New Zealand Journal of

SPORTS MEDICINEOfficial Journal of Sports Medicine New Zealand Inc

Volume 38 • Number 3 • 2011

NZ JOURNAL OF SPORTS MEDICINEInstructions to Authors

GENERALThe New Zealand Journal of Sports Medicine is the official journal of Sports Medicine New Zealand, publishing material relevantto sports medicine and related disciplines. The New Zealand Journal of Sports Medicine welcomes submissions of originalmanuscripts from both members and non-members of Sports Medicine New Zealand in the following areas: sports medicine,sports physiotherapy, clinically relevant sports science, rehabilitation, coaching issues as they relate to sports medicine, exerciseprescription and training, sports chiropractic, sports podiatry, and sports psychology.

Manuscripts must not have been published elsewhere except in abstract form. Manuscripts will be reviewed by the editorial boardand/or experts in the field of interest. Submissions are in the following categories:

a Original Research b Case Reports c Review Articles d Editorialse Letters to the Editor f Sports Medicine Pearls g Policy Statements

SUBMISSION DETAILSManuscripts are to be sent to The Editor, New Zealand Journal of Sports Medicine, Sports Medicine New Zealand, PO Box 6398,Dunedin, New Zealand. Telephone +64 3 477 7887, facsimile +64 3 477 7882, email smnznat@xtra.co.nz. The manuscript textshould be submitted in MS Word format (if using Vista please save the file as Office 2003 compatible, ie, .doc. Please do not usestyles for headings, etc, ensure your manuscript is in the style ‘Normal’. (For submission of graphics, please see Tables, Illustrations,Figures, Photos below). The manuscript may be sent via email however one hard copy must also be submitted, including anytables, figures, and photographs. Manuscripts should be double-spaced with wide margins. Each page should be numbered. Themanuscript should include the following: title page; structured abstract (followed by five key words); introduction; methods;results; discussions; conclusion; acknowledgements; references; tables; figures.

Case reports are to have no more than two figures and are not to include an abstract. There should be no more than 12 referencesfor a case report. The structure of a case report is as follows: introduction; case report; discussion.

Structured abstracts are to be no longer than 300 words and should use the following subheadings: aim; study design; setting;participants/subjects; interventions; outcome measures; results; conclusions.

Abstracts for review articles should use the following headings: aim; data sources; study selection; data extraction; datasymphysis; conclusions.

The title page should include the title of the article and a running title not exceeding 45 letters and spaces, authors’ names (firstname, middle initials, last name), degrees, affiliations with institutes, contact details for the corresponding author (to include name,address, telephone, fax, and email).

The standard for spelling is to be in accordance with the Oxford Dictionary.

TABLES, ILLUSTRATIONS, FIGURES, PHOTOSOne hard copy of tables, illustrations, figures, photos, etc, must be submitted. Tables should be included on a separate sheet ratherthan in the body of the text. Identify all illustrations with the manuscript title, name of author, figure number, and. if necessary,identification of the top of the image, on the back of the illustration in pencil. All markings should be removed from x-rays beforephotographing. Please do not produce graphics in Microsoft Word. Graphics should be supplied in TIF, EPS or PDF format,preferably at a resolution of no less than 300 dpi.

STYLEDrug names: generic only are to be used. Abbreviations: the American Medical Association Manual of Style (9th edition 1998)(published by the American Medical Association, 535 North Dearborn St, Chicago, IL 60610, USA) is to be used for abbreviationstyle. The List of Journals Indexed in Index Medicus (Superintendent of Documents, US Government Printing Office, Washington,DC 20402, USA, DHEW Publication No. (NIH) 83-267;ISSN0093-3821) is to be used for abbreviations for journal titles.

REFERENCESReferences are to be numbered in alphabetical order. Names of journals should be abbreviated according to the format approved byIndex Medicus. All references listed must be sited in the text. Journal titles that are single words only should be spelt out in full.All authors must be listed. Pagination should be inclusive. Examples of the appropriate formatting of references are given below:

Journal Article: Speedy D B, Kelly M, O’Brien M. The effect of pre-exercise feeding on endurance exercise performance.NZ J Sports Med 1998; 26:34-37.

Book: McRae R. Practical fracture treatment. Edinburgh; Churchill Livingstone, 1989.Chapter in Book: Figoni S F. Spinal cord injury. In, Wikgren S (ed.): ACSM’s exercise management for persons with chronic

diseases and disabilities. Champaign: Human Kinetics, 1997; 175:179.COPYRIGHTThe New Zealand Journal of Sports Medicine is copyrighted by Sports Medicine New Zealand Inc. No portion(s) of the work(s)may be reproduced without written consent from the publisher. Permission to reproduce copies of articles for non-commercial usemay be obtained from Sports Medicine New Zealand Inc, PO Box 6398, Dunedin, New Zealand, phone +64-3-477-7887, fax +64-3-477-7882, email smnznat@xtra.co.nz.

The opinions expressed throughout thisjournal are the contributors’ own and donot necessarily relfect the view or policyof Sports Medicine New Zealand (SMNZ).Members and readers are advised thatSMNZ cannot be held responsible for theaccuracy of statements made inadvertisements nor the quality of the goodsor services advertised. All materialscopyright. On acceptance of an article forpublication, copyright passes to thepublisher. No portion(s) of the work(s)may be reproduced without written consentfrom the publisher.

PUBLISHERSPORTS MEDICINE NEW ZEALANDPO Box 6398, DunedinNEW ZEALANDTel: +64-3-477-7887Fax: +64-3-477-7882Email: smnznat@xtra.co.nzWeb: www.sportsmedicine.co.nz

ISSN 1175-6063 (On-Line)

EDITORDr Bruce Hamilton

ASSISTANT EDITORMr Chris Whatman

Contents

EditorialBruce Hamilton ___________________________________________ 64

Letters to the Editor ________________________________________ 66

Best of British _____________________________________________ 68Chris Milne

ArticlesTHE SUPERIOR LABRAL ANTERIOR TO POSTERIOR ______ 72(SLAP) LESION: AN ELUSIVE PATHOLOGYDiarmuid Molony, Khalid Mohammed

NUTRITIONAL CONSIDERATIONS FOR FLAT _____________ 80RACING JOCKEYSStephen Gurr

ACUTE OCULAR TRAUMA: RECOGNITION AND _________ 85MANAGEMENT IN THE SPORTS ARENAAlbert Vosseler, Graham Wilson

Cardiology ConundrumsROLE OF EXERCISE STRESS TESTING IN ATHLETES _____ 90WITH REPOLARISATION ABNORMALITIESMathew Wilson, Othman Salah, Bruce Hamilton,Sanjay Sharma, Hakim Chalabi

Conference ReviewsUK SPORT AND EXERCISE MEDICINE (UKSEM) ___________ 94CONFERENCE 2011Chris Whatman

NZ SPORTS MEDICINE CONFERENCE ____________________ 97Ian Murphy

ReportsHIGH PERFORMANCE SPORT NEW ZEALAND ____________ 98CHANGES TO ENHANCE NZ SPORTSPEOPLE WINNINGON THE WORLD STAGEDuncan Reid, Tony Edwards, Sharon Kearney

SPORTS MEDICINE NEW ZEALAND 2011 _________________ 100NATIONAL CHAIRMAN’S REPORTStuart Thomson

Conference AbstractsSELECTED ABSTRACTS FROM THE 2011 _________________ 101NZ SPORTS MEDICINE CONFERENCE

New Zealand Journal of

SPORTS MEDICINE

NZJSM Vol 38 No 3, 2011

SPORTS MEDICINENEW ZEALAND

EDITORIAL

64 NZJSM

Scurvy, Gissy and the Plague of

Tendinopathy

When Englishman Captain James Cook landed in Poverty Bay on October 8 1769 (less than a kilometer fromwhere I grew up in Gissy), little did he know that he would set off a chain of events that would, amongstother (obviously less notable) things, culminate in the publication of this journal. Cook of course was not

the first European to discover NZ, that honour belonging to Dutchman Abel Tasman who parked his ship off theNelson area a few years earlier, many centuries after our Polynesian ancestors first inhabited this fine land. However,Cooks journey was notable for more than just charting NZ, as his was a voyage of scientific investigation (observingthe traverse of Venus from Tahiti), as well as one of exploration. It was this combination of tasks that resulted in aprolonged tour but it was the low incidence of scurvy on board Cook’s ship that separated his voyage from that of hispeers. Life was tough in those days, and Cook must have been concerned about the voyage, as for over 150 years,scurvy had plagued sailors and resulted in thousands of lives lost, ships abandoned and ultimately failed missions.Typically, up to 50% of sailors on board “long haul” voyages may have been expected to suffer a slow and agonisingdeath, and between the years 1500 - 1800 up to 2 million sailors may have perished from scurvy. Cook however wasfacilitated in his journey by the endeavours (excuse the cheap pun) of his sailing forebears, for without their attemptsto find a cure for scurvy, it is unlikely that Gissy, New Zealand and for that matter much of the southern hemispherewould have been known to Europeans until many years later. Unlike many of his peers, Cook instigated all thecontempory theoretical and practical means of preventing scurvy, and while the specifically successful treatmentwasn’t known, he was the first mariner to successfully combat scurvy, and hence have enough surviving sailors toenable his successful navigation of the globe. It was only in the late 18th century, when it became clear that navaldominance could be achieved through the elimination of scurvy, that any real investment in a cure was made, andshortly after the recognition of citrus fruit as a prevention was identified. Remarkably, the presence and absence ofscurvy amongst naval seamen may have played a crucial role in the independence of both America (from Britain) andBritain (from Napoleon) respectively. Scurvy is now known to result from a deficiency of Vitamin C (ascorbic acid),found in fresh fruit and vegetables in abundance, but scarce on long haul shipping due to the inability to store freshfruit and vegetables and the use of copper pots which reduced Vitamin C availability. Despite this, the managementof scurvy continued to fluctuate with its reappearance in 19th and early 20th Century polar exploration, and it continuesto appear in nutritionally deficient countries. Remarkably however, 300 years earlier in 1601, Sir James Lancasterstumbled across a genuine cure for scurvy, lemon juice, but due to the lack of scientific evidence of its curative ability,this effective treatment was slowly lost over the years, only to be replaced by multiple unsubstantiated theories andconcoctions, resulting in thousands of deaths and vast costs; hence, the treatment for scurvy remained elusive foralmost 200 further years. The medical thinking of the time was focused on the balance of the humors, which restrictedthe ability of clinicians of the day to consider deficiency as a cause of such a profound disease, and technology limitedtheir ability to investigate adequately.1

Vitamin C is of course involved in the synthesis of collagen, the absence of which results in collagen breakdown andsymptoms of scurvy result from this. It would be brave or foolish to try and link the high frequency of tendinopathythat we observe in many sports with a deficiency of vitamin C (although a quick search in “journal google” will reveala clear and profound relationship), and fortunately, I am not going to try that today. However, such are the vast numberof aetiological theories and treatment options currently available for the treatment of tendinopathy,2 a comparison withthe convoluted history of understanding scurvy seems more than reasonable. In the late 1990’s, the term tendinitis wasdiscarded as representative of an age of dogma, and not reflective of the newly identified histo-pathology. Tendinitiswas replaced by the catchy terms “tendinopathy”, “tendinosis” and to describe the histopathological changes observed,the term “degenerative”. In the last 10 years there has been an abundance of research trying to establish the aetiology,pathophysiology and best management of this challenging condition, and it is clear that we have come a long way inour understanding of its complexity.3 However, despite the abundance of both in vivo and in vitro research and theexplosion in information availability through the internet, we appear only marginally closer to a definitive understandingof either the aetiology or management of “tendinopathy”. Many fundamental questions remain unanswered, andauthors are now questioning the use of terms such degenerative when describing the pathology. Management approachesnecessarily remain pragmatic, regional and inconsistent in the absence of a clear aetiology.

Given our necessarily temperocentric views, one wonders if we are making the same mistakes as our 18th centurycolleagues. Is it that we actually have the answers in front of us, but are unable to put the puzzle together, blinded by

EDITORIAL

our beliefs or recycled dogma - as was the case in the 17th century management of scurvy? Or is it simply that we don’tyet have the tools required to answer the questions we are asking, or the understanding to ask the right questions?Asking the right questions is a good start, but as we are finding out, providing the answers is a lot more challenging.As practitioners in the burgeoning field of Sports and Exercise Medicine it is incumbent on us all to challenge dogmaand search for the most appropriate means of managing injuries such as tendinopathy. While not all of us are in theprivileged position of being able to perform high level clinical trials, critical self analysis and the accumulation ofobjective, quantifiable data is achievable and mandated for us all in order to ensure we are offering our patients thehighest level of care. In critical reasoning and with the accumulation of such data, perhaps we will avoid the delaysthat our medical forefathers faced in understanding equally fascinating clinical conditions.

References1 Bown S. Scurvy: How a Surgeon, a Mariner, and a Gentleman Solved the Greatest Medical Mystery of the Age of Sail. 2005,

New York, Thomas Dunne Books. St. Martins Griffen.

2 Cook J and C Purdam. “Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy.” British Journal of Sports Medicine 2009; 43: 409-416.

3 Eliasson P, Andersson T, et al. “Influence of a single loading episode on gene expression in healing rat Achilles tendons.”Journal of Applied Physiology 2011; Online before print October 2011. doi 10.1152/japplphsiol.00858.2011.

Dr Bruce HamiltonEditor

This issue of the NZJSM is special in that it marks only the second time in over 40 years of publication that it is beingproduced immediately after winning the Rugby World Cup. I would like to add my congratulations to all thoseinvolved, particularly from the Sports Medicine and Science side, who clearly had a significant impact on the result.Of course, rugby was not the only international sporting code to have great success this year, and New Zealand shouldgo into next year’s Olympics with confidence that it has both the the athletes and the support services needed toperform exceptionally well.

It was great being back in NZ for the Annual Conference held recently in Queenstown. Having not been there for 20years, it was great revisiting the beautiful area, re-uniting with old friends, making new friends and both watching andengaging in most interesting presentations and discussions. My thanks to Ian Murphy and the Organising Committeefor putting on such a great meeting and I look forward to next year’s conference in Auckland

In this journal, you will find a selection of the abstracts from the conference as well as a broad range of articles. We areconstantly looking for ways of improving the content of the journal and we hope to continue to add features as wemove into 2012 - your involvement in your journal is always appreciated. In the New Year, you should once again bereceiving a hard copy of the journal in the post. We recognise that while electronic journal access is convenient, theattraction of the paper copy remains, and as such we intend to print an annual edition of the journal, including all of thecontent published electronically during the year.

I would like to thank all those who have contributed articles to the journal over the last 12 months, those that haveacted as reviewers and in particular Brenda Allum for her ongoing hard work in preparing the journal.

Enjoy and see you next year!

Bruce

Vol 38 No 3, 2011; 65

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Reply to review on

“The Central Governor of exercise performance:

Fact or fiction”

I appreciate Professor Cairn’s carefully balanced review of the Central Governor Model (CGM) – The central governor of exerciseperformance: Fact or fiction5. I am especially grateful for his conclusion that the model “is an extremely valuable concept toinvestigate further and apply to all forms of sporting events along with clinical exercise situations” (p.50).

Indeed models are developed for exactly that reason. They make predictions which can be tested. By testing those predications wecan determine whether or not the model is helpful. By modifying the model or indeed rejecting it if there is no other option, weadvance our understanding especially of complex phenomena like the regulation of human exercise performance.

What many may not remember is that when it was first proposed in 199812, the CGM represented a significant mindshift in ourdiscipline. For then everyone “knew” that, according to the traditional A.V. Hill model11,14,15, exercise performance was “limited”solely by the development of a catastrophic peripheral fatigue in the exercising muscles. Indeed this interpretation continues to beargued in some of the world’s leading journals7. To have suggested that the brain is the final regulator of exercise performance was,at that time, considered to be too ludicrous to be taken seriously.

Now, of course, the argument has changed. As the evidence of the brain’s importance in the regulation of exercise performancecontinues daily to accumulate (for example – 2,3,9,10,22), the traditional “brainless” model17 of human exercise performance

becomes increasingly less defendable.

As a result the argument has now become in effect: “Of course we know that the brain is important. That is not new. In fact wehave always known it. But that regulation has nothing to do with a mythical central governor”. This is in keeping with thelegendary statement of Louis Agassiz who more than 100 years ago described how scientific knowledge advances: “Every greatscientific truth goes through three phases. First people say it conflicts with the Bible. Next they say it has been discovered before.Lastly they say they always believed it”.In this way some of those who only a few years ago were influential backers of the A.V. Hill model of exercise regulation havesuddenly undergone a Damascus Road transformation without ever having to acknowledge it. Instead the villain becomes theperson who first suggested that there was a need for a new interpretation4,7,19.

It must by now be reasonably obvious16,17 to most reasonable and disinterested scientists that the brain is indeed the final regulatorof human exercise performance. Whether or not this is due to a so-called “central governor” is largely irrelevant. The achievementof the CGM has been to focus the debate in this field by developing an alternative and easily testable model as Professor Cairnacknowledges. To quote Albert Einstein: “The mere formulation of a problem is often more essential than its solution, which maybe merely a matter of mathematical or experimental skill. To raise new questions, new possibilities, to regard old problems froma new angle requires creative imagination and marks real advances in science”.

Elsewhere11,16 I have reviewed why this alternative approach conforms with the Popperian model of scientific inquiry but contrastswith the authoritarian Kuhnian model which, in my view, has prevented a reasonable debate of this topic for perhaps the last 50years or so.

My sole point of contention with Professor Cairns’s article is his claim that “(Noakes) totally refutes the occurrence of peripheralfatigue”. In my article to which Professor Cairns refers, I specifically referenced studies showing the presence of peripheralfatigue and included them in the most recent diagram of the model. My point is simply that for at least three reasons, peripheralfatigue acting perhaps as a peripheral governor as McIntosh and Shahi8 suggest, cannot be the factor “limiting” exercise performance.

Firstly, the development of peripheral fatigue or alternatively a peripheral governor cannot explain the anticipatory components ofexercise control – especially the choice to begin exercise at different intensities dependant entirely on the anticipated or knownduration of the planned exercise bout13,23.

Secondly, these peripheral phenomena cannot explain the exercise “endspurt” 13,23 since how would a peripheral governor confinedto the muscles “know” for certain exactly when the end of any exercise bout is rapidly approaching?

But, most tellingly, neither of these mechanisms can explain why subjects slow down or indeed terminate all forms of dynamic1,9,18,20,21

or isometric6 exercise without a 100% recruitment of all the available motor units in their exercising limbs.

For, as repeatedly argued18, peripheral mechanisms can only regulate or limit the force output of muscle fibres that are activelycontracting since these peripheral models explicitly require that “fatigue” is caused solely by continuous contractile activity.According to that model, these peripheral mechanisms will cause the termination of exercise only when all the available motorunits are contracting and all have fatigued, causing the reduction in the work output that we define as “fatigue”.

LETTERS TO THE EDITOR

66 NZJSM

Thus the absence of complete recruitment of all available motor units in the exercising limbs at the point of fatigue or exercisetermination is the single best evidence that central, and not peripheral mechanisms regulate exercise performance18.

Whenever exercise terminates with motor unit recruitment reserve, then the sole conclusion must be that the central nervoussystem is the ultimate regulator of that exercise performance (regardless of the extent to which a peripheral governor or peripheralfatigue will also be active at that moment).

Professor T D Noakes OMS

MBChB, MD, DSc, PhD (h.c.), FACSM, (hon) FFSEM (UK)DISCOVERY HEALTH PROFESSOR OF EXERCISE & SPORTS SCIENCEAT THE UNIVERSITY OF CAPE TOWNDepartment of Human Biology, University of Cape TownSports Science Institute of S.A.Boundary Road, Newlands 7700South AfricaE-mail: Timothy.noakes@uct.ac.zaTel: +27-21-650-4557

References1 Albertus Y. Critical analysis of techniques for normalising electromyographic data. PhD thesis, University of Cape Town 2008:1-219.2 Amann M, Dempsey JA. Locomotor muscle fatigue modifies central motor drive in healthy humans and imposes a limitation to exercise

performance. J Physiol 2008; 586(1):161-173.3 Amann M, Eldridge MW, Lovering AT, Stickland MK, Pegelow DF, Dempsey JA. Arterial oxygenation influences central motor output

and exercise performance via effects on peripheral locomotor muscle fatigue in humans. J Physiol 2006; 575(Pt 3):937-952.4 Bassett DR, Jr., Howley ET. Maximal oxygen uptake: “classical” versus “contemporary” viewpoints. Med Sci Sports Exerc 1997;

29(5):591-603.5 Cairns SP. The central governor of exercise perfomrance: Fact or fiction? NZ J of Sports Medicine 2011; 38(2):47-50.6 Dideriksen JL, Enoka RM, Farina D. Neuromuscular adjustments that constrain submaximal EMG amplitude at task failure of sustained

isometric contractions. J Appl Physiol 2011; 111(2):485-494.7 Levine BD. VO2max: What do we know, and what do we still need to know? J Physiol 2008; 586(1):25-34.8 MacIntosh BR, Shahi MR. A peripheral governor regulates muscle contraction. Appl Physiol Nutr Metab 2011; 36(1):1-11.9 Marcora SM, Staiano W. The limit to exercise tolerance in humans: mind over muscle? Eur J Appl Physiol 2010; 109(4):763-770.10 Marcora SM, Staiano W, Manning V. Mental fatigue impairs physical performance in humans. J Appl Physiol 2009; 106(3):857-864.11 Noakes TD. Challenging beliefs: ex Africa semper aliquid novi: 1996 J.B. Wolffe Memorial Lecture. Med Sci Sports Exerc 1997;

29(5):571-590.12 Noakes TD. Maximal oxygen uptake: “classical” versus “contemporary” viewpoints: a rebuttal. Med Sci Sports Exerc 1998; 30(9):1381-

1398.13 Noakes TD. The central governor model of exercise regulation applied to the marathon. Sports Med 2007; 37(4-5):374-377.14 Noakes TD. How did A V Hill understand the VO2max and the “plateau phenomenon”? Still no clarity? Br J Sports Med 2008;

42(7):574-580.15 Noakes TD. Testing for maximum oxygen consumption has produced a brainless model of human exercise performance. Br J Sports

Med 2008; 42(7):551-555.16 Noakes TD. Is it Time to Retire the A.V. Hill Model?: A Rebuttal to the Article by Professor Roy Shephard. Sports Med 2011; 41(4):263-

277.17 Noakes TD. Time to move beyond a brainless exercise physiology: the evidence for complex regulation of human exercise performance.

