir
Dis
17.
63:459-71.
Godfrey
1982 13.
Den-Dov
14.
wIthour Henriksen humidny
15.
constriction. Ben-Dov
the
Cockcroft gen-induced Allergy
S: Exercise-induced
asthma
respiratory heat loss. Thorax 37:730-l. 1982 JM. Dahl R. Lundquist CR: Influence of relative and repeated exercise on exercise-induced bronchoAllergy I. Bar-Yishay
36:463-70, 1981 E. Godfrey S: Refractory
lowing exercise induced heat loss. Am Rev Respir 16.
Ben-Dov
asthma unexplained by Dis 125:530-4, 1982
DW. Ruffin RE, Dolovich increase in non-allergic 7:503-13,
1977
period
fol-
respiratory
J. Hargreave FE: Allerbronchial reactivity. Clin
I, Amlrav
response
challenge.
I. Shochina
S: The effect
csf asthmatic Thorax
M.
of negative
38:584-g.
children
Xmirai
iomzatiun to cxer(
633
I. B&r-\r‘i,hai 01 In+)!&
E. air on
L:X: irr histanune
1982
18.
Lipin I. Cur I. Amitai Y. Amirav I. God&y S. ‘The rtfccr ot positive ionizalion of inspired air on the rebpc,nse ot acthntatlc children to exercise. Thorax (in press)
19.
Ben Dov I. Bar-Yishay E. Godfrey S: Relation between effiLacy of sodium cromoglycate and baseline iung function in exercise and h,vperventilation induced a.>thmi. IV J Mrd Sci I in press)