LurERS

belSS melilU5. ProviS10na~report Ol i WHO C:OnsuU\1fIOn. DiabelMedlei". 1996: 15; 539·553

2. Colmar. PG, Thoma:; O~, Zim.mel PZ, el a~. New Cl~sifjcatjonand crileria for dl3gnOSlS ef diabetes melhlus. Position Slste·ment from ine AustralDsian Diitbctes Scciery. New Zealandsoeiety 10<Iha Sludy ol oi<lbetes. Royat College ol Patnotog;stsol Au"",ta'ia and Auslralas,an Associalion ol Clinical Bio·ohemi'''. Med J AuS11999: 170: 375·376.

3. ShaW JE. Zimmat PZ. de Co,men M. el a1.lmpaired lasting glu·case or impaired gfucose tolerance. Wnat eest predicts futlXediabetes on Maurilius? DiaOe,es Cate 1999; 22. 399·402.

4. American Diabetes ~sociatjOn ..~ep?rt ot th~ expen comrnlt·lee en tne diagnosls and claSSlflcatlon of diabetes meltltus.Diabeles Care 1997: 20; t 163·1197.

S. Perry RC. Baron AD. Impaired glucose tolerance: why is il neta dis,os," Dia06les Care 1999:22: 663·665. Q

Severe allergen-induced asthmadesplte the use of Buteykobreathing technique

. John M Weiner,' Jonathan G W Burdant

• Allergist. t DireClor, Dspartmenl of Rp.spiralory Medicine,'SI Vincent', HospilOI Melbourne. 41 Victoria Parade,Fitzroy, Vie 3065. Email: jw@allergy.cx

To the Editor: The Buteyka breathing tech.:..nique (BBT) is a method of shallow breath-ing ',that raises the partial pressure afcarbon dioxide (PaC02). Irs proponentsteacn that the cause OI asthma is hyperven-tilarien leading to hypocapnia and bron-chcconstriction.' Two Australian ran-domised controlled trials have shown thatBBT reduces hyperventilation," reduces theuse of B,-agonists,2,) and improves quality oflife.J

We report the case of a 40-year-oldwornan with life-long asthma who requireda short-acting i32-agonist once a day unlessshe took 400 ug bec1omethasone daily.Since completirig a course ofBBT in janu-ary 1994, s~d not used beclomethasoneor a B,-agornst regularlYj she practised BBTtWtce a day, and whenever sneaevelopedasthma symptorgs, .li1August 1995 her FEV1 (forced expi-

ratory velurne in one second) was 1.88 litres(74% predicted) with a 14% (significant)improvemerit af ter bronchodilator. Skin-prick tests were positive to various aero-allergens,' including a 15 mm weal tO horsehair. She was given information on allergenavoidanee, advised to continue using low-dose inhaled corticosteroids, and alsooffered allergen immunotherapy. Shede~lined these interventions. In April 1999she reported that BET had generally pro-vided "tremendous relief" over the previousfive years and three months. She still carrleda B2-agonist but bad had 00 need for regu-lar medieation. However, she had deve10pedsevere bronchoconstriction on three occa-si~~ arter exposure to lf.Qrses~hich BBTfa.~ reverse .. One epis~Qe resulted inurgent hospitalisanon with a'severe attack of

MJA Vol 171 19 July 1999

asthma, the other [WO settled after she uscd.the i32-agonist.

Doctors dealing with patients who chooseto use BBT for their asthma need to explain- in a mariner mat is understanding, infor-mative and non-threatening - that, whileBBT may reduce the need for rnedication,~e ris~ of sudden bronchospasnlandpos·:_~sible life-threatening asthrna remains. Wc:suggest the folIowing pl~ pati;nts whochoose BBT as their sole asthma interven-tion:• Lung function (spirometry) befor.e_.stan-

ing BBT, then at lease every three monthsfor one year, and subsequently annually;

• AE.ess:nent of aeroallergen seE~Eivity l?Yskin or blood tests; andA conventional wrinet). asthma manage-_mept plan whjch als?> jncludes the fol-:"lo~ing information:"The Euteyko breathing technjqw:...ma.yreduce the need for vom reliøver spzaysand may improve your asthma-relatedquahty of life. However, th~asthmaticnature of your airways _may persist andsudden attacks of asthma may stilloccur, If asthma sy~ptoms-Occ:urm;;;than three times a week (excluding withexei'clse) iben vour asthma m.:4Y..llQJ •.be .•.controlled. even if BW-CJIkai.t.praailed-reg-uiarly. If you are allergi c to airborn~t9ggers Csuch as pallees, dmr mi.>~,mould spores or anjmal ba;t) II relieyerspray should alwavs be carrjed, beC21lSe_aliergen exposure ean lead to sudden,severe, life-threatening asthma, evert ijB!ueyko is practlsed regularty. '

1. Slalmatski A. Freedom from astnma: ~uteykO'SrcvolulIonaryJt.realment. Hale Clonic Heallh LibrDry+ondon: KyleCDlhio Lid.

