You don't need to be signed in to read BMJ Blogs, but you can register here to receive updates about other BMJ products and services via our site.

Letter to the editor

Cape Town Medical 10, running race for health professionals

25 Mar, 13 | by Karim Khan

Hennie Muller and grandson

Letter to the Editor

The 35th staging of the Medical 10 will take place in Cape Town, South Africa, in November 2013. It is a 10 kilometre running race for health professionals. The race started in 1978 after a physician, Hennie Muller (shown in the photo with his grandson), discovered that the doctors in Finland held a 10 kilometer race to show that they practiced what the preached about a healthy lifestyle. The aim was to run it in 40 minutes but allowed a handicap of a minute for each year of age over 40.

Race organizers cut the handicap to half a minute and made it open to all health professionals and walkers, however, the event continues to be held annually at the end of November.

Is this race still held in Finland? Or are similar events held in any other country? I am interested to know.

Please contact me at: sydneyc@surgcare.co.za

Yours sincerely,

Sydney Cullis (Race Director)

Applicability of muscle injury classification system in The Munich Consensus Statement? (Letter to the Editor)

31 Jan, 13 | by Karim Khan

 By Drs. Del Buono, Best and Maffulli 

Letter to the Editor

In response to: Terminology and classification of muscle injuries in sport: The Munich consensus statement. Mueller-Wohlfahrt HW, Haensel L, Mithoefer K, Ekstrand J, English B, McNally S, Orchard J, van Dijk CN, Kerkhoffs GM, Schamasch P, Blottner D, Swaerd L, Goedhart E, Ueblacker P.  Br J Sports Med, 2012.

 Dear Prof Khan,muscles of the back

 

“The soul in darkness sins, but the real sinner is he who caused the darkness”

Victor Hugo, Les Miserables

 

We commend the authors for their efforts to provide a much needed new classification of muscle injuries in their article Terminology and classification of muscle injuries in sport: The Munich consensus statement (open access); the fact that highly experienced clinicians became involved in this field increases the potential impact upon both daily practice and future research fields 1. However, we wish to express our concerns regarding the actual applicability of this proposed classification system in clinical practice, especially for what concerns the translation to management of these injuries.

Notably, criticizing traditional terminology, as ‘passè and confusing’, the authors highlight the need for a more standardized definition and universal classification that reflects both functional and structural features of muscle injuries. We respectfully point out that the term ‘functional’ is not well defined, and it is used with various ambiguous and at times inconsistent meanings, such as fatigue-induced muscle disorder or delayed-onset muscle soreness (DOMS). We underline that both functional and structural disorders may lead to functional limitations in athletes, and these latter may also hide misunderstood structural changes of the muscle. Therefore, from a diagnostic view point, both the terminology and the ability to distinguish these two entities pose challenges. For structural changes, the authors also suggest that the term “tear” better reflects the structure of the muscle, recommending not to use the term “strain”. The latter, conversely, implies the biomechanics of the injury 1. We point out that the term “strain” reflects some radiological features (MRI and US). In fact, a strain is defined as a Grade I injury, in which less than 5 % of muscle fibers are disrupted, with a feathery oedema-like pattern, and intramuscular high signal on the fluid-sensitive sequences at MRI. This condition is well differentiated from grade II (partial tear) and III (complete tear) lesions 2. The proposed distinction is further complicated by the fact that it is unlikely that MRI is sensitive enough to detect the presence of microscopic disruptions, which may be decisive in differentiating ‘functional’ from ‘structural’ muscle injuries.

We recently proposed that a novel anatomic system was to classify acute muscle strains 2. Realistically, we suggest that the proper identification and description of the injury site could be prognostic for muscle recovery. Arising from the traditional imaging classification (MRI and US), we have simply considered the anatomy of the muscle, and classified the lesion as type I, when involving the proximal MTJ, type 2, for muscle belly injuries, and type 3, when the distal MTJ is torn. We accept that this classification system relies on clinical findings but also MRI (or ultrasound) scans. Specifically, to subcategorize muscle belly injuries, both coronal and axial views have to be taken into account. On coronal and sagittal imaging scans, the muscle belly may be injured proximally, in the middle, or distally. On axial sequences, we defined the injuries as intramuscular, myofascial, myofascial/perifascial, myotendinous, and combined.

