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120 tract infection in the adult and to elucidate its patho- genesis. We thank Margaret Munyan, Kathryn Holmes, Nancy Wheeler and Thomas F. Smith for technical assistance. This work was partly sup- ported by grants from Pfizer, Inc. Upjohn Company, and the Minne- sota Lung Association. Requests for reprints should be addressed to K. J. T., Box 194, Mayo Memorial Building, University of Minnesota Hospitals, Minnea- polis, Minnesota 55455, U.S.A. REFERENCES 1. Halberstadter L, von Prowazek S. Zur atiologie des trachoms. Dtsch Med Wschr 1907; 33:1285-87. 2. T’ang F-F, Chang H-L, Huang Y-T, Wang K-C. Trachoma virus in chick embryo. Natl Med J China 1957; 43:81-86. 3. Gordon FB, Quan AL. Isolation of the trachoma agent in cell culture. Proc Soc Exp Biol Med 1965; 118: 354-59. 4. Schachter J. Chlamydial infections. N Engl J Med 1978; 298: 428-35, 490-95, 540-49. 5. Halberstadter L, von Prowazek S. Ueber chlamydozoenbefunde bei blen- norrhoea neonatorum non gonorrhoica. Berl Klin Wschr 1909; 46: 1829-40. 6. Dunlop EMC, Jones BR, Darougar S. Chlamydia and non-specific urethritis. Br Med J 1972; ii: 575-77. 7. Berger RE, Alexander ER, Monda GD, Ansell J, McCormick G, Holmes KK. Chlamydia trachomatis as a cause of acute "idiopathic" epididymitis. N Engl J Med 1978; 298:301-04. 8. Rees F, Tait IA, Hobson D, Johnson FW. Chlamydia in relation to cervical infection and pelvic inflammatory disease. In: Holmes KK, Hobson D, eds. Nongonococcal urethritis and related infections. Washington, D.C: Ameri- can Society for Microbiology, 1977; 67-76. 9. Mårdh PA, Ripa T, Svensson L, Weström L. Chlamydia trachomatis infec- tion in patients with acute salpingitis. N Engl J Med 1977; 296: 1377-79. 10. Beem MO, Saxon EM. Respiratory tract colonization and a distinctive pneu- monia syndrome in infants infected with Chlamydia trachomatis. N. Engl J Med 1977; 196:306-10. 11. Harrison HR, English MG, Lee CK, Alexander ER. Chlamydia trachomatis infant pneumonitis—comparison with matched controls and other infant pneumonitis. N Engl J Med 1978; 298:702-08. 12. Jawetz E, Rose L, Hanna L, Thygeson P. Experimental inclusion conjuncti- vitis in man: measurements of infectivity and resistance. JAMA 1965; 194:620-32. 13. Wentworth BB, Alexander ER. Isolation of Chlamydia trachomatis by use of 5-iodo-2-deoxyuridine-treated cells. Appl Microbiol 1974; 27: 912-16. 14. Hobson D, Rees E, Johnson FWA, Tait IA. Effect of penicillin on Chlamydia trachomatis in vitro and in vivo. In: Holmes KK, Hobson D, eds. Non- gonococcal urethritis and related infections. Washington, D.C: American Society for Microbiology, 1977; 227-29. 15. Blackman HJ, Yoneda C, Dawson CR, Schachter J. Antibiotic susceptibility of Chalmydia trachomatis. Antimicrob Agents Chemother 1977; 12: 673-77. 16. Saravolatz LD, Burch KH, Fisher E, et al. The compromised host and legionnaire’s disease. Ann Intern Med 1979; 90: 533-37. 17. Myerowitz RL, Pasculle AW, Dowling JN, et al. Opportunistic lung infection due to "Pittsburgh pneumonia agent". N Engl J Med 1979; 301: 953-58. BLOOD-PRESSURE RESPONSE TO SWIMMING IN ICE-COLD WATER ROBERT J. ZENNER DANIEL E. DE DECKER DENIS L. CLEMENT University Hospital, Department of Cardiovascular Diseases, Gent, Belgium Summary The cardiovascular responses to cold were studied in a group of 28 subjects who enjoyed swimming in ice-cold water in winter ("ice- bears"). History and clinical examination had revealed no abnormalities