Appl Physiol Nutr Metab 2011; 36(1):23-35.18 Noakes TD, St Clair Gibson A. Logical limitations to the “catastrophe” models of fatigue during exercise in humans. Br J Sports Med

2004; 38(5):648-649.19 Shephard RJ. Is it time to retire the ‘central governor’? Sports Med 2009; 39(9):709-721.20 Sloniger MA, Cureton KJ, Prior BM, Evans EM. Anaerobic capacity and muscle activation during horizontal and uphill running. J Appl

Physiol 1997; 83(1):262-269.21 Sloniger MA, Cureton KJ, Prior BM, Evans EM. Lower extremity muscle activation during horizontal and uphill running. J Appl

Physiol 1997; 83(6):2073-2079.22 Swart J, Lamberts RP, Lambert MI, St Clair GA, Lambert EV, Skowno J, Noakes TD. Exercising with reserve: evidence that the central

nervous system regulates prolonged exercise performance. Br J Sports Med 2009; 43(10):782-788.23 Tucker R, Lambert MI, Noakes TD. An analysis of pacing strategies during men’s world record performances in track athletics.

Int.J.Sp.Phys.and Perf. 2006; 1:233-245.

LETTERS TO THE EDITOR

Vol 38 No 3, 2011; 67

BEST OF BRITISH

August

The August issue of BJSM was headedup by a useful editorial entitled“Changing gears: bicycling as thepanacea for physical inactivity”.Written by Adrian Bauman andcolleagues, the article summarised thehealth benefits and risks of cycling andnoted individual, social andenvironmental barriers to cycling. Itdocuments the controversy withregard to helmet use and efforts withinvarious communities to get morepeople cycling. In summary, cyclingis not a panacea for physical activity,but it has great potential and this isonly partly realised at present.

Later in the same issue was a usefularticle on Injury-prevention prioritiesaccording to playing position andprofessional rugby union players. Thisstudy demonstrated individualposition-specific differences in matchinjury profile; for example forwardssustain injuries to their shoulder, kneeand ankle most frequently, whereas forthe backs the most frequently injuredsites were the shoulder, hamstring andknee. With this data an appropriateinjury prevention programme can betailored for each playing position.

The issue concluded with another in-series of A to Z of NutritionalSupplements. This issue concentratedon leucine, lecithin and gamma-linolenic acid. The expert reviewerscommented that although lecithinmaintains plasma choline levels afterexercise, there does not seem to be agood reason to take supplementarylecithin in the hope of improvingperformance. Likewise, there is littleevidence that supplementary leucineor gamma-linolenic acid is necessaryfor peak sporting performance.

The September Injury Prevention andHealth Protection issue sponsored bythe IOC contained a landmarkconsensus statement on the health andfitness of young people throughphysical activity and sport. The IOC

assembled an expert group in January2011 and their findings are detailedover 10 pages. The article concludeswith recommendations for sportsorganisations, governments, non-governmental organisations andresearchers. As befitting itscomprehensive nature, 168 referencesare supplied. Sedentary behaviour inyouth is a major concern in mostdeveloped countries. Increased screentime, either in front of a television orcomputer monitor, is associated withsedentary behaviour and there isstrong evidence that children spendincreasing time being sedentary asthey grow older. This article byRussell Pate and co-workers dovetailsnicely with a second article in the sameissue entitled “Sedentary behaviourinterventions in young people: a metaanalysis”. The authors comment thattheir literature review indicated theinterventions designed to reducesedentary behaviours in young peopletended to have only small effects.They comment that this may be dueto strong environmental cues and thattime spent away from a screen maybe allocated to other sedentarybehaviours, e.g. listening to muscle,talking or sedentary hobbies. Clearlythere are major challenges to gettingour children on their bikes, or at leastout of the house.

In the same vein, Van Sluijs and co-workers examine the effect ofcommunity and family interventionson young people’s physical activitylevels. Their conclusion is thatalthough the study quality isimproving, the effect of family andcommunity based interventionsremains uncertain.

Later in the same issue is an articleexpressing more optimism; LyleMicheli, who has previously been aspeaker at our SMNZ Conference, andfellow experts see great promise inimproving the fitness and health ofchildren through sport. Their articlestarts with the well-known African

proverb “It takes a village to raise achild”. They comment that it is aglobal village that needs to step intoaction and sport is the logical vehiclefor improving the physical activityprofile and fitness of our youngpeople.

September

The routine September issue waschock full of useful articles: I evengot one published myself entitled“Practising sports and exercisemedicine in an environment of risingmedical costs”. This is one of themajor challenges facing today’sclinicians. Fifty years ago the limitsto medicine were largely around whatwe could do. Now the limits areincreasingly around what we canafford. We clinicians are increasinglyfacing questions from well informedpatients requesting high technologyimaging, for example. It has been asignificant contributor to risingmedical costs. I advocate acollaborative approach whereclinicians, administrators, funders andthe patient all have to play a role inaccepting that there needs to be somerationing of access to expensivediagnostic and therapeuticinterventions, and increasingly peoplewho wish to have an extrainvestigation for their own reassuranceshould be asked to fund thesethemselves.

Sudden cardiac death is a hot topic atpresent. Jonathan Drezner andcolleagues ask the pertinent question:Where did the science go? Theycomment that systematic reportingsystems are crucial. ECG screeningdoes not need to be mandatory but itcan be recommended for at-riskpopulations such as competitiveathletes. They comment that addingan ECG greatly increases thesensitivity to detect conditions at riskof sudden cardiac death and has beenshown to enhance the cost-effectiveness of a screening process.The issue is one of ongoing debate.

68 NZJSM

BEST OF BRITISH

Later in the same issue was an articleby Lynley Anderson of OtagoUniversity entitled Bloodgate: werethe punishments fair? This refers toevents of April 2009 during a rugbymatch between Leinster andHarlequins when a Harlequins playerfaked a blood injury and thephysiotherapist and doctor were bothclosely involved in the scam. Thedoctor was given a warning by theMedical Council but thephysiotherapist was struck off beforebeing reinstated by a High Courtdecision in January 2011. Andersoncomments that the health aims ofdoctors and physiotherapists may bedistorted by the environment ofprofessional sport. Teaching ethicsand creating professional guidelinesmay not be enough; we need torecognise the pressures and provideadequate support and protection tohealth professionals involved in sport.

Innovation is necessary to remain atthe head of the pack. A trans-Atlanticcollaboration between Cathy Speed ofthe UK and Bill Roberts of the USAprovides a background for why peopleinnovate in high performance sportsmedicine and provides advice on howto do this. They argue for a diversegroup that is likely to be more creative.

Chronic exertional compartmentsyndrome can often be difficult todiagnose. There is a very useful headto head series of articles within theSeptember issue. On the one hand,Mark Hutchison of Chicago arguesthat all four compartments in each legshould be tested as then one hasabsolute proof of the pressuresgenerated by exercise. By contrast,Matt Hislop and Mark Battrecommend a minimalist approach andconclude that not all compartmentsneed to be measured routinely. Theyadvocate additional time spent inhistory-taking to try and identifywhich particular compartments areinvolved and test only the moresymptomatic leg, thus reducing thenumber of needle insertions. Finally,

they conclude that measuring restingpressures is not necessary in theinvestigation of chronic exertionalcompartment syndrome. For anyclinicians with an interest in thiscondition, these articles make veryworthwhile reading.

Upper respiratory tract infections arethe commonest infection seen in thecommunity. David Nieman, who haspublished widely on these issues, andcolleagues studied a group of 1002adults aged 18 to 85 years andfollowed them for 12 weeks during thewinter and autumn seasons whilstmonitoring respiratory tract symptomsand severity using the WisconsinUpper Respiratory Symptom Survey.They found that those subjects whoperformed aerobic exercise for five ormore days per week had a 43%reduction in the number of days withURTI compared to those who werelargely sedentary, i.e. performing onlyone day or less of aerobic exercise perweek. The message is clear - get outthere and get active and you shouldstay healthier.

Wrapping up this busy Septemberissue was the usual section onnutritional supplements. Leptin is ahormone which plays a crucial role inthe regulation of appetite, body fatmass, basal metabolic rate and gonadalfunction. Theoretically, it could beused as an anabolic agent whencombined with strength training. Thereviewers conclude that there iscurrently insufficient knowledgeregarding this substance and do notrecommend supplementation.Magnesium supplements arefrequently used, but unless there isevidence of deficiency there is noevidence for any benefit frommagnesium supplementation.Medium chain triglycerides are usedcommonly by bodybuilders, howeverthey frequently cause gastrointestinaldistress and any theoretical metabolicbenefits are heavily outweighed bythis side effect. Therefore, the authors

do not recommend their use assupplements.

October

The October issue included an articleby the guru of achilles tendinopathytreatment, Hakan Alfredson, whopresented at our conference someyears ago. His concentric theneccentric strengthening regime hasbeen very successful in treating mostpeople. In those cases whereimprovement did not occur andoperation was necessary, he found anenlarged plantaris tendon in 58/73consecutive tendons. These peoplewere treated with ultrasound andDoppler guided scraping andextirpation of the plantaris tendon, i.e.the plantaris tendon was cut andremoved. He often found richlyvascularised fat tissue interposedbetween the achilles and plantaristendons and hypothesised that theplantaris tendon could be considereda co-factor in treatment resistantmidportion achilles tendinopathy.Watch this space.

Could genetics play a role in achillestendinopathy? A combined groupfrom Australia and South Africaexamined this issue via a pathwaybased approach. They investigated theassociation of sequence variance.Independently, no associations wereobserved between any of thepolymorphisms tested and the risk oftendinopathy. However, the allelecombinations of five polymorphismswere found to have a highly significantrelationship with achillestendinopathy. No doubt this is an areafor further research.

Later in the same issue was anintriguing article entitled “Referralsfrom a primary care-based sportsmedicine department to anorthopaedic department: aretrospective cohort study”. Thisstudy examined nearly 5000 patientsseen at a sports medicine departmentin Fort Worth, Texas. Only 2.4% of

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those patients required referral to theorthopaedic department, the remaindercould be managed non-operatively. Ofthe referred patients, surgery wasoffered to 68% of them. The averagewait for initial consultation decreasedfrom 97 to 19 days in generalorthopaedics, and 199 to 70 days inthe orthopaedic spine clinic. Theauthors comment that expansion ofprimary care-based sports medicineservices could relieve over-burdenedorthopaedic departments of patientswith conditions not requiring surgery.To that I say “hear, hear” as this is anissue in many countries around theworld.

Later in the issue is a review articleon injection treatments for patellartendinopathy. The authors found 11articles on seven different injectiontreatments including dry needling,autologous blood, high volume localanaesthetic, platelet rich plasma,sclerosis, corticosteroid injections andaprotinin. The authors comment thatall seven different injection treatmentsseem promising but that steroidtreatment often showed a relapse ofsymptoms in the long term. Theycomment that results should beinterpreted with caution as few highquality studies have been conducted,and recommend further research.

The series on nutritional supplementscontinues with comments onmelatonin and jetlag. It is unclearwhether the main action is hypnoticor chronobiotic and they comment thatmild heat loss by peripheral vasculardilatation following melatoninsecretion may be the mechanism thatinitiates sleep. Certainly melatonin iswidely used and there seem to be fewside effects reported.Methylsulphonylmethane is anorganic sulphur compound which isclaimed to improve osteoarthritic pain.However, there is a lack of high qualityevidence for many of the beneficialclaims and the authors state that nodefinite recommendations can be

made on current evidence. Melamineis a substance that was much in thenews in late 2008 as it was added toinfant milk formulas. It is toxic tohumans, even at low quantities, andthe authors do not recommend itssupplementation. Athletes should beaware of possible melaminecontamination in protein-richfoodstuffs.

Finally, there was a systematic reviewentitled “Is exercise effective inpromoting wellbeing in older age?”This was indexed on thePhysiotherapy Evidence Database.The meta analysis pooled the resultsfrom four trials using the SF-36 mentalhealth measure and a self-esteemmeasure. The review provided supportfor the role of exercise in improvingthe mental wellbeing of older people.The message is as previously - keepon keeping on.

Dr Chris MilneSports PhysicianHamilton

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2012 NEW ZEALAND

SPORTS MEDICINECONFERENCE

Pullman Hotel, Auckland14-17 November

Preliminary Programme

Wednesday, 14 NovemberHigh Performance Sport Workshop

Thursday, 15 NovemberMult-disciplinary Sessions

Welcome Reception

Friday, 16 NovemberMulti-disciplinary Sessions

Conference Dinner

Saturday, 17 NovemberSports Physicians/Doctors Specialist Day

Sports Physiotherapists Specialist Day

For information contact:smnznat@xtra.co.nz

ARTICLE

Abstract

AimThe SLAP (Superior Labral Anterior to Posterior) lesion has become a popular clinical and radiological diagnosis.The purpose of this article is to review the international literature of the SLAP lesion and describe our experience withthe diagnosis and surgical treatment of this lesion in a New Zealand practice.

Data SourcesWe reviewed the available literature on SLAP lesions based on an index medicus Pubmed search and proceedingsfrom relevant international meetings attended by the senior author (KDM). We included original articles, reviewarticles and metaanalyses in our search. We also include data from a 2 year period of the senior subspecialist practice.

Data ExtractionThe data from these studies was reviewed in combination with that form the senior authors practice and is included forillustration purposes with associated referencing.

ConclusionsThe clinical presentation, imaging diagnosis and arthroscopic diagnosis are variable and imprecise. There is debateabout the clinical relevance and treatment of SLAP lesions. There is no universally agreed clinical test to diagnosea SLAP lesion. Surgical treatment results range from very good to unsatisfactory. Patient populations differ frompredominantly young baseball throwing athletes in USA and some Asian series, to older non throwing populations inEuropean studies. These groups may differ from a New Zealand patient population. With selective indications, weachieved good results in our patients.

Key WordsShoulder, Arthroscopy, Superior Labrum, Biceps, Repair

The Superior Labral Anterior to

Posterior (SLAP) Lesion: An

elusive pathology

Diarmuid C Molony, Khalid D MohammedDiarmuid C Molony MB, BAO, MCh, FRCS(Tr&Orth)Fellow in Shoulder and Elbow SurgeryDepartment of Orthopaedic and Trauma Surgery, University of OtagoLevel 3, Christchurch General HospitalChristchurch, New Zealand

Khalid D Mohammed MB, ChB, FRACSConsultant Orthopaedic SurgeonDepartment of Orthopaedic and Trauma Surgery, University of OtagoLevel 3, Christchurch General HospitalChristchurch, New Zealand

Corresponding Author:Mr K D Mohammed.Consultant Orthopaedic SurgeonElmwood Orthopaedic CentreSt George’s Medical Centre249 Papanui RoadChristchurch 8014, New ZealandPhone: +64-3-3552393Fax: +64-3-3552483

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

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Introduction

In 19852 Andrews described theSuperior Labral tear in overheadathletes. Snyder47 coined the

acronym SLAP (Superior LabralAnterior Posterior) lesion in 1990.Snyder’s original classification is quitelong and descriptive but can besummarised as follows:

Type 1 Marked fraying of the superiorlabrum with a degenerativeappearance but no disruption of eitherthe labral attachment or that of thebiceps anchor.Type 2 The biceps anchor and superiorlabrum are detached or partiallydetached from the superior glenoid.The biceps labral anchor is unstable.Type 3 Disruption of the superiorlabrum with a “bucket handle” tearthrough the labrum with the peripherallabrum and biceps anchor remainingfirmly attached.Type 4 Bucket handle labral tear whichextends into the biceps tendon. Theremainder of the tendon and labrumare intact.

Other subtypes have beendescribed33,36 but the SnyderClassification is most commonly used.There is general agreement that a Type1 may be asymptomatic and notrequire treatment, with the surgicaltreatment option being debridement.Type 3 and 4 lesions can be recognisedand treated at surgery. For Type 3 and4 lesions treatments include excisionof the bucket handle tear with orwithout repair of any residual biceps /labrum detachment, or tenodesis. TheType 2 lesion is more frequentlyreported, but more difficult todiagnose, with more diversity ofopinion on treatment.

This article focuses on the Type 2SLAP lesion. What is the normalanatomy? How do you get a SLAPlesion? How do you diagnose a SLAPlesion? What are the results oftreatments internationally and locally?We attempt to answer these questions.

Anatomy

To understand the SLAP lesion, wemust understand the normal anatomy.At the 12 o’clock position on the‘glenoid clock’, articular cartilage

extends 4 or 5 mm over the superiormargin of the glenoid, beneath thebiceps and labrum. The superiorlabrum at the 12 0’clock position hasa meniscoid margin which covers thesuperior extension of articularcartilage.6 Forty to sixty percent of thebiceps insertion is into thesupraglenoid tubercle with theremainder inserting into the labrum.Histologically, usually most of thebiceps insertion into the labrum is intothe postero-superior labrum.49, 50 In thepostero-superior 10 o’clock position,the labral attachment to the glenoid ismeniscal in shape in 50% and roundedin 50%. By comparison the inferiorlabrum of the shoulder from the 4o’clock to the 8 o’clock position is arounded extension of articularcartilage with hyaline cartilagetransitioning to fibrous tissue with afirm attachment.

There is a loose connective tissueattachment of the superior labrum tothe glenoid which has elasticity. Thisconstruction indicates the naturalmobility of the superior labrum and itsclose relationship with the long headof biceps (LHB). There are variationsin the attachment of the mobile antero-superior segment of the labrum to theglenoid, including a sublabral foramen(present in 3.3%), middle cord pattern(present in 8.6%) and the Bufordcomplex (present in 1.5%).44 It isimportant to recognise these normalvariants as surgical fixation of themmay restrict external rotation.

The superior labral and biceps anchorcomplex function is a topic of debate.The labrum is widely accepted to actto deepen the concavity of the glenoidand widen its diameter improvingconcavity compression and excursiondistance in rotation. In conjunctionwith the glenohumeral ligaments andbony anatomy it acts as a staticconstraint to instability. The superiorlabral complex (SLC) has a role toplay in anterior stability and inexperimental models SLAP lesionshave been shown to increase the loadon the inferior glenohumeral ligament(IGHL), reduce ability to resistexternal rotation and increase anteriorand superior translation underload.35,40,45 The LHB itself has also

been shown to affect translation41

especially in mid abduction and inshoulders that are unstable for otherreasons.19 The LHB is also thought toact as a depressor of the humeral headin the presence of rotator cuff tear.26

Pathogenesis

Causes of SLAP tears can largely bedivided into traumatic, attritional anddegenerative. Traumatic lesions mayoccur in compression due to falls ontothe outstretched limb, more commonlyin the forward flexed position9 or withdirect impact onto the shoulder. Theycan also occur in tension. Examplesinclude using the limb to break a fallfrom a height, grasping at a heavyobject below waist level or beingpulled anteriorly as in waterskiing ordrag ski lifts. These events causesudden tension on the LHB tendon inthe superior, inferior or anteriordirections. The position of thehumeral head in the glenoid at the timeof impact or traction plays a role inthe type of injury sustained.3

Attritional injuries may occur inoverhead and throwing athletes.Considerable investigation of thepathogenesis of SLAP tears in thesepatients has been performed. Onetheory suggests that the primarypathology is a tight posterior capsularcomplex coupled with a relativelyloose anterior capsule frequently seenin this group.6 This may be associatedwith increased humeral retroversionand may develop as an adaptiveanatomical variation in throwers. Theincreased external rotation achieved inthe late cocking phase of throwing iscontributed to by postero-superiorhumeral migration at this point whichallows greater tuberosity clearance.This has been borne out by cadaverstudies.15 Such increased externalrotation puts increased tension on thefibres of the LHB anchor resulting ina so called “peel back” lesion as thesuperior labrum complex displacesmedially over the glenoid rim. Theposterior vector produced by suchmotion puts the superior labrum at riskas it is weakest in this direction46 andSLAP lesions may result.

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Degenerative tears of the superiorlabrum are commonly seen in elderlyand middle aged patients and may bethe result of age related degenerationof the labral tissue rather than anyspecific event or attrition. They arenot always symptomatic.

In summary, there is no specifichistory for a SLAP lesion. They mayoccur in different patient populationsspontaneously, gradually ortraumatically from a variety ofmechanisms.

Diagnosis

The clinical presentation of SLAPlesions is extremely variable.Coexisting pathology may be presentand more symptomatic. It is essentialthat the clinician determines therelative significance of the clinicalpresentation, imaging and operativefindings.25,30 The patient may presentwith a history of gradual or suddenonset of symptoms, with a wide rangeof trauma mechanisms possible.

Symptomatic SLAP lesions causepain, but the pattern is variable.25 Pain,which may be sharp or dull, istypically felt deep inside the shoulderand may radiate either anteriorly orposteriorly mimicking anterior orposterior labral lesions or indeedacromioclavicular pathology.Exacerbation of pain can be expectedwith heavy lifting, overhead motionand pushing. Throwing athletesfrequently report pain in the latecocking and early acceleration phaseof throwing.

Weakness in these positions may alsobe a feature and development of labraltear related cysts and suprascapularnerve compression may causeinfraspinatus weakness. Lack of trustin the shoulder and a sensation ofgiving way are also commonespecially in the overhead position.Patients may report mechanicalsymptoms of clicking and locking.Essentially the SLAP lesion maypresent with the symptoms of anyother shoulder pathology and given thepropensity for concomitant pathologyit is difficult to delineate which is trulythe cause of the patient’s symptoms.