1997:175.2. Bowler SD, Green A, Mi'ch.1I CA. Buteykc breathing 18Ch·

niques in asthma: a blinded ranaomised controlled Irial. MedJ Ausr 199B: 169: 575·578.

3. Opal A. Cohen M. Bailey M. Abf"""on M. Tne 6u'eyI<o brealh·ing ,~~c~,~ue in asuvna: a etinicat uial (abstra:!l. Respirology

4/199y--UPPI; A24. U

Hospital in the home: arandomised controlled trial

HJ,lgh G Dickson: David A Confortlt

• Prolessor ol Aged Care and Rehabilitation, and DepulyMsdlcal Director, t Dlreclor ol Rehabililation endGeriatrics, Division of Medietne, Liverpool Hospital.PO Sox 103, Liverpool, NSW 2170Emaa: hugh.dickson@swsshs.nsw.go,/.au

To the Editor: The article by Caplan et a[lis an important study concerning the opti-mal site for delivery of medical services tOelderly patients, The evidence presentedsuggests that, in comparison with hospital-isation, a ''hospital in the home" (HrH)model can deliver equivalent benefits and

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The effects of carbon dioxide on exercise-induced asthma: anunlikely explanation for the effects of Buteyko breathing training

TRE INCREASING USE of alternativetherapy in First World countries has ledtO suggestions mat the relationshipsbetween hcalthcare professionals andscciety need to be reviewed.1 There isalso a ne ed tO investigate the efficacyand therape utic rnechanisrns of alterria-rive rrearmentsj--' once a treatment hasbe en rigorously resred and shown to beeffective, the distinenon berween alter-native and conventional therapybecomes irrelevant."

One alternative treatment for themanagement of asthma, Buteyko breath-ing trainirig (BBT), has been wide lypublicised in Australia and New Zealandand, more recently, in the United King-dom.' 'Ibis technique af intermirtent,regular, controlled, shallow breathingand breath holding was developed byButeyko in the 1960s, and evolved fromthe meditative Eastern traditions such astai chi, which ernphasise the importanceof conscious breathing control for phys-ical and mental well-being.> Buteykosuggests mat hyperventilation and theassociated hypccarbia in asthma terid tole ad to reduced tissue oxygenaticn,which leads in rum to bronchial and.arreri al spasm and inflammation. 5

According to the Buteyko hypcthesis,restcring "normal" ventilation by vol-untary hypoventilation training will alle-viate asthma by increasing the level ofcarbon di oxide and reversing thisprocess. Hypoventilation is used bothregularly and at the onset of an asrhmaattack.

Exercise is a common trigger of acutebronchoconsrriction in people withasthrna, and a previous study has sug-

Wael K Al-Delairny, Scotl M Hay, Kevin R Gain, David T Jones and Julian Crane

Objectives: To examine the effect at breathing 3% CO, on exercise-inducedasthma (EIA), as a raised airway CO, level is suggested to mediate the effectsof Buteyko breathing training (SST).

DesIgn: Double-blind erossover study, using a standard laboratory-basedexercise challenge, with EIA defined as a tall af 15% or greater In Ihe lorcedexpiratory volume in ane second (FEV,) wlthin 30 minutes ol completing astandard exerclse protoco/.

Subjects: 10 adults withconlirmed EIA.

Intervention: Air enriched with 3% CO, during and for 10 rnlnutes afterexercise.

Outcome measures: MaximUm percentage tall In FEV, after exercise. Areaunder curve (AUC) of the decrease in FEV, with time.

Results: Msan maximum fall in FEV, was similar: 19.9% with air, and 26.9%with 3% CO, (P= 0.12). The mean AUC lor the total 30-minuts post-exerciseperiod was 355 for air and 520 tor 3% CO2 (P= 0.07). Atter discontinuing the 3%CO2 at 10 mlnutes after sxercise, there was a further and .sustainad fall in FEV l'

Mean AUC for the perlod 10-30 minutes post-exercise was signlficantly greaterfor CO2 than air (275 and 137, respectively (P= 0.02]). Mean minute ventilationwas Increased when subjects exercised breathing 3% CO2: 77.5 Umin for 3%CO2, compared wlth 68.7 Umin for air (P=0.02).

Concluslon: Breathing 3% CO, during exerclse does not prevent EIA. Theshape ol the FEV, response curve after 3% CO2 suggests that a greater degreeaf EIA (becauss ol increased minute ventilation during exercise) was opposedby a direct relaxant afiect of CO, an the airway. Increased airway CO, alone isan unlikely mechanism lor the reported benefits of SBT; nevertheless, furtherstudy af the effects of voluntary hypoventllation in asthma is warranted.