Therefore, different from the classification system presented, which describes structural and functional muscle disorders, we propose a novel classification based on anatomical and imaging features: these aspects have a higher impact on diagnosis and management of these injuries. Imaging (US and MRI) assessment is not only helpful to help management 3, but it would also be used for assessment of injury severity and to predict the time of return to sport activity 2. Both classification systems likely have strengths and limitations, perhaps the next step is the validation of these systems and their ability to predict convalescence from sport and time for return to play.

 

References

1          Mueller-Wohlfahrt HW, Haensel L, Mithoefer K, Ekstrand J, English B, McNally S, Orchard J, van Dijk CN, Kerkhoffs GM, Schamasch P, Blottner D, Swaerd L, Goedhart E, Ueblacker P. Terminology and classification of muscle injuries in sport: The Munich consensus statement. Br J Sports Med In press.

2          Chan O, Del Buono A, Best TM, Maffulli N. Acute muscle strain injuries: a proposed new classification system. Knee Surg Sports Traumatol Arthrosc 2012;20:2356-2362.

3          Boutin RD, Fritz RC, Steinbach LS. Imaging of sports-related muscle injuries. Radiol Clin North Am 2002; 40: 333-362.

***********************************************************

Angelo Del Buono 1, Thomas M. Best 2, Nicola Maffulli 3

1 Department of Orthopaedic and Trauma Surgery, Campus Biomedico University, Via Alvaro del Portillo, 200, 00128 Trigoria, Rome, Italy

2 Division of Sports Medicine, Department of Family Medicine The OSU Sports Medicine Center, The Ohio State University, Columbus, OH, USA

3 Centre for Sports and Exercise Medicine, Barts and The London School of Medicine and Dentistry, Mile End Hospital, 275 Bancroft Road, London E1 4DG, England.

 

 

Debate! Is education more effective than mandating helmets for skiers and snowborders? – Guest Blog from Canada Safety Council

4 May, 12 | by Karim Khan

The Canadian Paediatric Society has called for legislation mandating helmet use for all skiers and snowboarders. The Society says that through mandatory helmet legislation, governments can send a strong message that helmets are important and reduce the risk of brain injury and disability.

For the record, I am a strong advocate for helmets for skiers and snowboarders and have been so for years. I just do not support, with all its attendant issues and challenges, mandating their use. Public education and public awareness is more effective, cheaper, no public/user push-back, etc, etc. And with no taxpayer-funded inspectors roaming these facilities armed with citation books and empowered to hand out fines and other penalties.

Terrible tragedies, including the skiing death of actress Natasha Richardson at Quebec’s Mont Tremblant in 2009, always spark discussion and debate about wearing a helmet when skiing or snowboarding. Should skiers and snowboarders wear helmets?  Without question, the answer is yes!  Helmets are proven critical life-saving and injury -prevention equipment. A Norwegian study published in February 2006 in the Journal of the American Medical Association found that using a helmet was associated with a 60 percent reduction in the risk of head injury. Blows to the head are among the most devastating and lethal types of injury. Although head injuries are quite rare, an estimated 60 percent of skiing fatalities involve a head injury. Even if it is not fatal, such an injury can have lifelong consequences.

Some experts do question whether helmet use also prevent the most serious types of head injuries while skiing and snowboarding. Dr. Jasper Shealy, an American researcher who is recognized as an expert on the subject, supports helmet use but points out the rate of skiing fatalities has not dropped despite much greater helmet use on the slopes. In other words, helmets just cannot prevent catstrophic injuries in some ski hill accidents.

While children are most likely to wear a helmet, the recent surge in helmet use on Canadian hills, according to the Canada Safety Council, is reflected in all age groups. Today’s helmets are so light and stylish that many skiers consider them not only effective safety equipment but also as a fashion accessory. According to the Canadian Ski Council, helmet use has risen dramatically over the last few years for skiers and snowboarders. Nova Scotia, which recently passed legislation mandating helmet use,  already had one of the highest rates of helmet use on ski hills in Canada at 88 %.

The Canada Safety Council does not favour mandatory helmet use, which brings into question enforcement and its related challenges. Public education, public awareness, commonsense, adults and parents teaching by example, and working with operators to further educate skiers and snowboarders  are the way to go to get that many more skiers and snowboarders to wear helmets on the slopes.

Emile Therien,
Public Health and Safety Advocate,
Past President, Canada Safety Council,
326 Frost Avenue,
Ottawa. ON.
Tel:613-737-4965.

 

Related BJSM articles

Sports helmets now and in the future. 2011. Andrew Stuart McIntosh, Thor Einar Andersen, and Roald Bahr et al. 

The effectiveness of helmet wear in skiers and snowboarders: a systematic review. 2010. Michael D Cusimano, Judith Kwok.