Clinical examination for SLAP tearsis rarely decisive. It is important toexamine the shoulder for otherpathologies e.g. instability, rotator cuffdisorders, capsulitis and painsyndromes. Wasting of infraspinatusmay indicate suprascapular nervecompromise which may be secondaryto compression by a sublabral cyst.These are frequently associated withSLAP tears. Posterior capsulartightness may be present and may bea contributor to the pathogenesis ofSLAP tears. It is important todifferentiate apprehension from painand important also to remember thatBankart lesions in combination withSLAP tears are common, especially inthose under 40.30

While many special tests have beendescribed27,28 concerns regarding theaccuracy of these techniques havebeen expressed.24,34,43 Biceps tests, likeSpeed’s test, may aid in suggestingpain in from the long head of biceps.Several tests to isolate the superiorlabral complex have been describedincluding the Kim’s biceps load tests(I and II), Liu’s Crank test, Jobe’srelocation test, McFarland’scompression rotation test, forcedshoulder abduction test and O’Brien’sactive compression test.16,27,28,32,34,37,39

These tests aim to provoke pain bystressing the superior labrum and longhead of biceps. Perhaps the mostcommonly used is O’Brien’s activecompression test. O’Brien reported asensitivity of 100% and a specificityof 98.5% but independent assessorshave been unable to reproduce theseresults for this or other describedtests.24,34,42,43

Imaging plays a central role in thediagnosis of SLAP lesions. Magneticresonance imaging (MRI) is the bestmodality to assess the labrum.Whether MRI arthrography or noncontrast MRI is most useful indiagnosing SLAP lesions has yet to beresolved.18 We prefer MRIarthrography for examination of thelabrum. The interpretation ofpathology in this region is impeded bythe variability of the local anatomyhowever specific findings suggestiveof SLAP lesions include tracking of

contrast under the superior labrum,best seen on coronal cuts, andincreased signal intensity in labraltissue and the biceps anchor on T2axial cuts.22,48 It has been suggestedthat positioning the arm in theabducted and externally rotatedposition may improve diagnosis bydisplacing the lesion.8,23 Nonethelesseven with arthrography one studyreported that sensitivity may be as lowas 89%, specificity 78% and accuracy82%.20

Arthroscopy is the gold standard fordiagnosis but even at arthroscopy itcan be difficult to agree on what is andwhat is not a type 2 SLAP lesion.Gozebie et al12 surveyed the opinionof fellowship trained expert shoulderand sports surgeons. Members of theAmerican Shoulder and ElbowSociety and the American OrthopaedicSociety of Sports Medicine were askedto comment on arthroscopic videos.There was high interobserver andintraobserver variability and difficultydistinguishing a Type 2 SLAP lesionfrom normal. Jia et al, however,reported good reliability in a smallstudy group of experienced shouldersurgeons.21

Treatment

Type 1 SLAP lesions may need notreatment or debridement. Little hasbeen written regarding outcomes oftreatment of the less common Type 3and 4 lesions. Few studies existdocumenting the natural history ofconservatively treated SLAP lesions.10

In cases with a concomitant rotatorcuff tear, cuff repair with debridementof the SLAP 2 tear1 or with tenotomyof the LHB11 have better outcomesthan repair. These studies involvedpatients ranging from 45-60 and over50 years of age respectively. Morerecently Koh et al have shown nodifference except in the appearance ofa popeye sign between patients treatedwith tenotomy rather than tenodesiswhen treating biceps pathologyidentified at rotator cuff surgery.31

Reported results of surgical treatmentof isolated Type 2 SLAP lesions witharthroscopic repair vary considerably.Some North American literature

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reports favourable results. Morgan etal36 reported 97% good and excellentresults in 102 patients. The mean ageof their patients was 33 years. Fifty-three were throwing athletes with anaverage age of 24 and all had dominantarm injuries. The other 49 were nonthrowers with a single traumatic eventand an average age of 40. Twenty-nine patients had dominant arminjuries and 20 had non dominantpathology. Kim et al,29 reported 94%good and excellent results in 34patients in their Korean series. Themean age was 26. Eighteen wereoverhead athletes, 12 were contactathletes and 4 were not involved inorganised sport. In a Japanese seriesof 40 overhead athletes,17 Ide et alreported 90% good and excellentresults in 40 overhead athletes with amean age of 24. Brockmeier andAltchek5 studied outcomes at 2 yearsof isolated SLAP type 2 lesion repairsin 47 patients with a mean age of 36years. In total 28 of 47 were overheadathletes of varying levels. Overall 25patients had a specific traumatic eventthat triggered their pain and 22 had aninsidious onset with 20 of these beinginvolved in overhead sports. Eighty-seven percent of patients in this studyreported good or excellent results with71% returning to premorbid level ofsports participation. Having anidentifiable traumatic event wasassociated with improved outcome inboth subjective assessment and levelof competition.

Conversely, poor results of SLAPlesion repair have been reported inEurope. The French ArthroscopySociety presented a multicentreretrospective study comparing repairof Type 2 SLAP tears to tenodesis.The mean age of their patients was 36years, 52% had a traumatic, 30% hada progressive and 18% had mixedaetiologies. Thirty-three patients hada repair and 20 had tenodesis. In thetenodesis group 90% were satisfied orvery satisfied, whereas only 57% ofthe repair group were satisfied or verysatisfied (p<0.01).14 In their nonrandomised prospective study, Boileauet al also published superior results forbiceps tenodesis compared to SLAPrepair.4 There were differences in the

ages of each patient group (37 in theSLAP repair group versus 52 in thetenodesis group) and small samplesizes (10 repairs and 15 tenodeses).The authors reported significantlybetter results in the patients withbiceps tenodesis. Eighty percent ofpatients in the tenodesis group weresatisfied compared with 40% in therepair group. Return to sports was alsosuperior in the tenodesis group with87% of athletes returning to theirprevious level of competitioncompared with 20% in the SLAPrepair group. Eighty percent ofpatients in the SLAP repair group and60% patients in the tenodesis groupwere overhead athletes. Overall 60%reported a specific traumatic event.

Despite these geographical differencesit is generally recognised thatoverhead throwing athletes, especiallybaseball players have inferioroutcomes after SLAP repair than otherpatients.5,13,17,29,30,51 It is also widelyaccepted that poorer outcomes areseen with SLAP repairs performed inthe presence of other pathologies, suchas rotator cuff tears. Debridement ortenotomy/tenodesis rather than repairis preferred in combination withtreatment of the major pathology.1,11

Further debate exists about the repairof SLAP tears in older patients38 butdespite this recommendations leantowards repair in appropriate casesunder 40 and tenodesis or tenotomyabove this age.7

A New Zealand

Perspective

Patients and MethodsOver a two year period, between 1st

November 2007 and 31st October2009, of new patients attending thesenior author (KDM), 457 had an MRIscan of the shoulder. Of these 148(32.39%) had a report which includeda SLAP lesion. During the sameperiod the senior author performed 41arthroscopic SLAP repairs. In 24 ofthese cases other significantprocedures were performedconcomitantly, usually arthroscopicstabilisations for glenohumeralinstability, acromioplasties or lesscommonly rotator cuff surgery.Excluding these 24 patients and 4

other cases requiring treatment of Type3 SLAP lesions left 17 cases where therepair of the Type 2 SLAP lesion wasthe isolated therapeutic procedure. In5 of these 17 cases there was aparalabral cyst. There were 15 malesand 2 females. The mean age atsurgery was 35 years (range 19-51years). All were funded by theAccident Compensation Corporation(ACC).

The injury mechanisms are listed intable 1. Most patients had alreadyreceived physiotherapy and 4 patientshad subacromial cortisone injectionsprior to referral to our practice. Themean time from injury to surgery was25 months (range 4 months – 8 years).All had an MRI diagnosis of a SLAPlesion. All were repaired with aknotless anchor technique, using 1postero-superior anchor in 12 casesand 2 anchors (1 antero-superior and1 postero-superior) in 7 cases. Patientswere asked to complete the AmericanShoulder and Elbow Society Score(ASES) pre operatively and 6 monthspost operatively. At 6 months patientswere asked to report their satisfactionwith the options being dissatisfied, notsure, satisfied and very satisfied.Patients were asked at 1 to 3 yearsfollow up (mean 25 months) to onceagain rate satisfaction and alsoestimate the “percentage of normal”for their treated shoulder.

Mechanism of Injury NumberFall (Soccer, Snowboard, Bike, Stairs) 6Collision (Rugby, Soccer, Squash) 4Combat 2Heavy Lift 2Road Trafffic Accident 1Repetitive Overhead 1Repetitive Throwing 1

Table 1: Mechanism of Injury

Results:Sixteen patients completed the preoperative ASES score and 11 of these(69%) completed their 6 months ASESscores with an increase from 46 to 82points. The highest score on this scaleis 100 points. (Fig 1) Of those thatcompleted their 6 month assessment,

Vol 38 No 3, 2011; 75

82% were very satisfied with theremaining 18% satisfied. At aminimum of 1 year follow up, 14 outof 17 (82%) of our patients werecontactable. Once again there was ahigh satisfaction rate. (Fig 2) Themean percentage of normal rating was94% (85-100%).

One patient, who was not contactablefor follow up, was experiencing painwith collisions at rugby. At the indexprocedure he was noted to have a

Figure 1: Pre-operative and 6 month Post-operative ASES scores.

Figure 2: Satisfaction at minimum 1 year follow up.

ARTICLE

posterior labral tear that was debrided.He was offered further surgery with aview to posterior labral repair, but hassubsequently left New Zealand. Onepatient had a reoperation. He washappy with his shoulder but more thana year post surgery he reported apainless graunching sensation in hisshoulder. He had an arthroscopy at22 months following the indexprocedure to exclude suture anchorprominence. At surgery a labral flapwas debrided and the graunching has

not recurred. One patient had mildmedian nerve symptoms for severalmonths following surgery.Neurophysiological studies suggestedmild compromise of the median nervein the infraclavicular region and thecarpal tunnel. His symptoms resolvedadequately without intervention. In 2patients slow progress was reported intheir notes. One with aching at 1 yearreported he was ‘very satisfied’ andrated the shoulder as 90% normal atfinal follow up. Another with slowprogress recorded at 3 months postsurgery reported he was ‘verysatisfied’ and rated the shoulder as95% normal at final follow up.

Illustrative Case:A 20 year old elite swimmer (Olympictrialist) and surf life saver hit a lanerope swimming backstroke andexperienced sudden severe pain in hisright shoulder. His pain was ongoingdespite rest and physiotherapy. Hewas unable to swim or throw. He hadsharp pain reaching out. The shoulderdid not feel unstable to him. Onexamination he had a good range ofmovement, with pain on internalrotation in abduction and pain on theapprehension Test. O’Brien’scompression test was negative andSpeed’s biceps test was positive. Priorto referral he had cortisonesubacromial injection withoutimprovement and had seen aphysiotherapist. His MRI reported aSLAP lesion. Figure 3 demonstratesthe appearances of the superior labrumand biceps after debridement. Figure4 demonstrates the postero-superiorrepair with a single knotless anchor.Post operatively he wore a sling for 4weeks then started physiotherapy. At3 months from surgery he wascomfortable for activities of dailyliving and had regained near full rangeof movement (Figures 5) andrehabilitation included gymstrengthening. His ASES scoreimproved from 47/100 preoperativelyto 98/100 at 6 months postoperatively.He was able to swim and returned towork as a surf lifeguard. He reportedhe was ‘very satisfied’ with theoutcome on his 6 month post operativequestionnaire.

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Figure 3: Arthroscopic photograph of the debrided type 2 SLAP lesiondemonstratikng abnormal mobility of the superior labral and biceps complex.

Figure 4: Superior labrum and biceps anchor following SLAP repair.

Discussion

There are a wide range of proposedaetiologies for SLAP lesions, with anequally wide range of symptomsdescribed. No clinical presentation ortest will allow the clinician to diagnosea SLAP lesion with certainty. The

anatomy of the superior labrum isvariable. There is a normal recessbeneath the biceps insertion and thepostero-superior labrum may have ameniscoid shape. There is somemobility of the normal superior labrumand biceps. It can be difficult to

distinguish a Type 2 SLAP lesion fromnormal anatomy on MRI scans andeven at arthroscopy. In our practiceover a 2 year period, it was commonfor a patient’s MRI scan to include areport of a SLAP lesion withapproximately one third of MRI scansreporting a SLAP lesion, with orwithout other pathologies. In this timeperiod we performed just 41 SLAPrepairs. SLAP repair was an isolatedprocedure in only 17 of these.

The results of surgical treatment in theliterature are variable. We believe thatpart of this variation may relate todiffering patient populations. We havedescribed good results in a NewZealand practice but wish to stresshow selective we are in consideringwhether an MRI diagnosis of a SLAPlesion is clinically relevant.

If a patient has a traumatic event withonset of mechanical symptoms, thenlabral abnormalities may be relevant.With increasing age, however,degeneration of the labrum may occurand it is difficult to determine whatmay be normal for age and whetherthe labrum is a cause of symptoms.We consider most other pathologiese.g. instability, rotator cuff tears,capsulitis or regional pain syndromesto be dominant in causing symptoms.Not all labral tears remainsymptomatic and a period ofconservative treatment includingposterior capsular stretching andscapular stabilising is worth a trial inmost cases. Vigilance forsuprascapular nerve compression ishowever important. This can oftenoccur in patients with a paralabral cystrelated to SLAP tears and requiresmore urgent surgical intervention.

Our guidelines for selection forsurgical repair of a SLAP lesion are:

• Traumatic onset with mechanicalsymptoms

• Symptoms ongoing for more than6 months

• Patient age usually less than mid40’s and physically active

• No capsulitis, regional painsyndrome or other dominant

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3 Bey MJ, Elders GJ, Huston LJ, Kuhn JE,Blasier RB, Soslowsky LJ. The mechanismof creation of superior labrum, anterior, andposterior lesions in a dynamicbiomechanical model of the shoulder: therole of inferior subluxation. J ShoulderElbow Surg 1998 Jul-Aug; 7(4):397-401.

4 Boileau P, Parratte S, Chuinard C,Roussanne Y, Shia D, Bicknell R.Arthroscopic treatment of isolated type IISLAP lesions: biceps tenodesis as analternative to reinsertion. Am J Sports Med2009 May; 37(5):929-36.

5 Brockmeier SF, Voos JE, Williams RJ, 3rd,Altchek DW, Cordasco FA, Allen AA.Outcomes after arthroscopic repair of type-II SLAP lesions. J Bone Joint Surg Am 2009Jul; 91(7):1595-603.

6 Burkhart SS, Morgan CD, Kibler WB. Thedisabled throwing shoulder: spectrum ofpathology Part I: pathoanatomy andbiomechanics. Arthroscopy 2003 Apr;19(4):404-20.

7 Burns JP, Bahk M, Snyder SJ. Superiorlabral tears: repair versus biceps tenodesis.J Shoulder Elbow Surg Mar; 20(2Suppl):S2-8.

8 Chhadia AM, Goldberg BA, HutchinsonMR. Abnormal translation in SLAP lesionson magnetic resonance imaging abductedexternally rotated view. Arthroscopy Jan;26(1):19-25.

9 Clavert P, Bonnomet F, Kempf JF, BoutemyP, Braun M, Kahn JL. Contribution to thestudy of the pathogenesis of type II superiorlabrum anterior-posterior lesions: acadaveric model of a fall on the outstretchedhand. J Shoulder Elbow Surg 2004 Jan-Feb;13(1):45-50.

10 Edwards SL, Lee JA, Bell JE, Packer JD,Ahmad CS, Levine WN, et al. Nonoperativetreatment of superior labrum anteriorposterior tears: improvements in pain,function, and quality of life. Am J SportsMed 1456 Jul; 38(7):1456-61.

11 Franceschi F, Longo UG, Ruzzini L,Rizzello G, Maffulli N, Denaro V. Noadvantages in repairing a type II superiorlabrum anterior and posterior (SLAP) lesionwhen associated with rotator cuff repair inpatients over age 50: a randomizedcontrolled trial. Am J Sports Med 2008 Feb;36(2):247-53.

12 Gobezie R, Zurakowski D, Lavery K,Millett PJ, Cole BJ, Warner JJ. Analysis ofinterobserver and intraobserver variabilityin the diagnosis and treatment of SLAP tearsusing the Snyder classification. Am J SportsMed 2008 Jul; 36(7):1373-9.

13 Gorantla K, Gill C, Wright RW. Theoutcome of type II SLAP repair: asystematic review. Arthroscopy 2010 Apr;26(4):537-45.

14 Gossetin OS, F. Paratte, S. Clavert, P. Mole,D. Boileau, P. Type II SLAP lesions;Fixation or Tenodesis. In: Boileau P, editor.Shoulder Concepts, Arthroplasty &

Figure 5: Forward elevation 3 months post SLAP repair right shoulder.

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pathology such as a rotator cufftear.

• An MRI arthrography provenSLAP lesion with the presence ofa paralabral cyst an even clearerindication.

• Confirmation of the SLAP lesionat arthroscopy.

We prefer repair with 1 postero-superior anchor taking care not torestrict antero-superior labral mobilityto avoid stiffness in external rotation.

Conclusion

Diagnosis of SLAP lesions can bedifficult. Careful correlation ofclinical presentation and diagnostic

tools is essential to avoid poor surgicaloutcomes. Use of a well devisedalgorithm fro treatment can be of usein identifying which patients willbenefit from which intervention, butdefinitive indications are yet to bedetermined.

References1 Abbot AE, Li X, Busconi BD. Arthroscopic

treatment of concomitant superior labralanterior posterior (SLAP) lesions androtator cuff tears in patients over the age of45 years. Am J Sports Med 2009 Jul;37(7):1358-62.

2 Andrews JR, Carson WG, Jr., McLeod WD.Glenoid labrum tears related to the longhead of the biceps. Am J Sports Med 1985Sep-Oct; 13(5):337-41.

78 NZJSM

Arthroscopy; 2008; Nice: SurampsMedical; 2008. p329-34.

15 Grossman MG, Tibone JE, McGarry MH,Schneider DJ, Veneziani S, Lee TQ. Acadaveric model of the throwing shoulder:a possible etiology of superior labrumanterior-to-posterior lesions. J Bone JointSurg Am 2005 Apr; 87(4):824-31.

16 Hamner DL, Pink MM, Jobe FW. Amodification of the relocation test:arthroscopic findings associated with apositive test. J Shoulder Elbow Surg. 2000Jul-Aug; 9(4):263-7.

17 Ide J, Maeda S, Takagi K. Sports activityafter arthroscopic superior labral repairusing suture anchors in overhead-throwingathletes. Am J Sports Med 2005 Apr;33(4):507-14.

18 Iqbal HJ, Rani S, Mahmood A, BrownsonP, Aniq H. Diagnostic value of MRarthrogram in SLAP lesions of the shoulder.Surgeon Dec; 8(6):303-9.

19 Itoi E, Kuechle DK, Newman SR, MorreyBF, An KN. Stabilising function of thebiceps in stable and unstable shoulders. JBone Joint Surg Br 1993 Jul; 75(4):546-50.

20 Jee WH, McCauley TR, Katz LD, MathenyJM, Ruwe PA, Daigneault JP. Superiorlabral anterior posterior (SLAP) lesions ofthe glenoid labrum: reliability and accuracyof MR arthrography for diagnosis.Radiology 2001 Jan; 218(1):127-32.

21 Jia X, Yokota A, McCarty EC, NicholsonGP, Weber SC, McMahon PJ, et al.Reproducibility and reliability of the snyderclassification of superior labral anteriorposterior lesions among shoulder surgeons.Am J Sports Med May; 39(5):986-91.

22 Jin W, Ryu KN, Kwon SH, Rhee YG, YangDM. MR arthrography in the differentialdiagnosis of type II superior labralanteroposterior lesion and sublabral recess.AJR Am J Roentgenol 2006 Oct;187(4):887-93.

23 Jung JY, Ha DH, Lee SM, Blacksin MF,Kim KA, Kim JW. Displaceability of SLAPlesion on shoulder MR arthrography withexternal rotation position. Skeletal RadiolMar 8; 2011:8.

24 Karlsson J. Physical examination tests arenot valid for diagnosing SLAP tears: areview. Clin J Sport Med Mar; 20(2):134-5.

25 Keener JD, Brophy RH. Superior labraltears of the shoulder: pathogenesis,evaluation, and treatment. J Am AcadOrthop Surg 2009 Oct; 17(10):627-37.

26. Kido T, Itoi E, Konno N, Sano A, UrayamaM, Sato K. The depressor function of bicepson the head of the humerus in shoulderswith tears of the rotator cuff. J Bone JointSurg Br 2000 Apr; 82(3):416-9.

27 Kim SH, Ha KI, Ahn JH, Kim SH, ChoiHJ. Biceps load test II: A clinical test forSLAP lesions of the shoulder. Arthroscopy2001 Feb; 17(2):160-4.

28 Kim SH, Ha KI, Han KY. Biceps load test:a clinical test for superior labrum anterior

and posterior lesions in shoulders withrecurrent anterior dislocations. Am J SportsMed 1999 May-Jun; 27(3):300-3.

29 Kim SH, Ha KI, Kim SH, Choi HJ. Resultsof arthroscopic treatment of superior labrallesions. J Bone Joint Surg Am 2002 Jun;84-A(6):981-5.

30 Kim TK, Queale WS, Cosgarea AJ,McFarland EG. Clinical features of thedifferent types of SLAP lesions: an analysisof one hundred and thirty-nine cases. J BoneJoint Surg Am 2003 Jan; 85-A(1):66-71.

31 Koh KH, Ahn JH, Kim SM, Yoo JC.Treatment of biceps tendon lesions in thesetting of rotator cuff tears: prospectivecohort study of tenotomy versus tenodesis.Am J Sports Med 1584 Aug; 38(8):1584-90.