Ilt', '~.ill

i

I

gesred that air enriched with 6% CO2could reverse exercise-induced asthma(EIA).6 Given that an increase in CO, issuggested as a mechanism for theimprovement in asthrna folIowing BBT,we wished to exarnine whether breathingair enriched with COz during and afterexercise could prevent or reduce ELA...

Participants

People with a history af EIA wererecruited by advertisement in the localcomrnunity and through hospital-basedrespiratory clinics. Subj ects with a his-tory of cardiovascular discase or exer-cise-induced anaphylaxis were excluded .Volunteers who had had a severe exac-erbation or hospital admission withinthe previous three months were alsoexcluded. Before each srudy, short-acting ø-agonists were withheld for atleast six hours, and in one individualoral salbutarnol was withheld for 24hours. None of the partielpants weretaking Iong-aeting inhaled ~-agonists .

The number of participants 'needed!

....

Wellingi6nSchool:of Medielne; W~iljngtDn,New Zealarid.·· -. . .,WaelK~I~6~lairi;Y;.:MEl·aCh,·R~seårch;=~II~~;·Depårt~e;'(p.tPu~lii:H9:aith;'; ...: ..' ..' -. .Julian. CianeJ.fAACP,.H!'lGJ~rlnciparResea(ch)~'eIlDw/Departr'nentorMedidn~.:· : :.';" •. ' .;Re·s~I~~toryLa~ritoiy;We:iIjnitån ..pub.iic:H;:;s~ltai, W~lling-i~~;<Ne";Ze~l~itd.·..·Sco.t1M H~Y;RåsplratoryTetliiiida:i1;Kelllii RGalo, PhD,Seni6f l'echhlcal.OHicer;·.,%:;·i;·;'·;~j,~~6\,;~r.~I;bj:Jrg~~~·:~~0~~:.~i·~;:;~p~n~~~~e:;6~·:J~li~h:Cran~;.DeØartrn~n~.of.l,!lei;llc~nt;l.' We,lIl.ngtonSch.,!ol.ofMedICIn~. PO l?o?':r.~4~,:W(lllln.gto~~ew Zealand: '. ; ...'

;.C!'~n~~.VI~'rl;Bg;~,iic/ii.. \; ... ':':' > "'.'." ,,-"., '..' ".".72

.. '

MJA Vol174 15 January2001

c"scimated on the basis of a recent line FEV1 was within 10% ofthe previ-~dy rhat addressed sample-size calcu- ous study,

,\fI%tions for studies of EIA. Ten subjects The first ep en test was to confirrnwere require d. for a study ro have 90% EIA, defined as a 15% or greater fall inpower to show a 40% rednetion in EIA baseline FEV

1in th e 30 minures fol-

using area under the response-time lowing exercise. This was followed incurve, and seven subiects for similar

positive subiects by (WO randomisedpower using rnaximum fall in force dexpir at or y volume in on.e seco n d double-blind challenges, at Ieast 24

" hours apart. The exercise protocol was(FEV1)·7similar, exe ept that during exercise andfor la minures after exercise the subjectsbreathed a gas mixture via a mouthpiecefrom a Douglas bag. This gas rnix waseither air, or air enriched with 3% CO2

(oxygen 21 %). (An initial study in ancn-asthrnatic volunteer with 6% CO2

caused vasodilatatioo and s ever eheadache which prevented completionof the exercise prctocol.) The hjirnidiry(20% relative hurnidiry) and t;mpera:'ture of the gas mixtures in both ran-domised challenges were identical.

Minute ventilation wa s re cord edthroughout the exercise period in nine ofthe 10 subjects. Ae 10 minures af terexercise, the rnouthpiece was removedand subjects then breathed room air.

Intervention

The srudy intervention is surnrnarised inBox 1. Subje cts undertook three stan-dard exercise tests, running 00 aninclined treadrnill at a speed designed tobring the heart rate up to 70% of pre-diered maximum in one minure andthen at 90% of predicted maximum fora further four minutes. Using a Vitale-graph wedge bellows spirometer, werneasured FEV1 before exercise and thenafter exercise, at rwo-minute intervals forla minures and at five-rninute intervalsfor a further 20 minures. Each test wasperformed at"the same time of the day,at least rwo hours aner the previousmeal, and was conducted only if base-

1: Summary of the study Intervention

f 22 people wlth esthmarecruiled by

adverusemsnt andtrom hospital

\.. oulpalJenls

- 12 sub)ecis excluded:8 had c 15% tallin FEV 1 atter exarcJse

2 could not complete sxerclss chaJlenge2 had> 50% fallln FEV1

and requlred urgent bronehodilator

Standard exsrclse challengeon Incllned treadmlll:

1 min at 70% pradlcledmaxJmum heart rata, Ihen

4 min al 90% predlctadmaxlmum haart rats

2 randomlsed double blindexercise challenges

brealhing air or 3% CO2via mouthpleee trom

Douglas bag.Basellna FEV 1 wtthln

10% af prevlous challenge

10 sub)ects wlthbaselIne FEV 1 wlthln

10% of prevlouschallenge and> 15% faU

In FE::V 1 atter exarclse Qj>

~iiiI

Q)a'ti~'tioI~'ti

'E";::;i5Q)

~.:.:~

lE1iiD>-

.J:l"'O

Q)

"O";;;oo.c-,

~------ ~ ~ ~ ~3

After exerelse,FEV1 recorded al

2 minuts Intervals for10 mlnutes whlle

Bub)ects breathed alrar 3% CO2 from

Oouglas bag

-___ 8_ro_n_c_ho_d_lIa_t_or__ ...lI __

At 10 mlnules,moulhplece removad and

sub)ects braathed rcom airfor 20 minutas, wllhFEV1 racorded at5 mlnute Intervals

FEV, = foreed expiratory volume In one seeond.

MJA Vol174 15 January 2001

':1: I' I

Oufcome measures

Intervention studies af EL.l\ usuallymeasure rnaxirrrum decline in FEV1 2S"2

percerrtage of the baseline value, andarea under die FEV, response-timecurve, which provides an assessment afthe duration as well as the degree afposr-exercise airway obstruction. Wemeasured both these pararneters. Dif-ferences in mean values were cornpared'using palred t tests for norrnally distrib-uted data and the Wilcoxon signed ranktest for non-normally distributed data.

Ethics approval

The study was approved by the Welling-ton Regional Ethics Cornrnittee.

Twenty-rwo subjects with a his tory ofEIA were recruited (Box :). Eight sub-jecrs did not rneet our criteria for EIA,and rwo were unable to cornplete rheexercise test. A further two subjects wereexcluded be cause they exp eriericedsevere bronchoconstricrion (a decrease inFEV1 > 50% from baseline) immediatelyafter exercise, and required imrnediatetreatment with a bronchodilator. Tensubjects (six male) aged 18-46 yearscompleted the study, All subiects wereusing inhaled l3-agonists as required,seven were taking regular inhaled corti-costeroids, and all but one subject hadhad asthma since childhood.

Box 2 shows mean percentage fall inFEV1 folIowing exercise, breathing air arair enriched with 3 % CO2• The rneanmaximum percent fall in FEV1 afterex er ci s e was 19.9% (95% Cl,14.4%-25.1 %) for air and 27.4% (95%Cl, 19.7%-34.1%) for CO. (P=0.12)(Box 3). The mean AUC for the total30-mmute post-exercise period was 355(95% Cl, 216-493) for air and 520(95% Cl, 399-642) for CO2 (P=0.07).

Ten minures after exercise the mouth-piece was removed and subjects breathedroom air. This had no effect an FEV1when thesubjects were already breathingair, but when tbey changed from 3%cal to room air there was a significantfurther fall in FEV1 (Box 2). TherneanAUC for the period 10-30 minures anerexercise was significantly greater anerbreathing Cal than aner breathing air:

,II;

iI

I~iI·II

73

,r"M,., doc,",,, ;, ,,,,.dexplratory volume in aneseccnd (FEVj) for 30 minutesatter exercise breathing air (11:I)or 3% CO2 (.)

o .,--~----,rl0--lc-5 --=:..:::.:::.-:;:="'3

~ ·5.5!i ·10

'"g' ·15~~ ·20'"a.

æ ·25

'"::;·30

At 10 minutes after sxercise subjecls ramovedthelr rnouthpiacas end breathed room air for afurther 20 rnmutes. Error bars indicate standarderror of the mean.

3: Maximum percentage fali inFEV 1 foliowing exercise foreach subiect while breathing airand 3% CO,

suojsct Air 3% CO,

123456789

10Mean95% Cl

16.7%27.8%

6.8~ti19.2%33.6%19.6%18.4%23.5%25.8%

7.7%19.9%

14.4%-25.1%

18.3%15.4%21.1%19.3%27.5%38.7%19.2%47.0%43.6%26.2%27.4%

19.7%-34.1%

4: Effects of increasing inspiredCO, concentration on exerclse-induced asthma (EIA)

I· Increased insplred CO2 I~--~/~ ~~~--~

Increased mlnuteventilation

Incraased alrwayCO2

lIncreased alrwaydrying

Direct relaxanteHeetan airwaysmooth musclsIncreasad mast

eell medlalorrelease j

Decreasedbronchospasm

No overall etteet an EIA

74

275 (95% cr, 192-358) and 137 (95%Cl, 46-227) (P= 0.02), respectively,

Mean minure ventilation for the lastfour minutes of exercise (in the nine sub-jects in whorn it was measured) was sig-nificantly increased when s ubje ctsbreathed 3% CO2: 77.5 Umin (95% er,69-86Umin) for 3% CO2' comparedwith 68.7 Umin (95% cr, 59-78Umin)for air (P=0.02).