except hypertension (180/105 mm Hg) in 1, while 3 other subjects had a diastolic value of 95 mm Hg. Systolic blood-pressure increased significantly while the subjects were waiting undressed in cold air in the cabin by the pond. Neither immersion nor swimming in the ice-cold water caused further increase in systolic blood-pressure, and diastolic blood-pressure showed only a modest rise. 4 min later, blood-pressure had returned to control values. Electro and vector cardiographic signs remained unchanged. Although very high pressures were recorded in several subjects, no signs of left ventricular hypertrophy or of cardiovascular or cerebrovascular damage could be detected. Introduction THE hypertensive properties of cold have been widely recorded, and the cold pressor test was proposed as an index of vascular reactivity. In this procedure, however, only a small part of the body is exposed to cold. Much less is known about the effect of whole-body immersion in cold water. Methods In Dendermonde, a town of about 30 000 inhabitants, one of the Belgian "ice-bear" clubs has been flourishing for several years. Members are not selected in anyway and all swim regu- larly outdoors in cold water. Both sexes and all ages are rep- resented. The activities start in autumn, and whatever the weather, the more energetic members take a daily dive and swim for about 5 min in cold water. Sometimes, ice has to be removed to allow them to do so. Obviously the swimmers experience a gradual lowering of temperatures between autumn and the coldest winter days. In . September, 1978, we were asked to do a cardiological check-up of the 27 members. Examination included: history, physical examination, fluoroscopy, ECG, and VCG. Three orthogonal Frank leads were recorded simultaneously on magnetic tape and processed later by the Pipberger program version 3.6 on a Hewlett-Packard 2100 A computer. No absolute contraindications being discovered, the club continued to enjoy its activities as usual, and agreed to partici- pate in a repeat examination 4 months later. At that time, out- side air temperature was 0°C and water temperature 1-2 °C. Blood-pressure and ECG-VCG were recorded indoors, and im- mediately before and after 10 sec passive immersion and after 60 sec vigorous swimming in the pond, freed of ice. Some weeks later, 16 members had their blood-pressure taken before and after a regular cold shower (12°C). The data were ana- lysed by the paired t test. Results The basic examination revealed only modest abnor- malities (for example, old history of tuberculosis, moderate hypertension, obesity, left anterior hemi- block). As the 27 members were a very mixed population of both sexes and all ages, no statistics concerning weight and height were considered. In some cases, the "sport" had been faithfully performed for 5 years; in others, it had been pursued only recently or occa- sionally. The local barman took his first (and last ?) dive on the day of the examination. Because of the very rapid changes and the impossibil- ity of continuous recordings, heart-rate was not taken into account. In the VCGs obtained within 2 min before and after water contact, no significant rhythm or QRS disturbances were noted. As an isolated finding T waves in lead Z became sharper and deeper in 4 subjects. 22 subjects had normal blood-pressure (less than 140/95) at the first check-up, but 5 had respective levels of 140/95, 145/95, 155/95, 165/95, 180/105. After they undressed