32 Liu SH, Henry MH, Nuccion SL. Aprospective evaluation of a new physicalexamination in predicting glenoid labraltears. Am J Sports Med 1996 Nov-Dec;24(6):721-5.

33 Maffet MW, Gartsman GM, Moseley B.Superior labrum-biceps tendon complexlesions of the shoulder. Am J Sports Med1995 Jan-Feb; 23(1):93-8.

34 McFarland EG, Kim TK, Savino RM.Clinical assessment of three common testsfor superior labral anterior-posteriorlesions. Am J Sports Med 2002 Nov-Dec;30(6):810-5.

35 McMahon PJ, Burkart A, Musahl V, DebskiRE. Glenohumeral translations areincreased after a type II superior labrumanterior-posterior lesion: a cadaveric studyof severity of passive stabilizer injury. JShoulder Elbow Surg 2004 Jan-Feb;13(1):39-44.

36 Morgan CD, Burkhart SS, Palmeri M,Gillespie M. Type II SLAP lesions: threesubtypes and their relationships to superiorinstability and rotator cuff tears.Arthroscopy. 1998 Sep; 14(6):553-65.

37 Nakagawa S, Yoneda M, Hayashida K,Obata M, Fukushima S, Miyazaki Y. Forcedshoulder abduction and elbow flexion test:a new simple clinical test to detect superiorlabral injury in the throwing shoulder.Arthroscopy 2005 Nov; 21(11):1290-5.

38 Neri BR, Vollmer EA, Kvitne RS. Isolatedtype II superior labral anterior posteriorlesions: age-related outcome ofarthroscopic fixation. Am J Sports Med2009 May; 37(5):937-42.

39 O’Brien SJ, Pagnani MJ, Fealy S, McGlynnSR, Wilson JB. The active compression test:a new and effective test for diagnosinglabral tears and acromioclavicular jointabnormality. Am J Sports Med 1998 Sep-Oct; 26(5):610-3.

40 Pagnani MJ, Deng XH, Warren RF, TorzilliPA, Altchek DW. Effect of lesions of thesuperior portion of the glenoid labrum onglenohumeral translation. J Bone Joint SurgAm 1995 Jul; 77(7):1003-10.

41 Pagnani MJ, Deng XH, Warren RF, TorzilliPA, O’Brien SJ. Role of the long head ofthe biceps brachii in glenohumeral stability:a biomechanical study in cadavera. JShoulder Elbow Surg 1996 Jul-Aug;5(4):255-62.

42 Parentis MA, Glousman RE, Mohr KS,Yocum LA. An evaluation of theprovocative tests for superior labral anteriorposterior lesions. Am J Sports Med 2006Feb; 34(2):265-8.

43 Powell J. Diagnostic Utility of ClinicalTests for SLAP lesions: A SystematicLiterature Review. The Journal of Manual& Manipulative Therapy 2008; 16(3):59-79.

44 Rao AG, Kim TK, Chronopoulos E,McFarland EG. Anatomical variants in theanterosuperior aspect of the glenoid labrum:a statistical analysis of seventy-three cases.J Bone Joint Surg Am 2003 Apr; 85-A(4):653-9.

45 Rodosky MW, Harner CD, Fu FH. The roleof the long head of the biceps muscle andsuperior glenoid labrum in anterior stabilityof the shoulder. Am J Sports Med 1994 Jan-Feb; 22(1):121-30.

46 Shepard MF, Dugas JR, Zeng N, AndrewsJR. Differences in the ultimate strength ofthe biceps anchor and the generation of typeII superior labral anterior posterior lesionsin a cadaveric model. Am J Sports Med 2004Jul-Aug; 32(5):1197-201.

47 Snyder SJ, Karzel RP, Del Pizzo W, FerkelRD, Friedman MJ. SLAP lesions of theshoulder. Arthroscopy 1990; 6(4):274-9.

48 Tuite MJ, Cirillo RL, De Smet AA, OrwinJF. Superior labrum anterior-posterior(SLAP) tears: evaluation of three MR signson T2-weighted images. Radiology 2000Jun; 215(3):841-5.

49 Tuoheti Y, Itoi E, Minagawa H, YamamotoN, Saito H, Seki N, et al. Attachment typesof the long head of the biceps tendon to theglenoid labrum and their relationships withthe glenohumeral ligaments. Arthroscopy2005 Oct; 21(10):1242-9.

50 Vangsness CT, Jr., Jorgenson SS, WatsonT, Johnson DL. The origin of the long headof the biceps from the scapula and glenoidlabrum. An anatomical study of 100shoulders. J Bone Joint Surg Br 1994 Nov;76(6):951-4.

51 Yung PS, Fong DT, Kong MF, Lo CK,Fung KY, Ho EP, et al. Arthroscopicrepair of isolated type II superior labrumanterior-posterior lesion. Knee SurgSports Traumatol Arthrosc 2008 Dec;16(12):1151-7.

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Vol 38 No 3, 2011; 79

ARTICLE

Nutritional considerations

and challenges for flat

racing jockeys

Stephen Gurr BHlthSci(Nut&Diet), Grad Dip Ex & Sport Sci, IOC Diploma in Sports NutritionDepartment of Sports NutritionAspire Academy of Sports Excellence

Correspondence to:Stephen GurrAspire Academy of Sports ExcellencePO Box 22 287DOHA, Qatar

Abstract

Flat race jockeys need to maintain a low body mass that allows them to meet the weight handicaps assigned to the horses they areriding. This review examines the anthropometric characteristics, chronic and acute weight management and dietary practicesjockeys employ to maintain or make weight. It was found that most jockeys are small in stature and have low total body mass andbody fat levels. Typical means of manipulating body mass include food/fluid restriction, saunas, hot baths, diuretics, laxativesand appetite suppressants. These practices place jockeys at increased risk of heat related illness during race meeting and evenincrease the likelihood of falls and are therefore discouraged. Reported energy intakes are indicative of restrained eating behavioursand likely increase risk of low energy availability and poor bone health. The reported carbohydrate intake is unlikely to meet thedemands of training and competition. It is recommended that jockeys target a hydrated body mass that is within 2% of theminimum weight they perceive necessary to be able maximise riding opportunities. A long term approach needs to be made toweight loss, with moderate energy restriction and appropriate exercise. Acute weight loss for competition should be achieved viause of a low residue meal plan and moderate fluid and sodium restriction. Replenishment of carbohydrate stores and minimisingthe fluid deficit should be the focus of dietary food and fluid intake during race meetings.

Key words: Low energy availability, weight making, dehydration, heat stress, jockeys

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Introduction

“In horse racing it is widely accepted thatthe physiological status of the jockey issecondary to that of the equineathlete”18(p66)

Horse racing is one of the most popularsports in the world, enjoyed by billionsof people worldwide. However, as thisquote attests, it is the health andconditioning of the horse that is of primaryimportance.

Unique among weight category sports, theweight a jockey must attain for a givenrace is set by the weight-handicapallocated to the horse, which is based it’son ability or age.4 For each race in whichthey ride, jockeys will receive a basemonetary amount, plus a percentage ofany prize money on offer. The incentive

to achieve a weight that will maximiseriding opportunities, coupled with weighthandicaps that are often well below thejockeys natural weight, has seen manyjockeys adopt “extreme” weight makingbehaviours that are contrary to both healthand performance.21

While there have been studies examiningthe physical characteristics7,8 dietaryhabits10,11 and weight making practices10,11

of jockeys, there currently exists nopublished guidelines on the nutrientrequirements of jockeys in training andcompetition. This review examines someof the existing literature on flat racingjockeys, before making dietaryrecommendations for training and racing.Information presented in this review withregards racing regulations for competitionis specific to jockeys competing in

Australian race meetings, unlessotherwise stated.

Training

Jockeys typically ride early morning trackwork 5-6 days a week, lasting between 3-5 hours, which is often followed by trialor official race meetings later in the day.During track work, jockeys will ridemultiple horses, each of which they willbe required to “work” according to thetrainer’s instructions.11

Most studies suggest that jockeys will dosome form of training outside of theirtrack and racing commitments. Most ofthe cross training activities are aerobic innature, eg, running and riding.14,10 Ratherthan being driven by motivation toimprove specific “jockeyingperformance”, these cross trainingactivities are often used as a means of

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aiding in the maintenance of riding weightor as an acute weight making strategy.21

Concomitantly, it has been reported thatjockeys are reluctant to undertake anyresistance training for fear of gaining extramuscle mass.9

Competition

Race meetings are held all year round,meaning jockeys have the opportunity toride as often or as little as they like. Byextension, the timing and length of their“season” and “off-season” will vary.While one study reported that jockeys willaverage of 344 rides a year, the studyfound this did range from 10-1200.7

Jockeys can ride in up to 2-4 race meetingsa week, in which they will ride between1-8 races over a period of 5-6 hours. Racedurations range from 1-3 minutes, with thelength of time between races typically 30-40 minutes11. Jockeys are required toweigh-in no later than 45 minutes beforeeach race, while those on horses that earnprize money, along with the next bestfinisher, have to weigh in directly afterthe race as well4. Race meetings are heldin a wide range of environmentalconditions.

Physiological Requirements

of Training and Racing

The work of Trowbridge et al18 representsthe only empirical data on the physical

demands of horse riding. They studiedseven jockeys during fifteen racemeetings. They found average heart ratesranged from 136 to 178 beats. min -1 (peak- 162-198 beats. min -1) and were alwaysabove 80% of the jockeys’ measuredmaximum during races. Mean lactates,taken soon after races had finished, rangedfrom 5.1 – 11.7 mmol . l -1. The authorsnoted that lactates tended to be higher inthose races where the horses had a chanceof a top placing, suggesting that as thehorse works harder, the greater thephysiological strain placed on the jockey.

Though only involving a small number ofriders, this study suggests jockeys requirea high level of aerobic endurance to beable to tolerate long periods in the saddle,while at the same time have the anaerobiccapacity to be able to produce highintensity efforts during races and “fast”track sessions. The fact that thoroughbredhorses can weigh up to 500 kg and reachspeeds up to 60 km . h-121 suggests jockeysalso require a degree of upper bodyfunctional strength to be able to controlthe horse.

Optimal Physique

The optimal physique for a jockey is onethat simply allows him or her to maximiseriding opportunities. While the minimumweight for all races is 43.5 kg 4, it has beennoted that weight handicaps are usually

between 52-58 kg. As this is inclusive ofthe riding saddle and accessories, thismeans that in effect jockeys need to behalf to one kilogram lighter than this.Therefore jockeys need to maintain aweight below 55 kg to allow them to raceregularly.14

Table 1 summarises studies that haveexamined the anthropometricalcharacteristics of race jockeys. It showsthat they are typically small in stature,have low body mass index (BMI) and lowskinfolds or percentage body fat. Hill andO’Connor8 conducted somatotypeprofiling of jockeys, classifying them asectomorphic-mesomorphs, indicating thatmesomorphy (musculo-skeletal robustness)is dominant while ectomorphy (linearity,slenderness) is more dominant thanendomorphy (relative fatness).

Weight Management

Practices of Jockeys

The studies that have described the weightmaking practices of jockeys have foundmost regularly use one or more chronicor acute strategies to maintain or makeweight.7,11,14,10 Reported methods includethose designed to induce a reduction inbody fluid levels (restricted fluid intake,saunas, exercising while wearing sweatsuits, hot baths, diuretics), a reduction infat/muscle mass (energy restriction,appetite suppressants) or a reduction in

Publication Study Body Mass Height BMI % Body Fat Sum 7Population (kg) (cm) (kg.m2) Skinfolds

Hill et al (1997)^ 65 professional 52 ± 3.2 161 ± 6.4^ 20.1 ± 1.4 Not reported. Not reported.jockeys (42-60)^ (17.7 - 23.6)

Hill and O’Connor n = 8 (6 males, 52.6 ± 1.9 kg 161 ± 3 20.4 ± 1.0 9.9 ± 3.9 Not reported.(1999)^^ 2 females)

Hill and O’Connor (2000) 31 professional 51.8 ± 2.0 kg** 161.1 ± 5.4** 20.0 ± 1.3** 7.5 ± 1.8 (4.6%- 53.0 ± 11.3^^^(M) jockeys (28 males, (17.5-22.9) 10.9% (M)) 64.0 ± 3.9^^^(F)

3 females) 15.3 ± 0.6 (14.9-15.9)

Leydon and Wall (2002) 6 males 52.8 ± 2.4 (M) 162.3±4.4 (M) 20.1 ± 1.5 11.7 ± 2.9 (M)* Not reported.14 females 49.3 ± 3.4 (F) 156.2±4.0 (F) 20.2 ± 1.5 23.6 ± 3.8 (F)*

Moore et al (2002) 116 senior and 53 ± 0.4 (M) 162 ± 8.0 (M) 20.3 (M) Not reported. Not reported.apprentice jockeys 51 ± 0.6 (F) 157 ± 1.0 (F) 20.5 (F)male 91female 25

Pruscino et al (2008) 7 male jockeys 53.9 ± 2.7 164.1 ± 4.0 20.0** Not reported 32.9 ± 5.6

Warrington (2009) 27 professional 53.1 ± 4.1 160.0 ± 0.1 19.88 ± 1.26 8.99 ± 2.48 44.3 ± 10.2jockeys 7.88 ± 1.73 (Equation(17 flat and 10 national based on sum 7 skinfolds)hunt jockeys)

^ Self reported values via questionnaire. * Measured via DEXA scan^^ Did not provide separate figures for males/females ** Calculated from the mean height and weight provided^^^ Sum of 9 skinfolds

Table 1: Anthropometrical data of flat race jockeys (Mean ± SD)

gastrointestinal contents (laxatives,vomiting). While similar weightmanagement behaviours have beendescribed in other weight category sports,1

a major concern is that jockeys have tomake weight on a weekly basis, ratherthan just for a few major competitionsduring the year. The health andperformance implications of some of thesepractices are described briefly below (SeeFogelholm (1994); Walberg-Rankin(2006) and Sawka et al (2007) for moredetailed reviews).

Energy Restriction

The findings of the dietary surveys (SeeTable 2) would suggest many jockeysregularly use chronic or acute energyrestriction to manipulate body mass.Leydon and Wall11 suggested the reportedvalues for energy intake in their studywere well below the jockeys’ estimatedrequirements, which is consistent with thefindings of Hill et al,6 who found that theaverage reported total energy intake wasbelow the average calculated RestingMetabolic Rate (RMR), measured byindirect calorimetery (6190 ± 565 kJ;range 5535 – 7186 kJ). Periods of energyrestriction will lower RMR1, which ineffect will lower the energy prescriptionrequired to help jockeys maintain theirdesired weight. Further, chronic energyrestriction is also associated withinadequate intake of carbohydrate, proteinand a range of micronutrients1. Twostudies10,11 also reported that intakes of anumber of micronutrients, includingcalcium and iron, to be below theRecommended Daily Intake (RDI).

When the average energy intakes reportedin these studies are expressed kJ/perkilogram body mass, it suggests that manyof the jockeys are at risk of periods of lowenergy availability, which is known toresult in a suppression reproductivefunction and bone formation (See Manoreet al (2007) for review). The only studyto examine menstrual status in jockeysfound that 36% of the female jockeys intheir study reported menstrualabnormalities. Interestingly, a recentstudy of male professional jockeys foundno evidence of hypogonadism, but foundjockeys had whole-body osteopenia and12% were osteoporotic. Leydon andWall11 found that almost half of thejockeys (44%) in their study to beosteopenic. It has been suggested that thehigh prevalence of bone disorders andlower than expected bone mineral density(BMD) for their age was likely due to theprolonged periods of energy deficit,combined with other poor lifestyle factors,eg, smoking, and the small oestrogenicstimulus provided by horse riding.21 Thisis of special concern for jockeys, giventhe high risk nature of the sport.

Using the Eating Attitudes Test-26 (EAT-26), both King and Mezey9 and Leydonand Wall11 classified 20% of the jockeysas suffering from disordered eating, whileanother study3 found jockeys scoredhigher on the EAT-26 when undertakingacute weight loss compared to times whenthey were not. As the EAT-26 is knownto underestimate the true prevalence ofdisordered eating in athletes,1 trueprevalence of disordered eating amongstjockeys may be much greater. It has alsobeen shown that scores for depression,

anger and fatigue were significantlyincreased, and scores for vigoursignificantly reduced, when the jockeyswere undergoing rapid weight losscompared to times when they were not.3

Fluid Loss

Any degree of dehydration will reduce thebody’s ability to produce sweat, which inturn increases the risk of heat injury.20 Inaddition, dehydration of >3%, or lessextreme losses combined with heat stress,will negatively affect cognition, mood andmental status during exercise.17

Therefore, the high intensity nature ofhorse racing, coupled with the often severefluid losses jockeys will incur to makeweight, reported to be as high as 11% oftotal body mass,10 will not only predisposejockeys to suffering heat illness,especially during warm environments, butmay also increase the likelihood of falls.

Two studies which have measured thehydration status of jockeys have bothshown jockeys to have greater averageupon waking Urine Specific Gravity(USG) values on race days whencompared with non-race days.15,21 Further,Pruscino15 noted that despite a relativelymodest average acute weight loss (2.1 ±0.4%) and the cool to temperate (9-20˚C)environment in which they were racing,found that mean core temperatures injockeys still rose 1.2˚C above restingvalues after five races.

Dietary Recommendations

for Training

The dietary goals of professionals jockeysmay be broadly described as to:

Energy CARBOHYDRATE PROTEIN FAT

Publication Jockey Survey kJ kJ/kg g g/kg % of g g/kg % of g % ofPop Method Overall Overall Overall

Energy Energy EnergyIntake Intake Intake

Labadarios 93 senior 7 day food 8100 153 219 4.1 43.4 77 1.5 15.2 74 33.9et al (1993) male jockeys diary

Hill et al professional 7 day weighed 5781±828 112±15.1 180 3.4 50±9 65 1.2 18±3 46.9 30±5(1999) jockeys (6 male, food diary (4734-6964)

2 female)

Leydon and 6 males 7 day weighed 6769±1339(M) 128(M) 179±56(M) 3.4(M) 45.5±5.5 58±12 1.1(M) 15±4.5(M) 54±23(M) 34.5±7.2Wall (2002) 14 females food record 6213±1797(F) 126(F) 174±50(F) 3.5(F) 47±16 0.9(F) 13.5±3.0(F)

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Table 2: Reported dietary intakes of flat race jockeys (Mean Daily Intake ± SD)

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1 Provide sufficient carbohydrate tosupport the aerobic and anaerobicenergy production during track workand races.

2 Maintain a weight that maximisesriding opportunities and promotesmaintenance of RMR and lean bodymass.

3 Provide an adequate energy intake toensure normal physiological functionand avoid consequences of lowenergy availability.

4 To ensure adequate intake of allmicronutrients, especially calciumand iron.

Long Term Weight

Management

Jockeys should be encouraged to adoptdietary and exercise habits that allow themto achieve a hydrated body mass that iswithin 2% of the minimum weight theyperceive necessary to be able to maximiseriding opportunities. This will helpameliorate the need to adopt chronicenergy restriction and “extreme” acuteweight making strategies known to havedeleterious effects on health andperformance. Extremely low levels ofbody fat levels should be avoided, as thiswill reduce cushioning of internal organs,1

a major consideration of jockeys given therisk of falls during racing. When workingwith jockeys, health professionals,especially dietitians, always need to besympathetic to the incentive of jockeys toachieve a weight well below thatconsidered healthy to ride a particularhorse for a given race.

Assessment of energy availability shouldbe undertaken with jockeys. Table 3provides an example of a calculation ofenergy availability for a female jockey.Values 125 kcal.kg.FFM day-1 (30 kcal kgFFM-1.day) are indicative of low energyavailability.12

Carbohydrate Requirements

Data from Trowbridge et al,18 coupledwith reports of training volumesundertaken by jockeys, would suggestthey require at least 5-7 g/CHO/per kg/Body mass to support the aerobic andanaerobic demands of training and racing,although a target of 3-5 g/CHO/per kg/Body mass may be more appropriate onlight training/rest days. Both these targetranges provide the jockey with theopportunity to adjust carbohydrate intaketo reflect their daily training load.Interestingly, two studies6,7 whichexamined the carbohydrate intakes ofjockeys reported low intake values, likelyreflecting the jockeys’ desires to restrictoverall energy intake (see Table 2).

Protein Requirements

Jockeys should target a protein intake of1.2-1.6 g.kg-1.day-1. This level of intakewill promote better maintenance of leanbody mass, especialy during periods ofenergy restriction and/or inadequateintake of carbohydrate. The higher dietinduced thermogenesis (DIT) of protein13

and increased satiety associated withprotein rich food provides additionalsupport for jockeys to aim to achieve thehigher end of this intake target.

Calcium and Iron

Athletes following a low energy diet areat risk of suboptimal intake of a range ofmicronutrients, especialy iron andcalcium. Adequate intake of calcium isespecially important for jockeys given therole it plays in achieving and maintainingoptimum bone density.

Dietary Recommendations

for Competition

Preparation for Race DayThe dietary goals of jockeys in the leadup to race meetings are to achieve theweight required to ride the horses forwhich they have been assigned, ensure

Energy Availability = Energy Intake - Training Energy Expenditure*Body mass: 49.3 kg*% Body fat: 23.6Lean body mass: 37.7 kg*Mean energy intake: 6213 kJEnergy cost of daily training (3 hours track work): 4000 kJEnergy availability: 6213 - 4000 + 2213Energy availability: 6213 - 5000 = 2213/37.7 or 58 kJ per kilogram fat free mass(low energy availability)

Table 3: Example of energy avalability for a female flat riding jockey.

adequate carbohydrate stores and be wellhydrated. For jockeys that do not need tomake weight, they should aim to consume5-7 g/CHO/per kg/Body mass the daybefore to promote adequate glycogenstores. Those with a full schedule of ridesand that have undertaken early morningtrack work on the day prior, should aimfor the high end of this range, while thosewith a more limited schedule of rides, thelower end.