Breathing CO2-enriched air during andaner exercise did not prevent EIA.However, the unexpected observationthar the post-exercise FEVI dccreasedsigniflcantly when COl was discontinued10 minures aner the cessation of exercisesuggests that an increased airway CO2level does have an effect on ihe; airway.This observation requires explanation. -

EIA is thoughr to be caused by releaseof mediaters from mast cells triggered byairway drying," and this stimulus wil! bestronger with increased ventilation drivenby a high CO, level. However, a highCO. level wil! oppose this effect by adirect relaxant action en airway smoothmuscle. Q.IO Our results are consisrentwith these opposing effects (Box 4).Despite the increased minure ventilationinduced by the CO" the fall in FEVIwhen breathing air or 3% CO, was sim-ilar for the first 10 minures aner exercise,This suggests that an increased brcn-cho c ons tri ctor stimulus from th eincreased minure ventilation (greaterairway drying leading to greater media-tor release) was being countered by adirect relaxant effect of the increasedCOl on airway smooth muscle, After theCOl was discontinued, this direct relax-ant effect af COl was rernoved, allewingthe increased bronchoconstriction tomanifest as a sharp and sustained fall inFEV1•

A recent randornised controlled trial ofBBT in asthmatic patients found that, forthe BBT gro up compared with the con-trol group, there was a significant reduc-tion in minure ventilation and ~2-agonistuse and a substantial rednetion (49%) ininhaled corticosteroid use in the BBTgroup at three months.!' Despite thisreduction in mediearien use among theBBT gro up, there was no decline inmorning peak expiratory flow or FEVI.

End-tidal CO2 was similar in both groupsthroughout the srudy,

Could changes in airway COl explainrhe apparent improvement in asthma fol-lowing BBT? 'Ibis seerris unlikely, forseveral reasons:

we were unable to show that EIA isreduced in subjects breathing 3%COl;

end-tidal COl is not increased in sub-iecrs who have undertalren BBT; II

breathing 6% CO, is required to abol-ish ELI\. af ter exercise challenge.P Toachieve a similar effect by voluntaryhypoventilation would require severalminures of profound hyp oventilaticnor apnoea.Whatever the mechanisms for the ben-

efits of BBT, they are unJikely to resultfrom direct effects of CO, 011 theairway. Nevertheless, further study ofhypoventilation exercises and the effectsof CO. in asthrna are warranted giventhe results of the randornised con-trolied trial of BBT and our finclingsthat CO2 does affectairflow obstruction.

Thls study was supperled by a research granllrom tI,eAsthma and Respiratory Foundalion ol New Zealand.Julian Crane Is supporled by a senior research lellowshipIrom the Health Research Councl/ ol New Zealand. Theauthors would llke to thank all !he volunteers who tookpari In this stucy,

1. Kmletowicz Z. Complemenlary medicine should beintegrated into lhe NHS. BMJ 1997; 315: 1111-1116.

2. Hensley M. Glbson P. Promoting evidence-basedallernatlvemedlelne. Med J Aust199S; 169; 573·574.

3. Kent H. Ignore growing patient Inlerest In alternalivemedieine at your perlt, MOs warned. CMAJ 1997;157; 1427·1428.

4. Angetl M. Kassirer J. AlternAtive medlelne - therlsks ol unteslod ~nd unregulated remedies. N EnglJ Med 1995; 339; 639·841.

S. Arneisen P.Every breath you take. N orlh Sl1oroCity:Tandem. 1997.

6. Rsher H. Helton P, Buxlon SJ, Nadel J. Resislance10 brea)hlng durlng exercise-Inducec aslhmaattacks, Am Rev Resplr Dis 1970; 101: 885·696.

7. Holstra W. Sont J. Slerk p. et el. Sample size esti-malion In studies monltorlng exerclse·lndueedbronchoconstrlctlon In asthmalic chl/dren. Thorax1997; 52: 739·741.

8. Andersan SD. Daviskas E. Smilh CM. Exerejse-induced asthma: a dillerence In opinion regardingthe stimulus. Allefgy Proceedings 1989; 10: 215·226.

9. Herxheimer H. Hyperventilatian asthma. Lancet1946; 1: 83·S7.

10. Sterling G. The mechanlsm ol bronchoconstrictiondue te hypocapnla in men. elin Scl 1968; 34: 277.

11. Bowler S. Green A. Mitchell C. Butey\<o brealhlngtachniques In aSlhma: a bl/nded randomlsed con-trolled trial. Med J Auet 1998; 169: 575·578.

12. Fisher H. Hansen T. Sile ol action of inhaled 6 per-. cent carbon dlaxide in the lungs ol asthmatlc sub-

}ects belore and aller exercise. Am Rev Resp Dis1976; 114: 861·870.