Transcript of BLOOD-PRESSURE RESPONSE TO SWIMMING IN ICE-COLD WATER

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tract infection in the adult and to elucidate its patho-genesis.We thank Margaret Munyan, Kathryn Holmes, Nancy Wheeler and

Thomas F. Smith for technical assistance. This work was partly sup-ported by grants from Pfizer, Inc. Upjohn Company, and the Minne-sota Lung Association.

Requests for reprints should be addressed to K. J. T., Box 194,Mayo Memorial Building, University of Minnesota Hospitals, Minnea-polis, Minnesota 55455, U.S.A.

REFERENCES

1. Halberstadter L, von Prowazek S. Zur atiologie des trachoms. Dtsch MedWschr 1907; 33:1285-87.

2. T’ang F-F, Chang H-L, Huang Y-T, Wang K-C. Trachoma virus in chickembryo. Natl Med J China 1957; 43:81-86.

3. Gordon FB, Quan AL. Isolation of the trachoma agent in cell culture. ProcSoc Exp Biol Med 1965; 118: 354-59.

4. Schachter J. Chlamydial infections. N Engl J Med 1978; 298: 428-35,490-95, 540-49.

5. Halberstadter L, von Prowazek S. Ueber chlamydozoenbefunde bei blen-norrhoea neonatorum non gonorrhoica. Berl Klin Wschr 1909; 46:1829-40.

6. Dunlop EMC, Jones BR, Darougar S. Chlamydia and non-specific urethritis.Br Med J 1972; ii: 575-77.

7. Berger RE, Alexander ER, Monda GD, Ansell J, McCormick G, HolmesKK. Chlamydia trachomatis as a cause of acute "idiopathic" epididymitis.N Engl J Med 1978; 298:301-04.

8. Rees F, Tait IA, Hobson D, Johnson FW. Chlamydia in relation to cervicalinfection and pelvic inflammatory disease. In: Holmes KK, Hobson D, eds.Nongonococcal urethritis and related infections. Washington, D.C: Ameri-can Society for Microbiology, 1977; 67-76.

9. Mårdh PA, Ripa T, Svensson L, Weström L. Chlamydia trachomatis infec-tion in patients with acute salpingitis. N Engl J Med 1977; 296: 1377-79.

10. Beem MO, Saxon EM. Respiratory tract colonization and a distinctive pneu-monia syndrome in infants infected with Chlamydia trachomatis. N. EnglJ Med 1977; 196:306-10.

11. Harrison HR, English MG, Lee CK, Alexander ER. Chlamydia trachomatisinfant pneumonitis—comparison with matched controls and other infantpneumonitis. N Engl J Med 1978; 298:702-08.

12. Jawetz E, Rose L, Hanna L, Thygeson P. Experimental inclusion conjuncti-vitis in man: measurements of infectivity and resistance. JAMA 1965;194:620-32.

13. Wentworth BB, Alexander ER. Isolation of Chlamydia trachomatis by useof 5-iodo-2-deoxyuridine-treated cells. Appl Microbiol 1974; 27: 912-16.

14. Hobson D, Rees E, Johnson FWA, Tait IA. Effect of penicillin on Chlamydiatrachomatis in vitro and in vivo. In: Holmes KK, Hobson D, eds. Non-gonococcal urethritis and related infections. Washington, D.C: AmericanSociety for Microbiology, 1977; 227-29.

15. Blackman HJ, Yoneda C, Dawson CR, Schachter J. Antibiotic susceptibilityof Chalmydia trachomatis. Antimicrob Agents Chemother 1977; 12:673-77.

16. Saravolatz LD, Burch KH, Fisher E, et al. The compromised host andlegionnaire’s disease. Ann Intern Med 1979; 90: 533-37.

17. Myerowitz RL, Pasculle AW, Dowling JN, et al. Opportunistic lung infectiondue to "Pittsburgh pneumonia agent". N Engl J Med 1979; 301: 953-58.

BLOOD-PRESSURE RESPONSE TOSWIMMING IN ICE-COLD WATER

ROBERT J. ZENNER DANIEL E. DE DECKER

DENIS L. CLEMENT

University Hospital, Department of Cardiovascular Diseases,Gent, Belgium

Summary The cardiovascular responses to coldwere studied in a group of 28 subjects

who enjoyed swimming in ice-cold water in winter ("ice-bears"). History and clinical examination had revealedno abnormalities except hypertension (180/105 mm Hg)in 1, while 3 other subjects had a diastolic value of 95mm Hg. Systolic blood-pressure increased significantlywhile the subjects were waiting undressed in cold air inthe cabin by the pond. Neither immersion nor swimmingin the ice-cold water caused further increase in systolicblood-pressure, and diastolic blood-pressure showed only

a modest rise. 4 min later, blood-pressure had returnedto control values. Electro and vector cardiographic signsremained unchanged. Although very high pressures wererecorded in several subjects, no signs of left ventricularhypertrophy or of cardiovascular or cerebrovascular

damage could be detected.