If the jockeys need to make weight forrides, they should be encouraged to adopta low residue meal plan, in combinationwith a mild fluid and salt restriction. Sucha plan, based around low fibre,carbohydrate rich foods, may allowjockeys to achieve a 300-400 g decreasein body mass,4 while ensuring theadequate carbohydrate and energy intaketo promote optimal performance. Theamount of fluid restriction should beguided by the absolute amount of weightthe jockey needs to lose. It should belimited to the last 24 hours prior to therace meeting, given the negative impacthydration may have on ridingperformance.

Day of and During the Race MeetingThe goal of nutrient intake on the day ofa race meeting is to ensure adequatecarbohydrate stores and minimise fluiddeficit.

The requirement to weigh in after racesand the often short amount of timebetween each, act as obvious barriers tothe jockey practicing optimal nutritionpractices. Therefore, the decision on thetype and volume food/fluid consumed inbetween races should be guided by theirpost race weight and the weight they needto make for subsequent rides. Whileneeding to be mindful of the overallweight of the foods and fluids, jockeysshould aim to choose carbohydrat richoptions that will aid in re-fuelling. Forthose jockeys for whom weight is not aconcern, they should consider consumingsodium containing fluids and/or beencouraged to consume fluids with foods.For those jockeys for whom weight is aconcern, they should aim to consume lowsodium fluids in between meals, and bemore aggressive with their fluid intakeonce their riding commitments havefinished.

Vol 38 No 3, 2011; 83*Mean value reported from the study of Leydon and Wall (2002)

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Recovery

The goal of recovery after race meetingsis to refuel carbohydrate stores, promoterepair of damaged muscle tissue andpromote rehydration. Intake of 0.5-1 g/CHO/per kg/Body mass and 10-20 g ofprotein in the form of a meal or snack soonafter the race meeting serves as a usefultarget.1 Jockeys should aim to consumefluid 125-150% of estimated sweat lossesto promote optimal rehydration. In thesituation in which jockeys are unaware oftheir sweat losses, they should beencouraged to have available a range offluids that will promote voluntary intakeand consume these with their recoverymeal/snack. These targets are especiallyimportant if the jockey has track workcommitments the following day.

Conclusion

To optimise riding opportunities many flatrace jockeys adopt extreme weightstrategies that are contrary to both healthand performance. In this sense, the ends,ie, achieving a weight that allows them toride a horse in a race, justifies the means,ie, extreme weight loss practices such assevere energy restriction and use ofdiuretics/laxatives. Studies examining thedietary practices of jockeys provideevidence of restrained eating behaviours,compromising overall energy intake andthat of key macro and micronutrients.

It is recommended that jockeys take a longterm approach towards their weightmanagement, targeting a hydrated bodymass that is within 2% of the minimumbody mass they perceive necessary to beable to maximise riding opportunities. Thetarget weight must be one that can bemaintained without the need for severeenergy restriction and/or excessiveexercise behaviours. Acute weight lossfor competition should be achieved via useof a low residue meal plan and moderatefluid and sodium restriction.Replenishment of carbohydrate stores andminimising the fluid deficit should be thefocus of dietary food and fluid intakeduring race meetings.

Key Areas for Future

Research

• Examine the impact of pre-coolinginterventions on physiological strainand subjective markers ofperformance.

• Investigate the energy cost of jockeysduring track work and races.

• Examine the effects of the differentacute weight making strategies usedby jockeys on objective andsubjective markers of performance.

• Identify the physiological variablesthat impact on the performance of thejockey.

• Examine the typical sweat rates ofjockeys during training and racing ina range of environmental conditions.

• Investigate the health implications ofrepeated use of acute weight makingpractices on long term health.

References1 Burke L. Weight making sports. In L.

Burke, Practical Sports Nutrition. SouthAustralia: Human Kinetics, 2007; 289:312.

2 Cowley S, Bowman B, Lawrance M. (2007)

Injuries in the Victorian thoroughbred

racing industry, Br J Sports Med, 2007;

41(10):639-43.

3 Caulfield M J and Karageorghis C I.Psychological effects of rapid weight lossand attitudes towards eating amongprofessional jockeys, J Sports Sci, 2008;26(9):877-83.

4 Cox, G. Making weight in sports – Practicetips. In Burke L and Deakin V. ClinicalSports Nutrition, North Ryde, NSW:McGraw-Hill Australia, 2006; 189:196.

5 Fogelholm, M. Effects of BodyweightReduction on Sports Performance, SportsMed, 1994;18 (4):249-267.

6 Hill C A, O’Connor H T, Hooper M andWhite B. Energy intake and restingmetabolic rate of professional jockeys(Abstract), 5th IOC World Congress onSport Sciences, October 31-November 5th,1999.

7 Hill C A, O’Connor H, Abraham S,Richardson K, Hooper M, White B. andThompson. A descriptive study of the healthand lifestyle practices of professionaljockeys (abstract) Australian Conference ofScience and Medicine in Sport, NationalConvention Centre, Canberra, 7-10October, 1997, 154:155.

8 Hill C A and O’Connor H T.Anthropometric profile of professionaljockeys. �In Norton K, Olds T and DollmanJ. (ed.), Kinanthropometry Adelaide:International Society for the Advancementof Kinanthropometry, 2000; 105:120.

9 King M B, Mezey G. Eating behaviour ofmale racing jockeys, Psychol Med, 1987;17(12):49-53.

10 Labadarios A, Kotze J, Momberg D andKotze, T J W. Jockeys and Their Practicesin South Africa, World Rev Nutr Diet, 1993;71:97-114.

11 Leydon M A and Wall C. New ZealandJockeys’ Dietary habits and Their PotentialImpact on Health, Int J of Sport Nutr ExercMetab, 2002; 12;220-237.

12 Manore M, Kam C L and Louckes A B. Thefemale athlete triad: Components, nutritionissues, and health consequences, J SportsSci, 2007; 25(S1);S61-S71.

13 Manore M A and Thompson J L. Energyrequirements of the athlete. In Burke L andDeakin V. Clinical Sports Nutrition, NorthRyde, NSW: McGraw-Hill Australia, 2006;97:115.

14 Moore J M, Timperio A F, Crawford D A,Burns C M and Cameron-Smith D. WeightManagement and Weight Loss Strategies ofProfessional Jockeys, Int J Sport Nutr andExerc Metab, 2002; 12;1-13.

15 Pruscino, C., McGregor, M. Jones, M.,Flanagan, T. and Sullivan V. The effects ofhydration status on physiological andcognitive parameters of jockeys in mildconditions [9-20oC] – A study conducted bythe Victorian Institute of Sport (VIS) incollaboration with Victoria University (VU)for Racing Victoria (Unpublished), 2008.

16 Sawka M N, Burke L M, Eichner E R,Maughan R J, Montain, S J and StachenfedN S. Exercise and Fluid Replacement –Position Stand, Am College Sports Med,2007: 39(2):377-390.

17 Shirreffs S M. Conference onMultidisciplinary approaches to nutritionalproblems. Symposium on Performance,exercise and health Hydration, fluids andperformance, Proc Nutr Society, 2008;68(1):1-6

18 Trowbridge E A, Cotterill J V and CroftsC.E. The physical demands of ridingNational Hunt races, Eur J of Appl Physiol,1995; 70:66-69.

19 Waldron-Lynch F, Murray B F, Brady J J,McKenna M J, McGolrick A, WarringtonG, O’Loughlin G and Barragry J M. Highbone turnover in Irish professional jockeys,Osteoporosis Int, 2010; 21(3):521-525.

20 Walberg-Rankin J. Making weight in sports.In Burke L and Deakin V. Clinical SportsNutrition, North Ryde, NSW: McGraw-HillAustralia, 2006; 175-199.

21 Warrington G, Eimwear D, McGoldrick A,McEvoy J, MacManus C, Griffin M andLyons D. Chronic weight control impactson physiological function and bone healthin elite jockeys, J Sports Sci, 2009; 27(6):543-550.

Stephen GurrStephen graduated with a Bachelor HealthScience (Nutrition and Dietetics) fromQueensland University of Technology in 2005.Prior to his current role of Sports Dietitian atthe Aspire Academy for Sports Excellence inQatar, he worked as both a clinical andcommunity dietitian in Queensland, beforeundertaking the two year Nestle SportsNutrition Fellowship at the Australian Instituteof Sport. His major professional interests arein the area of nutrition for endurance and teamsport athletes.

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ARTICLE

Acute ocular trauma:

Recognition and management

in the sports arena

Albert Vosseler MBChB, Graham A Wilson MBChB, FRANZCO, MOPHTH

CorrespondenceDr G A WilsonEye DepartmentGisborne Hospital421 Ormond RoadGisborne, New Zealand

Introduction

Ocular trauma contributessignificantly to rates of visualimpairment and blindness

worldwide, and is the leading causeof unilateral vision loss.1 In developedcountries, sport and recreationalactivities account for up to 25% of allocular injuries.2-4 Remarkably, sportsrelated ocular injuries are often moresevere than other causes of oculartrauma (such as occupational) and aretherefore more likely to requirehospitalisation and cause long termvisual impairment.3,5,6 For children,sport and recreational activitiesaccount for more than 50% of allocular injuries, and thus children aredisproportionately affected and atgreater risk than the adultpopulation.7,8 Consequently, thelifetime impact of ocular trauma isoften far greater for children than foradults.

While there is relatively limited globaland regional data available on the ratesof eye injuries associated with sports,ocular injuries in Australiapredominantly occur from badminton,squash, Australian rules football andcricket.3 In contrast, North Americansports that account for the most eyeinjuries include basketball andbaseball,9 while soccer (football) andsquash accounted for the majority ofinjuries in Scotland.2 Interestingly, themajority of injuries requiringadmission from racket sports were dueto contact with the racket rather thanthe projectile itself.

The topic of ocular health is often notwell taught, and is perceived as acomplex and daunting subject. Whilerare, the appropriate recognition andmanagement of ocular injury iscritical; this article aims to provide apractical guide for practitionersworking with athletes in assessing, andappropriately managing acute ocularinjuries on the sports field.

Rapid Ocular Assessment in

the Sports Arena

The goal of the initial ocularassessment is to determine the natureand severity of the injury. This maybe assisted by having the appropriateequipment in your kit. (Table 1)

In a suspected ocular injury, as withany injury, assessment should beginwith a concise history.

1 Mechanism of injury; considerthe circumstances, severity andlikely objects involved. Is thislikely to be a blunt injury versusan open globe injury? An openglobe eye injury (where animmediate referral to anophthalmologist or emergencydepartment is warranted) may besuspected by history alone ifsecondary to flying objects(especially small objects with highspeeds) or motor vehicleaccidents, and may present withonly reduced vision or minor signson examination.

2 Vision is the best measure ofocular health: has vision changedsince the injury? Ask if contact

lenses are currently being worn asa lost lens may simply account forthe visual impairment.

3 Is there pain? What is the natureof the pain and where is itslocation. A deep aching pain issuggestive of a serious injury,while superficial pain andphotophobia are commonlyassociated with a corneal foreignbody or abrasion and is relievedby local anaesthetic drops.

4 Previous ocular history such asprevious ocular injury or ocularsurgery, laser surgery and/orvision loss (slightly decreasedvision in a patient’s previous lazyeye may not be the result of aninjury).

The ocular examination after acuteinjury is determined by the severity ofthe injury. A quick glance suggestingan open globe injury (ie, a deflatedglobe, asymmetrical pupil or signs ofherniated tissue) requires no furtherevaluation but immediate referral.

1 Visual AcuityIf the athlete is unable to open theireyes due to pain, instilling a drop ofanesthetic (amethocaine or lignocaine1%) can assist. If the eye becomescomfortable, the problem is likelyoriginating from the ocular surface.Use a Snellen chart or reading chartto test the vision (alternatively if noeye chart is available, using any printis fine) and record the distance fromwhich it can be read. With the adventof smart phones, various applications

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ARTICLE

are available that can help in assessingvision that remove the need to carryan eye chart. If nothing can be seenon an eye chart, counting fingersshould then be tested. Visual loss maybe graded into mild, moderate (visualacuity worse than 6/12) and severe(counting fingers or less). The exactdegree of vision is less important thangaining an overall appreciation for theseverity and persistence of vision loss.

Any reduced vision, without anobvious cause (ie, a corneal abrasion),that is not resolving should beconsidered a red flag for serious ocularinjury.

2 Examine the Globe and Pupil(see Figure 1)

When examining the globe, alwaysopen the lids from the bony orbitalmargins above or below the eye toavoid applying pressure to the globe,particularly until an open-globe injurycan be excluded (see Figure). Ensurethe eye is not deflated, check the pupilsfor size and shape and compare withthe opposite eye. A pupil dragged toone side indicates either a seriouscontusion or open-globe injury as thetissue in the eye has either been tornor is herniating out of the globe.Compare the pupils for size andreaction to light including direct andconsensual responses, as well as

looking for a relative afferent pupillarydefect (RAPD), which can be assessedby the swinging light test.

Pupil responses:i Direct: Pupil constricts with light

stimulationii Consensual: The pupil constricts

with light stimulation from theother eye

Swinging light test: In healthy eyes,when the light is moved from one eyeto the other eye, both remainedconstricted due to the direct andconsensual responses.

RAPD: Both pupils dilate when thelight is moved from the unaffected eyeto the affected eye, indicating aproblem with the sensory (afferent)component of the light reflex in theaffected eye.

Look at the front of the eye for bloodin the anterior chamber (hyphaema)located between the cornea and theiris. Note that while textbookstypically show a fluid level in the eye,initially the anterior chamber of theeye may simply appear hazy. Using anophthalmoscope, quickly check for ared reflex and compare with the otherside, absence of which may indicatebleeding deeper within the eye. Assessthe surrounding tissue including the

sclera, while maximising the view byexamining the eye turned in variousdirections. Take care in examining fordark masses underlying theconjunctiva which may signify globerupture and prolapsed intraoculartissue that has herniated through thesclera (white of the eye) (see Figure1). Look for any lacerations of theconjunctiva or sclera as this willrequire urgent opthalmological review.Look for foreign bodies on theconjunctiva or cornea, remembering toalways evert the lids when examiningfor a foreign body. Whilesubconjunctival haemorrhages areusually benign, take care with any thatencompass 360 degrees around thecornea or where the posterior aspectcannot be visualised, as this mayindicate a more serious injury such asglobe rupture or orbital fracture.10,11

3 CorneaExamine for corneal abrasions withfluorescein and a blue light either onan ophthalmoscope or alternatively atorch with a blue filter. If an abrasionis present, evert the upper lid to checkfor a foreign body. This can be doneby having the athlete look down andapplying light pressure with a cottonbud approximately 1 cm above the lashline. The eyelashes can then be gentlypulled away from the globe and overthe cotton bud allowing the lid to flipon itself. (See Figure 2)

4 The EyelidsLook at the lids for any contusions orlacerations. There are four mainanatomical regions to consider; theskin around the medial aspect of theeyelids, where the tear ducts drain intothe nose; the superotemporal area ofthe lids housing the lacrimal gland;lacerations involving the lid margin;and lastly lacerations with protrudingfat or associated ptosis. These areaswill require careful examination andsurgical repair. Always be cognisantto lid lacerations or superficial injuriesthat may be associated with anunderlying laceration to the globe. Donot remove any herniated fat.

5 Eye MovementsFinally, assess for any restricted eyemovements, particularly upgaze which

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Figure 1: Safely opening the eyes.

ARTICLE

may signify an orbital floor fracture.Look at the symmetry of the two eyes,a sunken eye or any forwarddisplacement of the eye that mayindicate a bleed behind the globe.Check for tenderness around the orbitas well as sensation over the cheeksand forehead (orbital fractures candisrupt the nerves which supplysensation to the forehead and cheeksleading to anaesthesia).

Management of Acute

Ocular Trauma in the

Sporting Arena

The majority of minor injuries inAustralasian sports where vision isminimally impaired or improving, arelikely to be abrasions and contusionsthat can be managed conservatively bya medical practitioner. However,following a careful assessment,referral is indicated with the followingindications:

1 Lacerations or penetrating injuriesof the lids or globe

2 Restricted eye movements(ophthalmoplegia) or, a black eyewith an associatedsubconjunctival haemorrhagewithout a visible posterior limit

3 A sunken or protruding eye4 Abnormal pupil size or shape

compared with the opposite eye5 Hyphaema6 Absent red reflex/asymmetrical

red reflexes7 Prolapsed tissue (appearing as a

dark mass under the sclera)8 Photophobia without a corneal

abrasion or foreign body9 Any degree of visual loss not

improving over 1-2 hours,including mild visual loss withoutan identifiable cause

If at any stage open-globe injury issuspected, including rupture from ablunt injury/contusion, intra ocularforeign body or penetrating injury,immediately cease the examination,place a non-pressure protective plasticshield over the eye, provide oralanalgesia and anti-emetics, keep the

athlete nil by mouth, and referimmediately to an ophthalmologist/emergency department. A completeexam is not required on the sports fieldand all topical ointment and dropsshould be avoided. If noophthalmologist is available, oralantibiotic (we recommendciprofloxacin 500 mg b.d [note thatciprofloxacin is relativelycontraindicated in some elite athletesdue to a suspected association withtendinopathy or rupture]) and tetanusprophylaxis should be initiated.12 Aconjunctival laceration may indicatean underlying scleral laceration,therefore the athlete should not returnto play but instead be referred for slitlamp evaluation that day.

For corneal abrasions consensussuggests that there is no benefit inpatching the eye when consideringeither healing time or pain. Patchingthe eye may actually decrease theexternal oxygen supply to the surfaceof the eye.13,14 Instead, manage theinjury with intensive topicalantibiotics (eg, Chloramphenicoldrops or ointment) and dark glasses tomanage the photophobia is sufficient.Isolated corneal abrasions do notrequire a referral unless visual acuityor pain fail to resolve within 1-2 days.Contact lenses should be avoided untilthe eye feels normal for one week andthe lesion is healed.

Corneal foreign bodies should beremoved with a moistened cotton budand the upper lid everted to exclude aretained foreign body. Note that manysymptomatic foreign bodies aremicroscopic, and running the cottonbud over the everted lid may removethese and improve symptoms. If youare unable to see the foreign body andsymptoms persist, or you suspect it haspenetrated the eye, do not attemptfurther removal and refer to anemergency department.

While many uncomplicated blunttrauma injuries will not result inclinically significant damage orrequire the athlete to stop play,significant ocular contusion can leadto hyphaema, traumatic iritis ordamage to the retina and associated

Vol 38 No 3, 2011; 87

Figure 2: Everting the eyelids.

ARTICLE

structures.15-17 Signs of seriouscontusion requiring immediate referralinclude photophobia, decreasedvision, a deep pain not relieved bylocal anaesthetic, a hazy appearinganterior chamber or blood aqueouslevel, and absent red reflex orasymmetrical pupil responses.Appropriate initial managementincludes oral analgesia (avoid oralNSAIDs due to the risk of re-bleeding)and cycloplegics which dilate the pupil(cyclopentolate 1% one drop 3 timesdaily). Steroid eye drops may only becommenced after a full ophthalmicassessment. The main complicationsof hyphaema are increased intra-ocular pressure from obstruction of thedrainage angle and re-bleeding. Strictbed rest is unnecessary if hospitaladmission is not required after anophthalmological assessment,however maintaining a upright orsemi-upright position, even whilesleeping, and limiting activity for 5-7days or until cleared by anophthalmologist is recommended.14

Orbital blowout fractures should besuspected when there is asymmetricalextra-ocular muscle movement withassociated diplopia. This is typicallyseen on upgaze with an inferior blow-out fracture. Urgent assessment by anophthalmologist and/or plasticsurgeon is warranted, along withmanaging the athlete by shielding theeye.8 Children can sustain ‘white-eyedorbital blow-out fractures’ where thereis a white ‘normal’ looking eyewithout surrounding bruising and theorbital soft tissue becomes trapped inthe fracture leading to tissueischaemia. This condition commonlymascarades as a head injury withheadache, nausea and vomiting alongwith irritablity, however there ismarked diplopia and pain with eyemovements. White-eyed orbitalfractures require prompt referral andmanagement.18 Avoid nose blowingwith orbital fractures due to the riskof associated infection from forcinginfected material into the orbit.11

Orbital roof fractures may present witha black eye and subconjunctivalhaemorrhage without a posterior limitvisible.11 With regard to flying ortravelling, there is generally no

contraindication with closed globeinjuries or orbital fractures and playersmay return home safely with themajority of injuries.19

Lacerations to the eyelids requirecareful examination and exploration,including checking for damage to theglobe. Lacerations involving the lidmargins, the drainage outflow system,the area of the lacrimal gland or thatcause ptosis or herniated tissue, shouldbe referred to an ophthalmologist forrepair within 24 hours. Cease play ifthese areas are involved.

Contact lenses present a specialscenario. If the sportsperson has anyocular pain or symptoms werecommend removing the contact lensin order to accurately assess. Whilethis can be done with a finger, thereare relatively cheap contact lensremovers that are available. Examinethe eye for any foreign bodies orcorneal abrasions and check for anytears in the contact lens.