(Received 12 Feb 1999. sccepted 19 Jul 2000) Q

MJA Vo11?4 15 January 2001

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We studied six patients with symptomatic hyperventilation,using new techniques to quantify baseline variability ofrespiratory variables, and to assess C02 sensitivity around thecontrol point using a stimulus not detectable by the subject.We compared them with six normal subjects and six patientswith mild asthma. Symptomatic hyperventilators had normalmean ventilation and end-tidal carbon dioxide tension(PETC02) at rest. Asthmatic subjects had higher ventilationand lower PETC02. Symptomatic hyperventilators had alarger number of sighs and abnormally wide fluctuations in baseline for inspiratory time,expiratory time, and PETC02. These could not be explained by an abnormal ventilatory responseto a transient C02 input; the transient response near the control point was undoubtedly normal.

Eur Respir J 1988; l: 846-851Copyright © ERS Joumals Ud 1988

Original Articles

C02 respons e and pattern of breathingin patients with symptomatichyperventilation, compared to asthmaticand normal subjects

J Hormbrey, MS Jacobi, CP Patil, and KB Saunders

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191"'1.' . 'HOME~'7:',·· A. Bruton and S. T. Holgate;,'......•Hypocapnia and ~sthma: .AMec~anism for Breathing Retraining?", __ Chest, May 1, 2005, 127(5). 1808 1811."c .• [Abstract] [Full Text] [PDF]

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G. Van Den Wittenboer, K. Van Der Wolf, and J. Van DixhoornRespiratory VariabiIity and Psychological Well-Being inSchoolchildren

~~==u Behav Modif, October l, 2003; 27(5): 653 - 670.[Abstract] [PDF]

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M Thomas, R K McKinley, E Freeman, C Foy, P Prodger, and D PriceBreathing retraining for dysfunctional breathing in asthma: arandomised controlled trial

IS. But this should not mask the special role of thenan in the cransrni.ssion of possible reratogens to the

~Healt11,

tomia1i. 9020. USA E. B. HOOK

IV or short-stav and discharge frommental handicap hospitals.art af the strategy for the discharge of patients from:ap hospitals money is available for distribution to theth authoriry for every long-stay patient who islID hospital. On the surface this seems commendablejs that the hospital will need less money to provide.ts remaining patients and that the lot af patientscornmunity facilities will be improved.nly transferred for patients who have been resident inany years. If a patient is admitted to a mental handicapIse of illness or behavioural disturbance at home andritable placement in the community he remains in:e the patient is no longer being supervised by thervices there is less urgency to find a suitable home forny individuals remain in hospital for same time.h regional and national policy proscribes Iong-termmental handicap hospitals there is a curious advantagech patients long-stay,ganise case conferences for such individuals I amwhether the patient is a long-stay or a short-stay! patient can be designated long-stay a eommunitysought eagerly because discharge will then be

by an agreed sum of money. The wheels are set in.thin a month or two visi rs have been arranged to bothestablishment and the training centre and the patientliseharged. Ifthe patienr is short-stay these initiatives.aken and the patient languishes in hospital.e a word it means just what I choose ir to rnean", saidipry in Lewis Carroll's Through the Looking G/ass. He.ate how long means short and short means long.

N E42 5NT. U 1< S. P. TYRER

Doctors' nours. Dec 22/29 editorial makes many criticisms, most of., of the excessive hours worked by doctors in theth Service. It also criticises the heads of agreementMinisterial Working Group as not addressing all thcunately your editorial is grossly inacenrate in certainh will dilute the impact of some of the well-directed~ sentence "Newly appointed consultants will have a-ernent in patient care when on call", far fromseniority of the group" is not in the agreement at all.ejudices most of the discussion in the subsequentthe need for consultant expansion. The agreement1.4 that it reaffirms a comrnitrnent to the Aehieving anent's objective of "rnaintaining existing rates of·ansion. Over and above this, additional career gradezconsultants, will be required in particular places andile agreernent goes on to detail some of the ways inaal consultants can help in the reduction of junior

rtes that consultants should not be required to beesident when on eall. There are many' ways in whichisultants ean help without being resident. Foraergency work a lot of uneeessary surgery is done atuld be handled with benefit by a fresh team led by anonsultanr the folIowing day. This would enableunior staff to take part in shift systems or have time off

af ter a night on call.I agree that rhe sums on offer are inadequate when ser beside the

money spent on implementing the larest NHS reforms. Far greaternurnbers of consultants are Tequired, with the fulI funding ofadditional secretarial and other staff, to help reduee junior doctors'hours.

The position in Scotland is even more difficult because thepresent rare of consultant expansion is 0·5%, a sixth of that inEngland and Wales. With the crisis management being used tobalance books before April l in· areas such as Lothian alreadythreatening cuts in consultant nurnbers, it is clear that adequatetargeted funding is the prime requirernent if a reduetion in juniordoctors' hours is to be achieved.