Introduction

THE hypertensive properties of cold have been widelyrecorded, and the cold pressor test was proposed as anindex of vascular reactivity. In this procedure, however,only a small part of the body is exposed to cold. Muchless is known about the effect of whole-body immersionin cold water.

Methods

In Dendermonde, a town of about 30 000 inhabitants, oneof the Belgian "ice-bear" clubs has been flourishing for severalyears. Members are not selected in anyway and all swim regu-larly outdoors in cold water. Both sexes and all ages are rep-resented. The activities start in autumn, and whatever the

weather, the more energetic members take a daily dive andswim for about 5 min in cold water. Sometimes, ice has to beremoved to allow them to do so.

Obviously the swimmers experience a gradual lowering oftemperatures between autumn and the coldest winter days. In

. September, 1978, we were asked to do a cardiological check-upof the 27 members. Examination included: history, physicalexamination, fluoroscopy, ECG, and VCG. Three orthogonalFrank leads were recorded simultaneously on magnetic tapeand processed later by the Pipberger program version 3.6 ona Hewlett-Packard 2100 A computer.No absolute contraindications being discovered, the club

continued to enjoy its activities as usual, and agreed to partici-pate in a repeat examination 4 months later. At that time, out-side air temperature was 0°C and water temperature 1-2 °C.

Blood-pressure and ECG-VCG were recorded indoors, and im-mediately before and after 10 sec passive immersion and after60 sec vigorous swimming in the pond, freed of ice. Someweeks later, 16 members had their blood-pressure taken beforeand after a regular cold shower (12°C). The data were ana-lysed by the paired t test.

Results

The basic examination revealed only modest abnor-malities (for example, old history of tuberculosis,moderate hypertension, obesity, left anterior hemi-

block). As the 27 members were a very mixed populationof both sexes and all ages, no statistics concerningweight and height were considered. In some cases, the"sport" had been faithfully performed for 5 years; inothers, it had been pursued only recently or occa-

sionally. The local barman took his first (and last ?) diveon the day of the examination.Because of the very rapid changes and the impossibil-

ity of continuous recordings, heart-rate was not takeninto account. In the VCGs obtained within 2 min beforeand after water contact, no significant rhythm or QRSdisturbances were noted. As an isolated finding T wavesin lead Z became sharper and deeper in 4 subjects. 22subjects had normal blood-pressure (less than 140/95) atthe first check-up, but 5 had respective levels of 140/95,145/95, 155/95, 165/95, 180/105. After they undressed

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and before they walked outdoors, systolic blood-pressuresignificantly increased by 15 mm Hg, whereas diastolicvalues did not change (see table). When they walked tothe edge of the pond, systolic blood-pressure rose furtherin all but 1 subject, who was not the most thoroughlytrained. The greatest rise was 65 mm Hg. There wasonly a small average diastolic rise of 7, although 2 sub-jects increased their diastolic pressure by 40. Blood-pres-sure did not undergo further significant change immedi-ately after 10 sec immersion in cold water. Vigorousswimming in ice water did not cause significant changes.

SYSTOLIC AND DIASTOLIC BLOOD-PRESSURE (mm Hg) UNDERVARIOUS CONDITIONS

Differences (A) are derived from the previous condition listed.n.s.-= not significant.

The barman’s highest value during the whole exercisewas 191/123, while most regular members never

reached 200 systolic or 110 diastolic. Some remarkabledecreases were noted in systolic pressure after exposureto cold (from 210 to 170 in 1 subject and from 180 to144 in another); and two impressive systolic/diastolic in-creases were seen (from 140/90 to 190/140 in 1 subjectand from 183/87 to 232/97 in another). Within 4 min,more or less normal values were restored in all but 1

subject. A young man, used to this activity, suddenlypeaked to a value of 250/110 4 min after leaving thewater, while he was shivering, and his pressure stayed at230/90 for some minutes. This reaction had never hap-pened to him before. After 15 min, this reaction disap-peared spontaneously.