Prevention

While up to 90% of ocular injuriesmay be preventable through education,appropriate eyewear and by removingcommon hazards, the practicality ofpreventative measures for ocularinjuries varies between sports.20,21

Despite easily available eye protectionfor sport, it is probably under utilised,with one Australian series reportingless than 2% of people in thecommunity wearing eye protection atthe time of injury.6 At all times thepractitioner should encourage eyeprotection when practical. Individualsat high risk, particularly those withfunctionally one eyed vision (visionless than 6/12 - the level required todrive), should consider avoiding highrisk sports or using properly fittingathletic eye protection, designed forthat sport, after appropriatecounselling on the risks involved.5,22

In addition, eye protection should beconsidered in those athletes withmyopia, diabetes mellitus, previouseye injuries or previous eye surgery.9

1 Open globe injury or suspicion fromhistory or exam

2 Scleral/conjunctival lacerations3 Foreign bodies imbedded in the globe4 Absent red reflex5 Suspected orbital fracture or a

protruding eye6 Severe pain7 Complete visual loss

Summary

The most important diagnosis toexclude in suspected ocular trauma isan open globe injury. Once you haveruled this out, you are essentiallydealing with either: a contusion to theglobe (which should be referred if ahyphaema is present, if vision isaffected or if you suspect traumaticiritis), an orbital fracture or a cornealabrasion/foreign body. Minorcontusions and corneal abrasions arenot uncommon and can generally bemanaged on the sports field. The redflags outlined above act as a basicguideline for referring, whileperforming a thorough assessment asoutlined will assist in ensuring that theathlete can safely and confidentlyreturn to play without a visionthreatening injury.

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Table 1: Eye Kit; Ocular SportsEquipment

1 Ophthalmoscope or torch with a bluelight

2 Local anaesthetic eyedrops3 Fluorescein strips/eyedrops4 Antibiotic ointment5 Eye pads and shields6 Cotton buds7 Contact lens remover8 Visual acuity chart/electronic

application9 Dark glasses

Table 2: Ocular Assessment

1 History2 Visual acuity3 Pupils4 Globe / Cornea / anterior chamber

and red reflex5 Lids (always evert the upper lid) and

face6 Extra ocular movements

Table 3: Signs and symptoms requiringurgent referral.

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Vol 38 No 3, 2011; 89

References1 Thylefors B. Epidemiological patterns of

ocular trauma. Aust N Z J Ophthalmol1992 May; 20(2):95-8.

2 Barr A, Baines PS, Desai P, MacEwenCJ. Ocular sports injuries: the currentpicture. Br J Sports Med 2000 Dec;34(6):456-8.

3 Fong LP. Sports-related eye injuries. MedJ Aust 1994 Jun 20; 160(12):743-7, 50.

4 Cillino S, Casuccio A, Di Pace F, PillitteriF, Cillino G. A five-year retrospectivestudy of the epidemiologicalcharacteristics and visual outcomes ofpatients hospitalized for ocular trauma ina Mediterranean area. BMC Ophthalmol2008; 8:6.

5 Duane TD, Tasman W, Jaeger EA.Duane’s Ophthalmology on DVD-ROM.2007 ed. Hagerstown, MD: LippincottWilliams & Wilkins.

6 McCarty CA, Fu CL, Taylor HR.Epidemiology of ocular trauma inAustralia. Ophthalmology 1999 Sep;106(9):1847-52.

7 Jandeck C, Kellner U, Bornfeld N,Foerster MH. Open globe injuries inchildren. Graefes Arch Clin ExpOphthalmol. 2000 May; 238(5):420-6.

8 McKeag D, Moeller JL, AmericanCollege of Sports Medicine. ACSM’sprimary care sports medicine. 2nd ed.Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2007.

9 Youn J, Sallis RE, Smith G, Jones K.Ocular injury rates in college sports. MedSci Sports Exerc. 2008 Mar; 40(3):428-32.

10 Pokhrel PK, Loftus SA. Ocularemergencies. Am Fam Physician 2007Sep 15; 76(6):829-36.

11 Kanski JJ. Clinical ophthalmology : asystematic approach. 7th ed. Edinburgh:Butterworth-Heinemann Elsevier; 2011.

12 Calder L, Balasubramanian S, Stiell I.Lack of consensus on corneal abrasionmanagement: results of a national survey.CJEM 2004 Nov; 6(6):402-7.

13 Turner A, Rabiu M. Patching for cornealabrasion. Cochrane Database Syst Rev.2006(2): CD004764.

14 Kirkpatrick JN, Hoh HB, Cook SD. Noeye pad for corneal abrasion. Eye (Lond).1993; 7(Pt 3):468-71.

15 Kearns P. Traumatic hyphaema: aretrospective study of 314 cases. Br JOphthalmol 1991 Mar; 75(3):137-41.

16 Cho J, Jun BK, Lee YJ, Uhm KB. Factorsassociated with the poor final visualoutcome after traumatic hyphema.Korean J Ophthalmol 1998 Dec;12(2):122-9.

17 Kuhn F. Ocular traumatology. Berlin ;New York: Springer; 2008.

18 Mehanna P, Mehanna D, Cronin A.White-eyed blowout fracture: another

look. Emerg Med Australas 2009 Jun;21(3):229-32.

19 Aviation Health Unit UCAA. Assessingfitness to fly. guidelines for medicalprofessionals [serial on the Internet].March 2008.

20 Negrel AD, Thylefors B. The globalimpact of eye injuries. OphthalmicEpidemiol. 1998 Sep; 5(3):143-69.

21 Brophy M, Sinclair SA, Hostetler SG,Xiang H. Pediatric eye injury-relatedhospitalizations in the United States.Pediatrics. 2006 Jun; 117(6):e1263-71.

22 Johnson DL, Mair SD. Clinical sportsmedicine. Philadelphia, PA: MosbyElsevier; 2006.

Dr Albert VosselerAlbert Vosseler is currently completing hissecond year as a Medical Officer in Gisbornewhich has included six months ofophthalmology training. Albert graduatedfrom the University of Otago where he alsoundertook research on laser eye surgery forthe treatment of glaucoma. He has sincegained his accreditation in the USA and hopesto enter into ophthalmology training inAustralasia. Albert’s vocational interestsalong with his surfing, skiing and tennishobbies have led to an awareness of oculartrauma in the sports arena.

Dr Graham A WilsonGraham is a general ophthalmologist workingat Gisborne Hospital and also in privatepractice. Graham has sub-specialty trainingin paediatric ophthalmology and strabismusfrom the UK and Canada. He is a member ofAmerican Society of Cataract and RefractiveSurgery, the Australian and NZ PaediatricSpecial Interest Group. He is also an honoraryclinical fellow at the University of Otago andhis research interests include population eyehealth, preventative ophthalmology andamblyopia. He is currently participating intwo HRC funded research projects includingthe Dunedin Multidisciplinary Health andDevelopment Study. In 2001 he won theAmerican Academy of Ophthalmology 5 kmrace making him the “fastest ophthalmologistin the world”!

CARDIOLOGY CONUNDRUMS

Role of exercise stress testing in

athletes with repolarisation

abnormalitiesMathew G Wilson,1 Othman Salah,1 Bruce Hamilton,1

Sanjay Sharma2 and Hakim Chalabi1

1ASPETAR, Qatar Orthopaedic and Sports Medicine Hospital, Doha, Qatar2Department of Heart Muscle Disorders and Sports Cardiology, St Georges Hospital, London

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○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

In the last edition of the NZJSM,we presented a case study of anasymptomatic athlete with deep T-

wave inversion in Leads II, III, V4-V6 together with ST segmentdepression in Leads II, III and aVF. Inthe clinical work up of this athlete, heunderwent maximal cardiopulmonaryexercise stress testing and theserepolarisation abnormalitiestransiently improved resulting in theappearance of a near normal ECG. Inthis cardiology conundrum, weexamine the diagnostic role of exercisestress testing (EST) in the evaluationof athletes displaying abnormal ECGrepolarisation patterns.

Management of Athletes

with Repolarisation

Abnormalities

In order to plan optimal managementand treatment strategies in athleteswith a suspected cardiomyopathy orion channelopathy, it is critical toestablish both an accurate diagnosisand underlying aetiology. This is oftendifficult given available technologicaland published evidential limitations.However in our experience, theminimum cardiac work-up required inthe presence of T-wave inversion inasymptomatic athletes include; 1)thorough personal symptom andfamily history questioning, 2) resting12-Lead ECG, 3) echocardiography,4) cardiac magnetic resonance, 5)maximal cardiopulmonary exercisetesting incorporating blood pressureresponse, 6) 24h Holter ECG(including 1 exercise training session),and where possible, 7) 12-Lead ECGand echocardiography of first-degreerelatives (> 10 years old). Despitebeing extensive, these evaluations will

minimise the risk of a false positiveor false negative result for the athlete.

Question: “Does the normalisation ofT wave inversion upon the onset ofexercise lessen the likelihood ofunderlying cardiac disease?”

Answer: The challenge of dealingwith athletes who demonstraterepolarisation abnormalities at rest,but often returns to normality duringexercise or adrenergic stimulation hasreceived surprisingly little attentionamong the sports cardiologycommunity. However, in ourexperience, only very few patientswith true hypertrophiccardiomyopathy (HCM) demonstratenormalisation of repolarisationabnormalities during exercise. Thus,whilst the normalisation ofrepolarisation abnormalities purportsa better prognostic outcome than afailure of normalisation or a worseningof abnormalities, the isolatedobservation of T-wave inversionnormalisation cannot exclude anunderlying pathology and thus furtherinvestigations remain warranted.

Case Based Evidence to

Support this Supposition

Athlete OneAn asymptomatic black maleprofessional football player with deepT-wave inversion in Leads I, II, III,aVF, V5-V6 (Figure 1).Echocardiography and lategadolinium enhanced cardiacmagnetic resonance (CMR)demonstrated no evidence ofcardiomyopathy per se; no ‘classic’features of dilated cardiomyopathy,arrhythmogenic right ventricularcardiomyopathy or hypertrophic

cardiomyopathy. EST on initialpresentation was negative for exerciseinducible arrhythmias, and hecompleted 11 min 02 sec of a rampedcycling protocol with a maximal heartrate of 181 bpm (maximal minutepower of 340 watts). Blood pressureresponse was normal during and post-exercise. Baseline T wave inversionsnormalised immediately at the onsetof exercise, and returned to negativity3 minutes into recovery. On the basisof the clinical and investigative results,the athlete was provided medicalclearance, given appropriate educationto seek immediate medical attentionif becoming symptomatic (eg,dizziness, palpitations, syncope, etc)and was required to undergo an annualclinical evaluation, including genetictesting. Three months after receivingmedical clearance, the athlete suffereda transient loss of consciousness after45 minutes of intense football training.A new 12-Lead ECG,echocardiogram, CMR scan,cardiopulmonary exercise stress test,and a 24hr Holter ECG were requestedand matched previous findings.Repeated EST demonstrated anappropriate blood pressure response toexercise, whilst baseline T waveinversions again normalised with theonset of exercise. However, starting at170 bpm (91% age predictedmaximum), and lasting past volitialexhaustion and into 5 minutes of staticrecovery, several episodes ofsupraventricular tachycardia and atrialfibrillation were recorded (Figures 2a, b), consistent with the presence ofan underlying cardiac pathology.

Athlete TwoAn asymptomatic black maleprofessional basketball player without

CARDIOLOGY CONUNDRUMS

Figure 1: Marked sinus bradycardia with 1st degree AV block, elevated ST-segment with an upward convexity followed by T-wave inversion in leads V2–V4, and T-wave inversion in Leads I, II, III, aVF, V5-V6.

Figure 2: Documented run of supraventricular tachycardia at 19 seconds into recovery (a), and atrial fibrillation at 1minute 35 secondsinto recovery (b). Note: T-wave modification in infero-lateral leads from negativity at rest (Figure 1) to positivity with exercise.

CARDIOLOGY CONUNDRUMS

Figure 3: T-wave inversion in V5-V6, with left anterior fascicular block and left axis deviation.

Figure 4: T-wave modification in infero-lateral leads from negativity at rest (Figure 3) to positivity with exercise.

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a family history of cardiovasculardisease or sudden death presented withT-wave inversion in V5-V6, with leftanterior hemiblock and left axisdeviation (Figure 3).Echocardiography demonstrated noevidence of cardiomyopathy and ESTwas negative for exercise induciblearrhythmias. Blood pressure responseto exercise was normal, whilst baselineT wave inversions normalisedimmediately at the onset of exercise(Figure 4). Subsequently, a CMR scandemonstrated no evidence ofhypertrophic cardiomyopathy or anyfibrotic infiltrate associated with anearly cardiomyopathic process. On thebasis of the clinical and investigativeresults, the athlete was providedmedical clearance, and given the samefollow-up advice as athlete one above.Ten months after attending pre-participation screening, the playercollapsed whilst playing basketball.On arrival to the A&E department, hecomplained of chest pain, wasirritable, restless, sweating and hadcold extremities. An ECGdemonstrated broad complexventricular tachycardia at a rate of 240bpm (Figure 5). He underwent a singlesynchronised DC shock of 360 joules;following which he reverted to sinusrhythm, and becamehemodynamically stable.

Specific Importance of

Exercise Stress Testing

As these two cases demonstrate, whenexamining an athlete with T-waveinversion on resting ECG, theresolution of this electrocardiographicabnormality with exercise does notimply that the T-wave inversion is aphysiologically benign finding. Therole of exhaustive exercise stresstesting in these athletes is usedprincipally to assess for thedevelopment of ischemic changes,abnormal blood pressure response, andarrhythmias. Thus in our opinion, theimprovement of repolarisationabnormalities with exercise isirrelevant and should not be utilisedin the diagnostic continuum. It isworth briefly mentioning thebeneficial role of integrating metabolicgas analysis with maximal EST.Sharma et al1 demonstrated thatmaximal cardiopulmonary exercisetesting can be used to differentiatephysiologic hypertrophy in eliteathletes from asymptomatic butgenetically confirmed HCM patientswith mild hypertrophy. Typical heartrate and blood pressure responses tomaximal exercise failed to distinguishthe two entities, but a peak-VO2 ≥ 50ml/kg/min or > 20% above thepredicted maximum VO2differentiated athlete’s heart from

HCM. Therefore, in those athleteswith T-wave inversion and with asurprisingly low VO2 maximum, apathological aetiology should beconsidered.

Take Home Message

• The normalisation of T-waveinversion upon the onset ofexercise does not lessen thelikelihood of an underlyingcardiac disease.

• Exercise stress testing specificallyassesses for the inducement ofischemic changes, abnormal bloodpressure response, andarrhythmias with the onset ofexercise.

• In our opinion, T-wavenormalisation with exercise stresstesting is an incidental findingonly, and should not be utilised forprognostication.

References1 Sharma S, Elliott PM, Whyte G, et al.

Utility of metabolic exercise testingin distinguishing hypertrophiccardiomyopathy from physiologic leftventricular hypertrophy in athletes. JAm Coll Cardiol 2000; 36:864-70.

CARDIOLOGY CONUNDRUMS

Figure 5: Broad complex ventricular tachycardia

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UK Sport and Exercise Medicine

(UKSEM) Conference 2011Topic: Sports science, medicine, conditioning, rehabilitation and performance coaching

Location: London

Dates: 23 to 26 November

Overview

This multidisciplinaryconference now in its thirdyear has replaced the British

Association of Sport and ExerciseMedicine conference. It is not onlyendorsed by this group but manyothers including FIFA, the FA, theIRB, the RFU, ACSM and BMJJournals and was opened by PrincessAnne – herself a former olympian. Theconference was promoted as Europe’slargest interdisciplinary conference onsports science, medicine,conditioning, rehabilitation andperformance coaching. The push tomaintain a multidisciplinaryconference (as is the focus in practice)is something we need to take note ofin New Zealand. It appears to me thatthere are an increasing number ofsubgroups holding conferences relatedto sport and exercise medicine in NewZealand and we should try and reversethis trend. Many of the presentersspoke of the importance of alldisciplines communicating well in themanagement of athletes and surely thismeans we should also be holding jointconferences. I note in the Novemberedition of SportsMedNewZ StuThompson’s called for lesscompetition and more cooperation insports medicine in New Zealand andthis is certainly the theme in the UK.

A theme of many of the presentationsI attended was the importance ofquality coaching in athlete success. Arepeated key of quality coaching wasa sound knowledge of movementcompetency from the young to the eliteathlete. There is reasonable evidencethat achieving (in youth athletes) andmaintaining (in elite athletes) optimalmovement patterns is important inmaximising performance and reducinginjury. Practitioners across alldisciplines including sports medicine,

sports science, physiotherapy,conditioning, coaching and educationspoke of the importance of physicalliteracy/movement competence.There were several sessions onbarefoot running and on the pros andcons of orthotics. There is goodevidence orthotics reduce injuries butcomfort is probably key to selectionrather than specific design. Barefootrunning requires further research butthe key is it may teach us aboutoptimal running technique which wasemphasised as more important thanarguing about whether or not to wearshoes!

Although based on the observations ofa journalist the key to producing eliteperformers (the so called “TalentCode”) is suggested to be maximisingreachfullness (practising on the edgeof your ability and embracingstruggle) and motivation. Thisobviously requires further research butprovides interesting food for thoughtfor coaches and trainers.

FIFA presented a number of studiesand there now seems good evidencefor their 11+ warm-up programme.They have published results showinga reduction in non contact injuries infootball and this programme seemsimmediately transferable to localsports including soccer and netball.

Selected Presentations

The format of the conference consistedmainly of the keynotes and invitedspeakers presenting 30-40 min oralpresentations with relatively feworiginal research offerings, thus I havefocused on these invited presentations.

Keynote presentations:

What we can learn about runningfrom barefoot runningDaniel LiebermanGiven the explosion of publicity onthis topic of late hearing ProfessorLieberman speak was certainly ahighlight of the conference as was hisvery measured approach to the topic.It is worth noting that ProfessorLiebermann is not a sports medicineexpert but an expert in evolutionarybiology. He reviewed his wellpublicised thoughts on how humanshave evolved to be endurance athletesand run considerable distances (10 to25 km), as until recently (inevolutionary terms!) this was how wecaught dinner! The major emphasis ofthe talk was the need to stop trying topolarise opinion on this topic whichshould not be a question of shoes orno shoes but a question of how to runwell. Professor Liebermannhypotheses that a barefoot runningstyle minimizes impact peaks (due toshorter stride and forefoot/midfootground contact), increasesproprioception and strengthens thefoot and this may decrease injury risk.Thus barefoot running may teach usthe key to running well is how you runnot what is on your feet. This is a clearmessage that needs to go out to athletesand support staff so they are educatedon this topic and we need to wait formore research in this area as wasemphasised by Professor Lieberman.Specific concerns noted byLiebermann were athletes thattransitioned too quickly, the unknowneffect of minimalist shoes onproprioception and the absence of anydata on children.

The impact of physiotherapy onsport and exercise medicineKim BennellThis was an excellent presentationsummarising many years of research

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CONFERENCE REVIEW

in the areas of patellofemoraldysfunction, tendinopathy and lumbarstabilisation. It was pleasing to hearthat physiotherapy treatment of thesecommon problems here in NewZealand is well in line with currentthinking. We still need to focus onmotor control (gluts and quads) andproximal control in the managementof patellofemoral issues, eccentrics arestill used in tendinopathy but in linewith the work of Jill Cook and CraigPurdam we need to recognise there aredifferent stages of this pathology andmanage accordingly and while motorretraining for low back pain(multifidus and TVA) is stillrecommended it may only work forsubgroups and overall may be nobetter than other structured exerciseprogrammes. Professor Bennell alsohighlighted the need for researchersand clinicians to continue to workclosely together to guide the mostimportant research questions – I thinkthis is something we are acutely awareof in NZ sports medicine.

The Blueprint of High PerformanceDaniel CoyleBest selling sports and sciencejournalist Daniel Coyle presented(without any slides!) a very thoughtprovoking and entertaining talk on thekeys to producing elite performers. Hisideas are based on four years visitingthe world’s greatest talent hotbeds insport, art, business and musicincluding a Russian tennis andBrazilian soccer club. He proposed thekeys to producing extraordinaryperformers were the right kinds ofpractice, coaching and motivation.Two points emphasised in the talk thatmade sense to me (although I have noexpertise in coaching) were tomaximise what Coyle termed‘reachfullness’ and motivation.Reachfullness is about valuing intensepractice on the edge of your ability andembracing the struggle and mistakesthat occur – it was suggested thismaximises the velocity of learning.Coyle suggested the key to motivationwas having someone successful “inyour windshield” to follow – he notedhow younger siblings were very oftenfaster than their older brothers andsisters. He noted that mixing age

groups, choosing spartan over luxuryand praising effort over ability as allbeing important. Obviously all this isbased on observations alone and I’mnot familiar with the state of researchin this field but it gives local coachesfood for thought.

Mindsight: Programmes for SuccessDan SiegelDr Siegel is a professor of psychiatryas well as an internationally acclaimedauthor. Although not an area I knowmuch about this presentation seemeda timely reminder of the importanceof mental function in sportperformance. It was interesting to hearpersonality features (resilience,outlook, social intuition, selfawareness, sensitivity to context andattention) are trainable and Dr Siegelspoke of the applications of this “braintraining” for athlete success. He alsomentioned frontal lobe brain functionsthat are trainable and the bestpredictors of life success at age three– and perhaps athlete success? – thesewere bodily regulation, attunedcommunication, emotional balance,fear extinction, flexibility, insight,empathy, morality and intuition. Interms of a practical tool he presentedthe “Healthy Mind Platter” a tool thatprovides a daily diet for a healthy mind– applicable to the athlete and thegeneral public! The platter includessleep time, physical activity time,focus time, connecting time, play time,and time in and can be downloadedwith additional information from;www.drdansiegel.com/resources/healthy_mind_platter.

The quest for physical literacyKelvin GilesThis was another interestingpresentation and is obviously a hotpolitical topic in UK sport. It did feellike a bit of a sales pitch (somewhatconfirmed by going to the websitepromoted by the presenterwww.movementdynamics.com) butthe message was still important. Localresearch suggests many schoolchildren don’t have appropriatelydeveloped motor skills and it wouldbe interesting to know how kiwi kidscompare! Giles proposed highperformance sport was built on what

had gone before and that thedevelopment of fundamentalmovement competency was essential.He suggested physical literacy was abasic right of every child alongside thethree R’s, being not only crucial tolater high performance but also togeneral health. Giles suggested thesolution was to put movementcompetency into the educationcurriculum but this was apparentlymeeting resistance as there was noroom for it! He went so far as torecommend physical literacy be testedalongside reading and writing. He alsocited the need for physical educationspecialists in primary school and forteacher and coach education to includemore on movement development. Imust say this seems very much inkeeping with the thoughts ofrehabilitation and conditioningpractitioners in NZ who considermovement competency/patterns key toperformance and injury prevention. Ifthis topic is not on the agenda of SportNZ then it should be.