41 Constitution Street.Dundee 003 6JH. UK

ARTHUR McG. MORRIS,Chairman, Scottish Commineefor Hospital Medical Services

'~*The passage in question was removed from a draft of theagreement at a very lare stage indeed, as was a sentence aboutyounger consultants being asked to do more emergency work thanolder ones. Perhaps it is not just fmancial commitment that needs tobe questioned in this discussion.-ED. L.

Exercise induced asthma: the protective roleof CO2 durinq swimming

SlR,-Reggiani et al' found less asthma associated with the lowermaximum minute ventilation (VE) in competitive swimming thanin running or cycling. It is well known that swimming eausesless exercise-induced asthma (EIA) than do other forms ofexercise'P-eindeed in some cases no EIA is seen. No explanation forthis has been fortacoming, although it has been postulated that thehumid air breathed dt!rir:ig ,wimming is protective. I suggest that theprotective effect of swimming might result from hypoventilationand hypercapnia due to constrained breathing patterns.

During swimming VE is mueh less than during either running orcycling.t+" The constrained breathing patterns necessitated by allthe competitive swirnming strokes, apart from backstroke, areprobably responsible for the lower VE seen with this form ofexercise. This, in rum, reslllts in some "retention" ofCO, as well asenhanced oxygen extraction." The increased alveolar CO, tension(P A CO,) might prevent EIA from swimming, either because iteauses bronchodilatation or. owing to its vasodilatory properties,because it preserves the bronchial bloodflow despite airway cooling .Preservation of bloodflow may prevent both excessive airwaydrying" and/or post-exercise reactive hyperaemia.?

A high anaerobic tolerance has been regarded as irnportant forcompetitive swimrners. t. common training programmeineorporates controlled frequeney breathing where swirnmersrestriet breathing frequencies from a normal breath every [WO armstrokes to every four, six, or eight strokes; this eauses a decrease inVE, and P ACO2 values can be as high as 6·95 KPa (52 mm Hg) whenbreathing once every six .~strolces.' The asthmatic swimmersstudied by Reggiani et al' were trained eompetitive swirnrners; allwere afforded completeprotection from EIA and even recorded amild brochodilatation after swimming, but after cycling or runningthey had a striking reduction in FEV,. To establish if humidity ofthe inspired air was irnportant Bar Yishay et aF standardised heartrate, oxygen eonsurnption, VE, tidal volurne, and degree afhumidity in their studies on untrained asthmatic ehildren. Wheneomparing running and swimming, under the same conditions ofrespiratory heat and water loss, they found a 13% fall in FEV, afterswimming and a 20% fall in FEV, while running. In their attemptto standardise the VE of swimming to running, they might haveremoved some of the proteetion against EIA afforded by thebiomechanics of swimming (ie, hypoventilation).

In most land-based forms of exercise, pattems of breathing arenot eonstrained, VE inereases proportionately throughout exereise,and end-tidal CO2 tensions are either normal or low." Therefore

180 THELANCET

there is no hypercapnic stimulus for bronchodilatation andasthmatics have no protection. In addition, it has been noted thatasthmatic subjects usually hyperventilate out of proportion to theirCO, produetion during exercise, whereas healthy subjects do not.

Although some workers believed that hypocapnia could berelevant' they could not dernonstrate this-perhaps merely becausean increase in CO2 acts as a more powerful bronchodilator than adecrease in CO, does as a bronchoconstrictor.

Because end-tidal CO2 tensions have not, as far as I am aware,been measured in asthmatics while swimming (although they havebeen well documented in healthy subjects in sports medicinejoumals) the potentially important protective propert y ofhypercapnia may have been overleoked.

lnstitute of Respiratory Medicine,Royal Prince Alfred Hospital,Camperdown. NSW 2050. Australia PETER M. DONNELL y

1. Reggiani E. Marugo L, Delpine Al Piastra G, Chiodini G, Odaglia G. A comparison afvarious exercise challenge tests an airway reacciviry in atopical swimmers. J SPOI'esMed Phy, Fimess 1988; 28: 394-401.

2. Bar- Yishay Ej Gur I, Inbar O. Neuman I, Dlin R, Godfrey S. Differences berweenswimming and running as stimuli for exercise-induced asthma. Eur J Appl Physiol1982; 48: 387-97.

3. Kohrt WM, Morgan DW,Bate5 B, Skinner ]S. Physiological responses of tri-athletes10 maximal swimming, cycling and running. Med Sci Sporu Exerøse 1987; 19:51-55.

4. Cocdain LJ Stager J. Pulmonary struerure and funcricn in swimmers. Sports Med1988; 6: 271-78.

5. Town GP~ Vanness 1M. Metabolic respenses to controlJed frequency breathing incompetitive swimmers. Med Sci Sports Exerase 1990j 22: 112-16.