The 5 individuals with higher basic pressures respec-tively attained levels of 165/100, 232/97, 200/112,210/80 and 240/110. The high values were found insubjects who were certainly not the least faithfulmembers or the worst trained (1 had been taking partfor 3 consecutive years).Only slight changes were recorded after cold shower-

ing. Values shifted within a range of 10-20 mm Hg sys-tolic and diastolic.

Apart from the one shivering reaction, no participanthad any subjective or objective signs of cardiovascularor cerebrovascular distress.

Discussion

Striking individual differences in response to coldwere noted, as had been observed by Hines, whodivided subjects into hyporeactors and hyperreactors tothe cold pressor test. These individual differences havebeen confirmed ;2 and, among other possible mechan-isms, the level of catecholamines may be involved.3,4In practice the greatest part of the pressor responsecame during exposure to cold air while the subjects werewaiting undressed at the edge of the pond; neither im-mersion or swimming led to important further increasesin pressure. Part of the blood-pressure response whileswimming was certainly unobserved, because technicaldifficulties interfere with blood-pressure recordingswhile the subjects are in the water. It seems impossibleto determine whether the increase of pressure while

waiting at the pond was due to contact with cold air orto the thought of jumping into the water--or both.Training did not change the response: very similar re-sponses were noted in subjects who had been used to thisperformance for 3 years and in more or less untrainedsubjects.A profound vasoconstriction of, for example, skin

arteries would be expected to be the main mechanism ofpressure response to cold. Yet systolic pressure increasedmuch more than diastolic in almost all subjects, whichpoints to an important role for cardiac output. Thecutaneous veins are known to react vigorously to cold;5-6since they play an important part in the regulation ofcardiac output, they may be prominent in this phenom-enon.

Although some very high pressures were recorded, nosubjective or objective signs were noted of cardiovascu-lar or cerebrovascular damage provoked by these activi-ties. Electro-vectorcardiographic analysis did not indi-cate left ventricular hypertrophy or repolarisationdisturbances. Blood-pressures returned to control valuesin a few minutes. Peak pressures, after short exposure to

cold, even if they were very high, seemed to have alimited impact on the cardiovascular system; they couldbe compared to the well-known peaks of blood-pressuredue to any exogenous stimulus in hypertensive patients.Continuous recordings of blood-pressure have shownthat these short peaks cause much less harm to the pa-tients than continuous states of raised blood-pressure.’

Requests for reprints may be directed to: R. J. Z., University Hospi-tal, Deparment of Cardiovascular Diseases, De Pintelaan 135, 9000Gent, Belgium.

REFERENCES

1. Hines EA. The significance of vascular hyperreaction as measured by thecold pressor test. Am Heart J 1940;19:408-16.

2. Clement DL, Mussche MM, Vanhoutte G, Pannier R. Is blood pressure vari-ability related to activity of the sympathetic system? Clin Sci (in press).

3. Johnson DG, Hayward JS, Jacobs TP, Collis ML, Eckerson JD, WilliamsRH. Plasma norepinephrine response of man in cold water. J Appl Physiol1977; 43:216-20.

4. Clement DL, Bogaert MG, Moerman EZ, De Schaepdrijer AF. Significanceof elevated plasma noradrenaline in patients with essential hypertension.In: Birkenhäger WH, Falke HE, eds. Circulating catecholamines andblood pressure, Rotterdam: Bunge Scientific Publications 1978. 17-21.

5. Vanhoutte PM, Shepherd JT. Effect of temperature on reactivity of isolatedcutaneous veins of the dog. Am J Physiol 1970; 218:187-90.

6. Vanhoutte PM, Lorenz RR. Effect of temperature on reactivity of

saphenous, mesenteric and femoral veins of the dog. Am J Physiol 1970;218:1746-50.

7. Sokolow M, Werdegar D, Kain HK, Hinman AT. Relationship between levelof blood pressure measured casually and by portable recorders and severityof complications in essential hypertension. Circulation 1966; 34: 279-98.