Other interesting oral presentations:

ACL rupture, treatment options andreturn to playRichard FrobellThis talk was a timely reminder thatnot everyone who ruptures their ACLneeds an immediate reconstructionand that although there are over 11,000published articles on the topic qualityevidence for best practice whendealing with ACL injury is still lacking– interestingly the majority of articlesrelate to surgery rather thanrehabilitation. The question of surgeryversus conservative management andall various combinations remainsunclear. Frobell made the interestingobservation that although the majorreason for reconstruction was to beable to return to sport only 60% do soand thus one has to wonder at theappropriateness of the surgery. Theemphasis of the talk was on the needfor prevention as this is where the bestevidence is and the focus on amultidisciplinary approach. Frobelldid comment that surgery is obviouslya very good option for many highperformance athletes but noted thatfurther research is required to match

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all individuals to the best managementand return to sport criteria still needwork.

Hamstring injury risk and return toplayCarl AsklingThis talk highlighted that there is stilllittle consensus on the management ofhamstring injuries. Re-injury ratesremain high and thus questions mustbe asked about treatment and returnto sport criteria. Askling suggestedtreatment needs to specifically targetthe involved part of the muscle (medialor lateral – although specific exercisesto achieve this were not presented –his publications may provide these)and muscle power was also noted asimportant. Two main mechanisms ofinjury were highlighted (i) anacceleration injury typical of sprintersand (ii) a stretching injury typical ofdancers. Stretching injuries weresuggested to take longer to recover(months) and in contrast the commentwas made that if there were nofindings on an MRI scan return wasnot surprisingly much quick (usuallywithin 10 days). Exercises combininghip and knee motion and lengtheningexercises under load were proposed asthe best management approach andthere may be some evidence thisprovides quicker return to sport.Askling has also developed an activeSLR test suggested as the bestindicator of readiness for return tosport and this may be worthconsidering. The test did howeverrequire bracing the knee in extensionwhich may not always be practicalclinically however the outcome wasbased on a simple subjective VASscale rating.

Update on Plantar FascitisSimon BartoldSimon is a well known Australianpodiatrist who gave a review on thecurrent thinking around plantarfasciitis. He highlighted the pathologyis likely to be similar to tendinopathy(degenerative rather thaninflammatory and due to a loweredenergy dissipation ratio in the fat pad)and risk factors included BMI, reducedpassive dorsiflexion, reduced 1st MTPROM, prolonged standing and a spur

on x-ray (which for years had beenconsidered irrelevant). In terms oftreatment he concluded no benefitfrom shockwave therapy or steroidinjection and benefit from taping(short-term), night splints (short-term), stretching the fascia, triggerpoint dry needling and soft orthotics(although from the talk by Benno Niggthe design of the orthotic does notseem important!).

Orthotics – what do they do – whatdo we know?Benno NiggDr Nigg is a very well knownbiomechanist who has publishedhundreds of articles on the topic ofhuman locomotion. In his presentationhe reviewed a number of his studiesand concluded that orthotics work buthe was still unsure exactly how! Hesummarised good evidence to show(as I think we all now know) thatorthotics do not re-align the skeleton– in his words “the skeleton doesn’tcare what you do to the shoe”. Fromhis studies kinematic changes withorthotics were small, subject specificand not systematic. There howeverwere substantial changes in jointmoments and muscle activity – thelatter seeming to be his preferredhypothesis as to how orthoticsinfluence performance and injury.There is evidence orthotics reduceinjury but this was based on orthoticsself selected for maximum comfort –non customised and prefabricated.

11+ nationwide implementation ofpreventative programme to reduceinjuries in footballMario BizziniThis was one of several presentationsfrom the FIFA Medical Research andAssessment Centre (F-MARC). The11+ programme is a series of 11exercises done as a warm-up – FIFApromote it as the “complete warm-up”.Results of a study looking at itseffectiveness (published in theAmerican Journal of Sports Medicinein 2011) have shown promisingreductions (around 10%) in non-contact injuries in football. The focusof the programme (as with othersimilar programmes) is onneuromuscular control and Dr Bizzini

96 NZJSM

emphasised the importance of coachand player education and compliance.He also highlighted the use of highprofile players as ambassadors for theprogramme. Given our local problemwith non-contact knee injuries innetball it would seem that we shouldbe looking at introducing these typesof education programmes/warm-upsin New Zealand – especially in youthsport. Obviously FIFA have a massivebudget and this made need someconsideration for implementationlocally.

Sports science in the media in 2011:From 10,000 hours to genes to unfairadvantagesRoss TuckerAn interesting presentation on the ageold debate of whether eliteperformance comes from training orgenetics or both. Tucker emphasisedtraining was important and hissummary statement was that “trainingis the realization of genetic potential”.He proposed that being dogmaticabout a magical number of hours suchas 10,000 was inappropriate and thatthe evidence shows there is a lot ofvariation between individuals – onceagain prospective studies are required.

Chris WhatmanSenior Lecturer/PhysiotherapistAUT UniversityAuckland

CONFERENCE REVIEW

Vol 38 No 3, 2011; 97

2011 NZ Sports Medicine

ConferenceLocation: Queenstown

Dates: 27 to 29 October

The 2011 Sports Medicine New Zealand Conference was held during October in the picturesque surrounds ofQueenstown. It provided an excellent opportunity for sports medicine practitioners from many disciplines tocome together for three days to hear a vast array of high quality presentations from a high quality range of

speakers from New Zealand and abroad.

We were extremely fortunate to be able to obtain the services of Per Hölmich and Kristian Thorborg on their travelsdown under to provide a workshop on the assessment of hip and groin pathology. The following morning saw PerHölmich present the Dr Matt Marshall Lecture. Alongside these two excellent presenters, we were also fortunate tohave Stefano Della Villa with us from Northern Italy where he works as a physiatrist. He was able to provide us withan excellent account of his approach to the rehabilitation of the elite athlete following injury. Dr David Hughes fromCanberra also accepted our invitation to present with a lecture on non-physical pain generators in whiplash injuryproviding a valuable insight around aspects of both pain generation and management that are not always considered inour setting.

In conjunction with these international speakers we were delighted with the vast array of presentations from localpractitioners. This was led by the keynote presentation provided by Dr Peter McNair on lower limb muscle performancechanges with injury. The conference programme followed the format of previous years, with the Saturday programmefocused on the individual discipline groups. Physicians and physiotherapists separated off to receive updates in keyareas relevant to their respective areas of sports medicine.

Also introduced was the great case presentation competition with a number of practitioners providing case presentationsfor the education of colleagues, whilst also introducing a competitive slant on things. It is hoped that this competitionwill obtain a regional and parochial focus in the future.

On the social front, an excellent conference dinner was enjoyed by the majority of delegates with highlights includingthe dual presentation of Dick Tayler and Sir Colin Meads. We were also lucky to have Dr Deb Robinson, the victoriousRugby World Cup All Black doctor with us who shared some anecdotes relating to her involvement with the teamduring the tournament.

We are grateful to all those who attended and especially to all those who made an effort to present in some formatduring the conference. Feedback to date has been very positive and we are grateful to those who have taken the timeto complete the feedback survey following the conference. This is already assisting us as we begin planning towardsthe 2012 conference in Auckland.

On behalf of the Organising and Scientific Committees, I look forward to seeing you there.

Dr Ian MurphyChairmanConference Scientific Committee

REPORT

As of 8 August 2011 there has beena change in the support structureand names of organisations

supporting elite sport in New Zealand. TheNew Zealand Academy of Sport (NZAS)has now merged with Sport and RecreationNew Zealand (SPARC)’s highperformance unit to form one nationalentity - High Performance Sport NewZealand (HPSNZ). This amalgamationhas come about with the goal of improvingthe use of resources supporting elite sportsperformance in New Zealand. The neworganisation is responsible for developingand supporting the country’s elite athletesand coaches, and expanding a network ofworld-class training facilities.

The Government’s expectations of theincreased high performance sportinvestment are:

• creating a more focussed highperformance system;

• ensuring the system is as efficient aspossible;

• effecting a cultural change with anincreased focus on excellence;

• implementing a one-stop shop for ourathletes;

• recruiting and retaining world classcoaches;

• maximising technology andinnovation; and

• increasing the number of dedicatedHP facilities.

The objectives of the merger of NZASNorth Island, NZAS South Island and theSPARC HP Unit to form HPSNZ are:

• simplify and streamline the highperformance system to the benefit ofathletes, coaches and sportsorganisations;

• lead to a culture change with anincreased focus on excellence;

• improve support for athletes, coachesand NSOs;

• improve collaboration and knowledgesharing; and

• reduce administrative and governanceoverheads.

As a result of changes over the last coupleof years, there are now less contractedproviders explicitly dealing with eliteathletes across the full range of disciplines,but especially in the rehabilitation area -medicine, physiotherapy, massage therapy,osteopathy and chiropractic. There are anumber of drivers for these changes asfollows:

1 There are less carded athletes in thesystem than when the academy wasfirst set up

2 There has been a centralisation ofservices to designated service centresin Auckland, Lake Karapiro,Wellington, Christchurch (until theearthquake struck) and Dunedin.

3 A desire to have key providersworking and being immersed in thesports they service

4 The need for consistent qualityreporting systems particularlyelectronic reporting

5 Improved inter-professionalintegration and team working in anathlete centered model

We will now expand on these drivers toprovide a rationale for the changes.

1 Less Numbers of AthletesThe previous Academy of Sport highsystem had reduced the number of cardedsports and set very high targets for athletesto be supported. The standard is “worldclass” (typically top 16 in the worldrankings), or on a development pathwayto medal in a pinnacle event such as Worldchampionships or Olympics. The fundingis now targeted to these four year cyclesto allow for adequate planning anddevelopment. There are now fewerathletes supported, and hence there arefewer providers required. The process ofdeciding who continued to provide servicewas based on a range of factors; thenumber of services provided in the lastyear, the number of providers already inthat area, and the geographical arearequired to provide services to athletes toname a few. There are still many providerswho actually meet the criteria to be aprovider but either saw very few if anyathletes or their service utilisation haddeclined. In cases where there is stillsignificant expertise, HPSNZ would liketo still use those providers on a case bycase basis, and when pre-approved by thesport paying for the services. Whereappropriate, HPSNZ has also retainedproviders with long standing and existingrelationship with key athletes. Howeverwith newly carded athletes, sports arebeing encouraged to use the establishedservice centers where possible as a greaterrange of coordinated service are providedat these centers than individual providerclinics.

98 NZJSM

High Performance Sport New

Zealand changes to enhance

New Zealand sportspeople

winning on the world stageDuncan Reid DHSc, Tony Edwards FACSP, Sharon Kearney BPhty

CorrespondenceDuncan ReidHealth and Rehabilitation Research InstituteSchool of Rehabilitation and Occupation StudiesAuckland Universty of TechnologyPrivate Bag 92 006Auckland 1142, New ZealandTel +64 9 921 9999 Ext 7806Fax 64 9 921 9620Email duncan.reid@aut.ac.nz○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

REPORT

Vol 38 No 3, 2011; 99

2 Service CentralisationIn order to provide a world class serviceto athletes most countries in the world havedeveloped designated service centers thatbring together the desired expertise inorder to ensure the athletes achieve theirgoals of ‘winning on the world stage’. Inthe early models of the academy it wasthought that having a wide coverage ofproviders to allow athletes to stay closerto home would be useful. However therewas mixed compliance to the reportingsystems required by the academy and alsofragmentation of how the various serviceswere delivered. This was not necessarilyintentional but more a function of thegeographical spread and lack of electronicreporting systems. With the new servicecenters up and running there have beensignificant improvements in coordinationof services, with teams of providersworking with athletes and along with thisenhanced quality control via appropriatereporting mechanisms.

3 Immersion of Key ProvidersWithin the service centers there has beena move to have key providers immersedinto the sports. A good example of this inthe Rowing NZ model. There now are fulltime physiotherapists employed to workwith the rowers along with a full timestrength and conditioning expert and abiomechanist. These providers aresupported by sports psychology, sportsmedicine, massage and nutrition in eitherfull or part time roles. The keyrehabilitation providers are also the onesthat travel with the teams on their overseascampaigns. It is envisaged that theseproviders will also be appointed toOlympic Games teams so that there iscomplete consistency of services. Manyothers sports now have some of or all ofthis immersion in place.

4 Quality Reporting SystemsThe rehabilitation centre at the AUTMillennium Campus was the first servicecentre to move to a full electronic clientrecord (ECR), implementing the Gensolvesystem. It is hoped that as the other servicecenters are developed that Gensolve willalso be used there. This system hasimproved the communication acrossproviders. It has also now been linked withthe new electronic Athlete ManagementSystem – ZED which contains all the keyinformation about the athlete. This systemis web based and accessible to authorisedproviders. The key drive in the system isthe athlete’s individual performance plan(IPP). All services must be coordinatedand monitored to ensure that theperformance goal is achieved and this isachieved more easily with coordination of

activities in the service centres. Key fieldsin the Gensolve ECR are uploaded dailyinto ZED so that providers in otherdisciplines can see appropriate parts of therehabilitation plan with less duplication ofpaper work.

5 Improved Inter-professionalIntegration

This is a key area of the new environment.The IPP and athlete centered approach iscritical to the new environment. Athletesappreciate services that are coordinated,where the goals are clear and when allproviders in the team are on the same pageand are talking together about the goals.There has been significant movement inthis area and there have been a number ofprofessional development days alreadyinstigated to ensure this inter-professionalapproach is enhanced. An example of thisis the inter-disciplinary approach is thedevelopment of the MovementCompetency Screen (MCS) developed byMatt Kritz and Professor John Cronin fromAUT University. This PhD projectdeveloped and validated a tool based onfive key movement patterns which is beingused as a communication tool betweenstrength and conditioning providers andrehabilitation providers. The five keymovements are used to decide if an athletemoves well or poorly and how theirmovement patterns might influencetraining and performance. The MCS helpsset appropriate loads for rehabilitationexercises and ensures all parties knowwhat the athlete can do and what needsmodification in the gym trainingprogramme. The MSC has now beenloaded into the Gensolve programme andthis has become a standard element of allathlete assessments upon presentation withan injury. It is also now the starting pointfor the previously applied muscle balanceassessments. Once the MCS is completedfurther sport specific tests can beundertaken by the physiotherapists.

There are two other key areas ofdevelopment. Firstly the philosophywithin the provider’s teams is performanceenhancement and injury prevention ratherthan injury treatment. To achieve this timeis allocated in the performance centers toallow for integration and time forproviders to work together to enhance thetraining programmes.

Secondly there has been an effort to embedresearch around the athlete performancedevelopment. This has been particularlysuccessful in the strength and conditioningarea where service providers are alsocompleting PhD and Masters researchprojects. This initiative will be extended

in the rehabilitation area to increase theresearch into injury prevention and themost effective injury rehabilitationprotocols. This will be lead by DuncanReid (Assoc Professor at AUT andDirector of the Rehabilitation Centre at theAUT Millennium campus).

Future Challenges

With a smaller number of providersintegrating with elite athletes there is a riskthat expertise will be lost. There is also arisk that getting to the top of this pyramidand working with truly elite athletesbecomes more challenging and as such,succession planning and career pathwaysneed to be considered. As there is nofunding for services to athletes that are notcarded, sports and HPSNZ need toconsider systems that encourage providersto get involved in sports at junior anddevelopment levels. This may be the socalled ‘hard yards’ that providers need todo to position themselves for opportunitiesthat may arise in the future. Fortunately,there are also opportunities to traveloverseas with teams, with key providersnot always available to travel. In this waysports need to develop touring providersand this model has worked well with sportslike Hockey where is a team of providersthat are available for tours on a rotationalbasis.

Conclusion

The changes to High Performance sportdescribed in this paper provide a rationalefor the future developments in this area.New Zealand is a country that has always‘punched about its weight’ in theinternational sporting arena. Supportservices to athletes have grown over timeand as these grow refinements are requiredto ensure we offer the most up to date andworld leading approaches. These changeswill ensure that an athlete has all therequired support to meet the overall goalof HSPNZ- “more new Zealanderswinning on the world stage.”

Duncan ReidRehabilitation Director HPSNZAUT Millennium Rehabilitation Centre

Tony EdwardsMedical Director HPSNZ

Sharon KearneyPhysiotherapy Director HPSNZ

REPORT

Sports Medicine New Zealand

2011 Chairman’s ReportPresented at the National Council Meeting held inQueenstown on 27 October

It is great to see that after a year of financial turmoil, earthquakes and ecological disaster, my first year as chairman has concluded with two significant positives: first, Sports Medicine New Zealand has continued to remaina financially sound organisation, and the All Blacks hold the Webb Ellis Trophy. I cannot truly claim to have made

any significant contribution to either, but I do want to offer my continuing thanks and appreciation for the fantasticwork that Brenda Allum continues to provide well above and beyond what we could ever expect. Thank you, Brenda.

Our esteemed President, Mr Chris McCullough, has nicely summarised the main focal points for SMNZ in 2011 in hisreport, so I will not repeat them.

Sports Medicine New Zealand has two main faces it shows to the world; our conference and our journal. This year’sconference again looks like it will be very successful with a great programme and a fantastic venue.

I encourage you all to support our journal and its new editorial team of Bruce Hamilton and Chris Whatman and Ichallenge each member of SMNZ to submit one single item for publication in the next 12 months. It doesn’t matterwhat the item is - a research paper, a review article, a brief commentary on a sporting or sports medical happening, aclinical pearl of wisdom (anything you have picked up that has helped you in your practice and could possibly helpothers), or even a letter to the editor. Bruce is also looking for case studies and journal article reviews and is developingtemplates and guidelines to assist anyone who wants to do something in this area. The journal is about Sports Medicinein New Zealand, and it is you, our members, who make up this sports medicine community. And it is only you who canwrite about it - for your colleagues and for the rest of the world. I believe that, with your input, the NZ Journal of SportsMedicine can inform, educate and report and be a valuable resource for us all. Bruce and Chris are working hard toachieve this, and I again thank them for their time, their energy, and their vision for our journal.

And what of Sports Medicine New Zealand in the future? SMNZ is the oldest of the organisations currently represent-ing sports medicine in New Zealand, and it is an umbrella organisation with a wide membership open to all those withan interest in the areas of medicine, sport and exercise in their broadest sense. But there are many other organisationscompeting for membership dollars and conference attendees. I believe there is a need to compete less and to co-operatemore and I hope to pursue this philosophy over the coming years through discussions with the various other groups.This philosophy is also reflected in the direction High Performance Sport New Zealand is moving. I hope we candevelop innovative ways to better work together, to share resources, to encourage continued membership and to de-velop and enhance relationships between the groups. Recent talks with Sport and Exercise Science New Zealand havebeen a start, as has the sponsorship High Performance Sport New Zealand has provided for our conference this year.

Finally, I wish you all an enjoyable conference, a happy Christmas and a hope that New Zealand will continue toprosper socially, culturally, economically and on the sporting fields of the world.

Dr Stuart ThomsonNational Chairman

100 NZJSM

CONFERENCE ABSTRACTS

Selected Abstracts from the

2011 NZ Sports Medicine Conferenceheld 27-29 October, QueenstownReproduced from the Conference Handbook published by Sports Medicine New Zealand.

CLINICAL ENTITIES INATHLETES WITH

LONGSTANDING HIP ANDGROIN PAIN - DIAGNOSIS,

TREATMENT ANDPREVENTION

Per HölmichChief Surgeon, Associate Research

Professor, Arthroscopic Centre Amager,Amager University Hospital,

University of Copenhagen, Denmark

Groin and hip pain in association withsports activities is a serious and recurrentproblem in sports medicine, in particularin connection with football, rugby andicehockey. The incidence of groin pain is5 – 18 % per year. The pain may originatefrom various anatomical structures suchas bone, joint, muscle, tendon or ligamentbut abdominal or gynaecologicaldisorders, referred pain and nerveentrapment can also cause groin pain.

The muscles of the femur, the abdominalmuscles and the muscles of the back allwork in synergy to balance the pelvis andto control the movements of the trunk inrelation to the pelvis and the legs.

Poorly understood terms as adductortendinitis, osteitis pubis, symphysitis,sports hernia, pubalgia and likewise areused in the literature. However, these termsdo not fulfil the demands for a true“diagnosis” and they are in relation tothese patients so far without scientificbasis. The term “clinical entities” issuggested relating the origin of the painto specific anatomic structures. Examplesof entities are Adductor related groin pain,Iliopsoas related groin pain and Inguinalrelated groin pain. (Hölmich BJSM 2007)Pathology in the hip joint is an importantcause of groin pain itself and apredisposing factor for primary as well assecondary groin pain as well.

Clinical ExaminationThe examination techniques used needs tobe standardised, reproducible and valid.This is imperative to make reliableconclusions, to report to and cooperatewith colleagues and to be able to workscientifically. A number of techniques havebeen tested and described in the literature,but there is still a need for further testingand validation.

TreatmentMost treatment modalities suggested in theliterature are based on the experiences ofclinical practice, lacking randomizedtrials. It is important to be aware of allcauses for the groin pain in the planningof a treatment program. The result oftreatment should be evaluated usingvalidated patient based outcome scores.(Thorborg et al, BJSM 2011)

Adductor-related Groin PainOne clinical randomized trial hasdescribed a specific exercise programfound to be highly effective in thetreatment of adductor-related groin pain(Hölmich et al, The Lancet 1999), and tohave a long lasting effect (Hölmich et alAJSM 2011).

The literature regarding tenotomy of theadductor tendons is contradictory and notscientifically based. It is the experience ofthis author that a tenotomy of the adductorsis rarely indicated. Most patients can betreated successfully with the above-mentioned training program combinedwith sufficient treatment of concomitantinjuries.