6. Andersen SD. Is mere a unifying hypothesis for exercise-induced asthma? J IlflergyGlin Immunol l~84; 73: 660--65.

7. M~.i'adden E~<.Jr. Exercise-induced asthma as a vascular phenomenan. Lance/ 1990j335: 880-il3.

8. Asmussen EJ Neilsen M. Studles in the regulatian af respi ration in heavy work. ACIQ

Physiol Scand 1946; 12: 171-78.9. Silverman M, Anderson SO, Walker SR. Merebette changes preceding exercise-

induced bronchoconstricrion. Br Med] 1972j i: 207-09.

What eauses motoneuron disease?SIR,-Your Oct 27 editorial is correct to emphasise the

epidemiological aspects of motoneuron disease (MND). Althoughthe ultimate truth may be found by molecular biologists, theepidemiological approach, in the short-term, is more likely to givedues as to cause and prevention. The ubiquinated inclusions foundin neurons of patients with lviND and other neurodegenerativedisease provide a marker for a sick neuron. However, Dr Swash andDr Martin (Dec l, p 1379) fail to mention that such inclusions arepresent in cells outside the nervous system and rnay be no moreimportant than lipofuscin. The importance of genetic factors inMND can be assessed by twin studies. We haveidentified 120 pairs,ofwhom only 2 are concordant. In a recent srudy of90 pairs,' nonewas concordant. There are only 2 other well-docurnented twin pairsand in both instances they were dizygotic and concordant.t-' Theevidence, therefore, points strongly to an environmental cause='such as a virus" ar chemicai agent. s

Supported by the Motomeurone Discase Association.

Department af Neuroloqy.Ipswich Hospital.Ipswich IP4 5PD. UK

C.H.HAWKESA. J. GRAHAM

l. Currier- RD. Conwill DE. lnfluenza and physical activiryas possible risk factors foramyotraphic lateral sclerosis: a srudy af twins. In: Rose FC, Norris FM, eds,Amyotraphic lateral sclerosis: new advances in toxicology and epidemiolcgy.London: Smith Gordon, 1990: 2:>-28.

2. Duman J, Macken J, de Barsy TH. Concordanee for arnyorrophic laterafsclerosis in apair of dizygous rwinsaf consanguineous parents.] Med Genet 1971; 8: 11~16.

3. Estrin WJ. Arnyorrophic lateral sclerosis in dizygaus twins. Neurology 1977; 27:692-94.

4. Kenncdy PGE. On the possible role of viruses in the aetiology of motor neuronedisease: a review.J R Soc Med 1990; 83: 784-8?".

5. Hewkes CH, Cavanagh, JB, Fax AJ. Moroneuron disease: a disarder secandary 1.0solvent expcsure? Lancet 1989; i: 73-75. .

SIR ,-D r Swash and Dr Martin rightly emphasise theimportance of rnolecular pathology and genetics in the investigationof the cause of moroneuron disease (MND). Although 90% of casesare sporadic with no family his tory of the disorder, familial casesconstirute the remaining 10% and can be adult onset, autosomal

dominant, and associsjuvenile-enset cases ayears and spasticity , fclinical feature. Inherhas been no report ol'same family l

The gene locus for(where degenerationspinal cord) has beenout, this fmding provodetermined degeneraimodel for investigatir:juvenile onset. There :DNA sampies from th

European Neuromuscular (3743JN Baarn. Netherland

l. Emery AEH, Hollaway ,139-45.

2. Melki), Sheth P, Abdelhs[O chromosome 5ql~-

SIR,-We stronglygeographical distri buiepidemiological studiethat the worldwide inciboth England and Walwe found that MN1population was a hall" <

and that men from tiEngland had half the nfrom MND comparedto Dr Swash and Dr iMi[chell's statement Omight yield newinsigh

Supperted by the Mote

Charing Cross Hospital,London W6 8RF. UK

Medieo-Social Research BeDublin, Republic af tretand

I. Elian M, Dean G. In: Ros:advances in toxicolcgy ~

Lang-tern1

SlR,- The natural hiarteries (C- TGA) with-remains poorly 'defimreported.':" We describ.C- TGA, in whom the <

the basis of non-invasidoppler echocardiograjand intravenous digital.

A 67-year-old man vfor evaluation of electrocsingle, accentuated seCOJfaint holosystolicrnurrmleft stemal border. EeGwith no septal Q wave irwaves in V3-V6, l, andenlarged, and the aseendright upper mediastinalMRl (figure), and DSAaorta arose from the left-heavy trabe~ulatio) -'arose from the rig. /intracardiac abno r -!

slight hypocontrac U:(anatomi cal tricusj

A 60-year-oldabnormality, had ,holosvstolic murmui"s-