ConclusionGroin injuries are difficult to treat. In manycases they tend to be ignored by bothathletes and trainers thus developing intoa chronic stage. The treatment should bebased on a systematic examination and anexact identification of the structurescausing the pain. Muscle imbalances andbiomechanical problems should beidentified. The physician, the therapist, thetrainer and the athlete need to be awarethat the treatment in most cases will belongstanding. Supervision, encouragementand patience are imperative to reach a goodresult.

ReferencesHölmich P, Uhrskou P, Ulnits L, Kanstrup I-L,Nielsen MB, Bjerg AM, Krogsgaard K.Effectiveness of active physical training astreatment for long-standing adductor-related groinpain in athletes: randomised trial. The Lancet 1999;353:439-443.

Hölmich P, Hölmich LR, Bjerg AM. Clinicalexamination of athletes with groin pain: anintraobserver and interobserver reliability study. BrJ Sports Med 2004; 38:446-451.

Hölmich P. Long-standing groin pain insportspeople falls into three primary patterns, a

“clinical entity” approach: a prospective study of207 patients. Br.J.Sports Med. 2007; 41:247-252.Hölmich P, Larsen K, Krogsgaard K, Gluud C.Exercise program for prevention of groin pain infootball players: a cluster-randomized trial.Scand.J.Med.Sci.Sports 2009.

Thorborg K, Hölmich P, Christensen R, Petersen J,Roos EM. The Copenhagen Hip and Groin OutcomeScore (HAGOS): development and validationaccording to the COSMIN checklist.Br J Sports Med 2011;45(6):478-91.

Hölmich P, Nyvold P, Larsen K. ContinuedSignificant Effect of Physical Training as Treatmentfor Overuse Injury: 8- to 12-Year Outcome of aRandomized Clinical Trial.Am J Sports Med 2011 Aug 3 Epub ahead of print

WHAT’S NEW IN SPORTSNUTRITION FROM THE IOCCONSENSUS MEETING 2010

Jeni PearceHead of Performance Nutrition,

English Institute of Sport

The first consensus conference to reviewthe evidence for the role and impact ofnutrition in sports performance met in1991 under the Medical Commission ofthe International Olympic Committee inSwitzerland. This was followed up in the2003 Consensus meeting producing aseries of journal articles, a book and videosof the meeting.

The latest developments in scientificevidence in sports nutrition were againreviewed in 2010 by a team of sportsnutrition experts. Day one of the two dayconference focused on the advances inscientific research in six specific areas(energy balance, carbohydrates for trainingand competition, fluids and electrolytes,protein and muscle growth and repair,special nutrients including vitamin D andantioxidants, and dietary supplements) insports nutrition.

The second day examining the practicalapplication of the science across a rangeof sports (strength sports, power sports,team sports, endurance sports, wintersports, aesthetic and weight class sports).A number of new developments in sportsnutrition were highlighted includingenergy availability, wider ranges in theguidelines for carbohydrate intakes, theamount and composition of carbohydrate,the timing and level of protein

CONFERENCE ABSTRACTS

Cyclist Discipline Age Training Comfort Pain Upper Low Butt- Knee Ankle-(years) Volume (%) (%) Body Back Hips (%) Foot

(hrs/wk) (%) (%) (%) (%)Competitive cyclists (n = 21) 37 ±11 8 ±4 86 33 29 43 43 50 7Recreational cyclists (n = 49) 41 ±9 7 ±3 85 41 52 48 43 87 9Mountain bikers(n = 13) 39 ±10 5 ±3 85 38 25 88 0 75 0Triathletes(n = 21) 38 ±10 6 ±2 79 58 13 25 25 75 38Total(N = 104) 40 ±10 7 ±3 85 38 30 41 28 61 9

Table I: Cyclists’ age and training volume, comfort during cycling, percentage of cyclists with pain, andbody sites of pain for recreational cyclists, mountain bikers, competitive cyclists and triathletes.

recommended for recovery from trainingsessions to maximise protein synthesis andsupport for a limited number of wellresearched supplements supported bystrong scientific evidence.

This session will review some of thehighlights and developments in thescience, the changes to therecommendations since 2003 and the finalconsensus statement produced on the thirdday of meeting.

PAIN FROM OVERUSE INJURYIN 104 COMPETITIVE AND

RECREATIONAL ROADCYCLISTS, MOUNTAIN BIKERS

AND TRIATHLETES

Rodrigo Bini2, Patria Hume1

1Sport Performance Research InstituteNew Zealand (SPRINZ)

AUT University, Auckland, New Zealand2Capes Foundation,

Ministry of Education of Brazil

Background: Occurrence of overuseinjuries and pain in cycling may differamong cyclists of different disciplines [1].The knee and low back have been reportedas the main injury sites in elite cyclists,but data have not been provided for othercycling disciplines and experience levels.

Aim: To describe the occurrence of pain incyclists of different disciplines andexperience level.

Methods: A survey of 104 cyclists (49recreational non-competitive road cyclists,21 competitive road cyclists, 13 non-competitive mountain bike riders and 21competitive triathletes) providedinformation on characteristics of existingpain during cycling, perceived comfort onthe bicycle (yes or no) and cycling trainingvolume (hrs/week).

Results and Discussion: Percentagevalues in Table I are presented within eachcycling discipline and for all cyclists. Forall cyclists surveyed, 38% had existingpain even though 85% reported they feltcomfortable on the bicycle. Fifty six

percent reported both pain and comfort,therefore, comfort on the bicycle isprobably not a good indicator for overuseinjury risk. The knee joint and low backwere frequently reported sites of pain forall the cycling disciplines and levels whichsupports findings from other studies onroad cyclists.1 A larger percentage oftriathletes reported pain compared to theother cycling disciplines. The largerpercentage of ankle-foot pain in triathletesduring cycling may be a cross-over effectdue to additional running training.

Conclusion: Triathletes report moreankle-foot overuse pain than other cyclingdisciplines. Comfort on the bicycle andcycling training hours per week areprobably not good indicators of overuseinjury risk. Training intensity and totaltraining volume of triathletes (includingrunning and swimming) should bemeasured to gain further understanding ofrisk factors for overuse injuries.

References1 Dettori N J and Novell D C, Non-traumatic

bicycle injuries: A review of the literature.Sports Medicine, 2006; 36(1):7-18

THE EFFECTS OF COMMUTERCYCLING FOR 10 WEEKS ONFITNESS, HEALTH AND BODY

COMPOSITION

James Novis, E Hargreaves, N RehrerSchool of Physical Education,

University of Otago,Dunedin, New Zealand

Introduction: Commuter cyclinginterventions in Northern Europe haveresulted in mixed effects to cardio-respiratory fitness,1,2,3 body composition,1,2

and blood pressure1,2 after eight,2 ten3 andtwenty-six weeks1. Mixed results betweenstudies may be due to methodologicalissues in the research. Therefore, thepurpose of this study was to examine theeffects of commuter cycling for 10 weeks

on peak oxygen uptake ( O2peak), bodymass, waist-to-hip ratio, blood pressure

and quality of life among healthy adultsusing a randomised controlled studydesign.

Methods: Fourteen men (mean age 37 ±7 years, body mass 76 ± 9 kg, O2peak 42.5± 8.5 ml•kg-1•min-1) and fourteen women(mean age 35 ± 9 years, body mass 70 ±10 kg, O2peak 31.5 ± 5.4 ml•kg-1•min-1)were recruited. Participants completed twotesting sessions before and after theintervention. In the first session, peakoxygen consumption and quality of life(SF-36 survey) were measured. In thesecond, blood pressure, body mass andwaist-to-hip ratio were recorded after a 12hour fast. Participants were stratified bygender and O2peak and randomised intointervention and control groups. Theintervention group (n=14) were givenbicycles and instructed to cycle to andfrom their work place three or more daysper week, for 10 consecutive weeks. Thecontrol group (n=14) were asked tocontinue commuting with their currentmode of transportation. Data wereanalysed using a two-factor (group x time)repeated measures ANOVA.

Results: There was 100% adherence in theintervention group, while one controlparticipant withdrew due to illness. A timex group interaction showed that O2peakincreased significantly (p = 0.02) by 3.2 ±4.6 ml•kg-1•min-1 in the intervention group,but did not change in the control group.While, diastolic blood pressuresignificantly (p = 0.05) increased by 8 ±10 (mmHg) in the control group, but didnot change among interventionparticipants. There were no significanteffects for body mass, waist-to-hip ratio,quality of life parameters, or systolic bloodpressure.

Conclusion: Ten weeks of commutercycling in New Zealand is beneficial forimproving cardio-respiratory fitness, butnot blood pressure, body composition orquality of life.

References1 de Geus B, Hoof E, Aerts I & Meeusen R.

Cycling to work: Influence on indexes of healthin untrained men and women in Flanders:Coronary heart disease and quality of life.Scand J Med Sci Sports 2008; 1: 498-510.

2 Møller N C, Østergaard L, Gade J A, Nielson JL, Andersen L B. The effect oncardiorespiratory fitness after an 8-week periodof commuter cycling — A randomizedcontrolled study in adults. Prev Med 2011 (notyet published).

3 Oja P, Manttari A, Heinonen A, Kukkonen-Harjula K, Laukkanen R, Pasanen M, Vuori I.Physiological effects of walking and cycling towork. Scand J Med Sci Sports 1991; 1: 151-157.

CONFERENCE ABSTRACTS

Vol 38 No 3, 2011; 103

CASE REPORTDIETETIC MANAGEMENT

FOLLOWING MULTIPLE JAWBREAKS IN AN ELITE RUGBY

UNION PLAYER

Kirsty Fairbairn, S T Kerridgeand T L Perry

Sports Nutrition and Exercise MetabolismResearch Group,

Department of Human Nutrition,University of Otago,

Dunedin, New Zealand

Introduction: In professional sport,injuries to key players can have crucialimplications on team performances.Severe injuries are common in rugbyunion, often followed by weeks tomonthsof recovery and rehabilitation.Often, body composition suffers duringthis rehabilitation period, due to reducedenergy expenditure via a reduced trainingload, combined with stable (or increased)energy intake due to boredom, and/or poorfood choices. Deficiencies in energy,protein, carbohydrate, fat, vitamins andminerals can negatively affect woundhealing1. The flow or catabolic phase ofthe body’s stress response entails a higherrequirement for glucose to heal tissues,and also involves greater proteincatabolism2. Good dietetic managementover the recovery period can not onlyaccelerate tissue repair and recovery, butalso ensure optimal body compositionwhen returning to play.

Case Report: This case describes thedietetic intervention strategies employedwith an elite rugby union player whosustained consecutive broken jaw injuries.There were three primary goals of dietarymanagement: 1) to provide a nutritionalenvironment that optimised the healingand recovery process; 2) to minimisechanges in body composition; and 3) assistthis player in achieving his goal of beingavailable for the All Black squad in 2011.

Early education regarding the stressresponse to injury and surgery wereprovided, and dietary strategies overdifferent time periods following thesubsequent surgery discussed. Theseincluded the need for a relatively highcarbohydrate, protein and energy intakein the immediate post- surgery period, toavoid substantial losses in body weightand muscle mass, further complicated bythe inability to eat solid food. In theabsence of established guidelines forathletes undergoing surgery, dietaryrequirements were extrapolated fromclinical guidelines. Estimated energyrequirements were 11-12 MJ/dayfollowing surgery, protein requirements

were estimated at 1.5g/kg body mass, andcarbohydrate requirements were estimatedat 3-5g/kg body mass. Practical advice wasprovided on the best way to achievenutritional goals via a liquid diet. Liquidsupplements including ‘Ensure Plus’,‘TwoCal HN’ and sports nutrition protein-carbohydrate supplements were providedto boost energy, carbohydrate and proteinintake. Regular reviews of dietary intakeand body composition were undertaken tomonitor the player’s ability to maintainenergy balance.

Discussion: Early dietetic intervention wasparamount in correction of misconceptionsregarding energy and carbohydraterequirements. Practical advice on liquidfood options and supplementation was wellreceived and adhered to. Regular dieteticmonitoring ensured maintenance of bodyweight within 3kg and of Sum of 8Skinfolds within 14mm for both injuries.Access to dietetic support following majorinjury/surgery can ensure optimalrecovery, particularly with regardmaintenance of body composition.

References1 Arnold M and Babul A. Nutrition and Wound

Healing. Plast Reconstr Surg 2006: 117(7)(Suppl): 42S-58S.

2 Hill G L, Douglas R G, Schroeder D.Metabolic basis for the management ofpatients undergoing major surgery. World JSurg 1993: 17(2): 146-153.

MUSCLE INJURY ANDREHABILITATION

Stefano Della Villa, Margherita RicciIsokinetic Medical Group,

FIFA Medical Centre of ExcellenceEducation Research Department

Bologna, Italy

Muscle Injuries are very common traumasin Sports Medicine. Depending on thetrauma mechanism muscle injuries areclassified as direct and indirect. The directform is the contusion, the indirect one isstrain. Muscle strains can be divided inthree grades according to their severity:mild (first degree), moderate (seconddegree) and severe (third degree).

An immediate and accurate diagnosis is thekey to plan an appropriate rehabilitativetreatment. The diagnosis is based on acareful history of the trauma followed bya physical examination and imagingprocedures. The initial imaging techniquewe require is the ultrasonography (US).Magnetic Resonance is preferred if thereis any discrepancy between the patient’ssymptoms and the ultrasonography and inthe evaluation of the deeper muscles.

Although the post acute management ofmuscle injuries known as RICE (rest, ice,compression and elevation) is alreadyaccepted there is no consensus about therehabilitation program. The primaryobjective of rehabilitation programmes arereturning the athlete back to competitionwith a minimal risk of re-injury. There isevidence that the risk of re-injury can beminimised by utilising core stabilitytraining (1) and eccentric strength training(2).

Our protocol consists of 3 phases, eachcharacterised by the achievement ofclinical and functional goals.

- Phase 1: Aerobic conditioning and rangeof movement recovery

- Phase 2: Strength and extensibilityrecovery

- Phase 3: General and specific conditioningon the field

The transition from one phase to the nextis allowed when the different progressioncriteria are met. Establishing criteria forthe return to sport remains a challenge forfuture research.

Our experience of 10 years consists of1343 injuries (non contact muscle lesions).The mean age was 30,4 and the 95% weremale. 79% injuries occurred in footballplayers and in the 37% were involved thehamstrings. We noticed a reduction of re-injury over the time.

References1 Sherry M A, Best T M. A comparison of 2

rehabilitation programs in the treatment ofacute hamstring strains. J Orthop Sports PhysTher. 2004; 34: 116-125

2 Askling C, Karlsson J, Thorstensson A.Hamstring injury occurrence in elite soccerplayers after preseason strength training witheccentric overload. Scand J Med Sci Sports.2003; 13: 244-250

TRAUMATIC ANTERIORSHOULDER INSTABILITY

Khalid MohammedDepartment of Orthopaedic Surgery and

Musculoskeletal Medicine,Christchurch HospitalUniversity of Otago

Elmwood Orthopaedic GroupChristchurch, New Zealand

Aim: To define the patient demographicsand pathology in patients in a NewZealand shoulder surgery practice,undergoing shoulder anterior instabilitysurgery and develop an algorithm for

CONFERENCE ABSTRACTS

surgical treatment of traumatic shoulderinstability.

Method: A 4 year cohort of patient’shaving shoulder stabilisations from 2005– 2008, were reviewed. A database wascreated using information obtained fromclinical notes, imaging studies, operativefindings and surgical procedures. Knownrecurrence rates were recorded andchecked against the digital imaging patientrecords.

Results: After excluding revisionstabilisations and posterior stabilisations,there were 193 primary anterior shoulderstabilisations. The mean patient age was24 (range 15 – 49) with the medianyounger. 80% were males. There was nearequal incidence of the dominant and non-dominant arm being affected. 85%reported playing sport, with 50 differentsports listed. Many participated inmultiple sports. Sports were classified as‘collision’, ‘contact and falling risk’ and‘overhead’. Approximately 50% listedcollision sports (rugby, rugby league orcombat). Approximately 50% listedcontact and falling risk sports (e.g.snowboarding, netball, mountain bike).Approximately 15% listed overhead sports(e.g. throwing, rock climbing). Withregard to glenoid bone lesions onpreoperative imaging, there were bonechanges in the glenoid in 15% of patients.On examination under anaesthetic at thetime of surgery 16% were Grade 4instability, where the shoulder is extremelyunstable and locks out of joint. Duringthis study period 64% of procedures wereperformed arthroscopically and theremainder through an open approach.Surgical decision making was on a case-by-case basis. For the 92 patients wholisted rugby as a sport, 60 underwent anarthroscopic stabilisation and 32underwent an open stabilisation. Withregard to recurrences (known dislocationsor subluxations) the overall rate was 13%.

Conclusions and Discussion: Knownrisk factors for recurrent instability aftershoulder stabilisation surgery includeyoung age, at risk sports and activities,hyperlaxity and bone lesions. Most NewZealand patients with shoulder instabilityare young, have an extremely high activitylevel and frequently play high-risk sports.There is a significant incidence of bonelesions. Each patient needs to beconsidered carefully with regard to thesefactors and the pathology of theirinstability. The surgeon should have arange of procedures in his / her inventoryto address each situation. Contemporaryoptions include open and arthroscopicBankart and capsular shift repairs, Laterjet

and bone block procedures for bonedeficiency and arthroscopic Remplissagefor Hill Sachs lesions.

UPDATE IN CHONDRALINJURY REPAIR/

REHABILITATION

Stefano Della Villa,1 E Kon,2

F Filardo,2 M Ricci,1 M Marcacci2

1Isokinetic Medical Group, FIFA MedicalCentre of Excellence, Bologna, Italy

2Department of Orthopaedic and SportsTrauma, Biomechanics Laboratory,

Rizzoli Orthopaedic Institute,Bologna, Italy

Cartilage knee injuries are frequentlyobserved in athletes and typically causedby high-impact stress and torsional loads.The management of chondral lesions isdifficult depending to the limitedregenerative capacity of articular cartilage.Several techniques have been appliedthrough the years for the treatment ofcartilage lesions including Microfractures,Osteochondral Autograft Transfer(Mosaicplasty), Osteochondral AllograftTransplantation and AutologusChondrocyte Implantation (ACI). Thetreatment has been recently improved bythe arthroscopic second-generation ACIwith three dimensional hyaluronan-basedscaffolds that reduces the joint surgerytrauma and may accelerate the recovery,when combined with proper rehabilitationprotocols.

The rehabilitation program after articularcartilage repair is a critical component ofthe treatment process and represents thekey for an optimal clinical and functionaloutcome. The post-operative rehabilitationprotocol should be progressive, goal-oriented, individualised and should takeinto consideration the patient’s age, thecartilage repair technique and the lesion’ssize and location. To ensure a successfuloutcome, rehabilitation should occur in acontrolled setting, with skilled therapistsand with access to rehabilitationswimming pool, gym, and field, under thesupervision of the orthopaedic surgeons.

We recently evaluated if the hyaline-liketissue obtained with the regenerative cell-based approach allows to these highlydemanding athletes a better functionalrecovery with respect to the outcomeoffered by the bone marrow stimulationapproach. We analysed the results obtainedin high-level football players affected byknee cartilage lesions and treated witharthroscopic second generation autologouschondrocytes implantation or

microfracture technique, and we comparedtime taken to recover, return to previousactivity level and functional outcome atshort and medium follow-up.

CARDIAC SCREENING/ECGINTERPRETATION IN THE

ATHLETE

Rob DoughtyProfessor, Heart Foundation Chair in

Heart Health,The University of Auckland,

Auckand, New Zealand

Pre-participation screening of athletes foridentification of cardiovascular diseasesthat predispose to sudden death duringsport is increasingly required for manysporting disciplines. Such screeningusually involves a medical history andphysical examination and, while the roleof a 12-lead electrocardiography (ECG)remains controversial, this is increasinglyrequired by sporting authorities. Thepurpose of ECG screening of athletes isto improve the detection of underlyingcardiac abnormalities that may beassociated with the risk of sudden death.Electrocardiographic changes in athletesare common and reflect the physiologicaladaptation to exercise training – so called“athletes heart”. Consequently it isimportant to correctly distinguish betweenthose ECG changes associated withexercise training and those which may bedue to other cardiovascular conditions.Controversy still exists with regard to ECGscreening of athletes. However, in thecurrent New Zealand context, ECGscreening is required in a number ofsporting disciplines and thus astandardised approach to ECG screeningis required. Recent recommendations fromthe Sections of Sports Cardiology andExercise Physiology of the EuropeanAssociation of Cardiovascular Preventionand Rehabilitation and by the WorkingGroup on Myocardial and PericardialDiseases of the European Society ofCardiology provides the mostcontemporary recommendations for ECGscreening of athletes.1

Reference1 Corrado D, Pelliccia A, Heidbuchel H, Sharma

S, Link M, Basso C, Biffi A, Buja G, DeliseP, Gussac I, Anastasakis A, Borjesson M,Björnstad HH, Carré F, Deligiannis A,Dugmore D, Fagard R, Hoogsteen J, MellwigKP, Panhuyzen-Goedkoop N, Solberg E,Vanhees L, Drezner J, Estes NAM, Iliceto S,Maron BJ, Peidro R, Schwartz PJ, Stein R,Thiene G, Zeppilli P, McKenna WJ.Recommendations for interpretation of 12-lead electrocardiogram in the athlete.European Heart Journal. 2010;31:243-259

Vol 38 No 3, 2011; 103

New Zealand Journal of

SPORTS MEDICINE

Change of address advice and business correspondence to:

Sports Medicine New Zealand IncPO Box 6398, Dunedin, New Zealand

Phone +64-3-477-7887 • Fax +64-3-477-7882 • Email smnznat@xtra.co.nzWebsite www.sportsmedicine.co.nz