Related BJSM Blogs

Injury prevention in high level snowboard: A need to return to first principles?

Is high level snowboard too dangerous to allow your children to participate?

Concussion: how do we reconcile risk-averse policies with risk-taking sports

We join the world in mourning Sarah Burke

Concussion Position Statement: Why it’s not a KO.

Letter to the Editor: Gate control pain modulation theory explains the effectiveness of prolotherapy

28 Jan, 12 | by Karim Khan

E-letter by:
Dr. Stavros Saripanidis, Consultant in Obstetrics and Gynaecology, Private Surgery, Thessaloniki, Greece
In response to:


Simon Petrides. 2011. The use of prolotherapy injections for elite athletes. Br J Sports Med ; 45: 2 (Electronic pages).

Photo of 'Spine' in Millennium Square, Bristol by Davecpayne, Flickr cc

Dear BJSM Editors,

The dorsal horns are not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occur. [18]

Via a series of filters and amplifiers, the nociceptive message is integrated and analysed in the cerebral cortex, with interconnections with various areas. [1]

The processing of pain takes place in an integrated matrix throughout the neuroaxis and occurs on at least three levels, at peripheral, spinal, and supraspinal sites. [9]

Knowledge of the modalities of pain control is essential to correctly adapt treatment strategies (drugs, neurostimulation, psycho-behavioural therapy, etc.).

Dysfunction of pain control systems causes neuropathic pain. [1]

Spinal Cord Stimulation modalities evolved from the gate-control theory postulating a spinal modulation of noxious inflow.   [16] [2] [7] [11] [12] [15] [17] [20] [22] [23] [24] [25] [26]

It has been demonstrated in multiple studies that dorsal horn neuronal activity caused by peripheral noxious stimuli could be inhibited by concomitant stimulation of the dorsal columns. [8]

Pain relief was more prominent at pain ascending through C fibers than pain ascending through Adelta fibers. [21]

Many theories on the mechanism of action of Spinal Cord Stimulation have been suggested, including activation of gate control mechanisms, conductance blockade of the spinothalamic tracts, activation of supraspinal mechanisms, blockade of supraspinal sympathetic mechanisms, and activation or release of putative neuromodulators.  [14]

At present, Spinal Cord Stimulation is a well established form of treatment for failed back surgery syndrome, complex regional pain syndromes (CRPS), low back pain with radiculopathy and refractory pain due to ischemia. [4] [3] [8] [13]

Stimulation produced analgesia can provide a level of analgesia and efficacy that is unattainable by other treatment modalities. [19]

Spinal Cord Stimulation for the treatment of chronic pain is cost-effective when used in the context of a pain treatment continuum. [14]

Precise subcutaneous field stimulation is targeted to specific areas of neuropathic pain. [6]

We aim at attenuation or blockade of pain through intervention at the periphery, by activation of inhibitory processes that gate pain at the spinal cord and brain. [9]

Segmental noxious stimulation produces a stronger analgesic effect than segmental innocuous stimulation. [10]

That is exactly what intradermal sterile water injections do!

This therapeutic approach should not be limited only to elite athletes.

It can work for every patient with back pain.

References

[1] Prog Urol. 2010 Nov;20(12):843-52. Epub 2010 Oct 20. Anatomy and physiology of chronic pelvic and perineal pain. Labat JJ, Robert R, Delavierre D, Sibert L, Rigaud J. Centre federatif de pelviperineologie, clinique urologique, CHU Hotel-
Dieu, 1, place Alexis-Ricordeau, 44093 Nantes, France.



[2] Int J Rehabil Res. 2010 Sep;33(3):211-7. Effect of transcutaneous electrical nerve stimulation on sensation thresholds in patients with painful diabetic neuropathy: an observational study. Moharic M, Burger H. Department of Physical and Rehabilitation Medicine, Linhartova 51, SI-1000Ljubljana, Slovenia.

[3] Conf Proc IEEE Eng Med Biol Soc. 2009;2009:2033-6. Spinal cord stimulation for complex regional pain syndrome. Shrivastav M, Musley S.Medtronic Neuromodulation, 7000 Central Ave NE, Minneapolis, Minnesota, 55432 USA.



[4] J Clin Monit Comput. 2009 Oct;23(5):333-9. Spinal cord stimulation: principles of past, present and future practice: a review. Kunnumpurath S, Srinivasagopalan R, Vadivelu N. St George's School of Anaesthesia, Tooting, London, UK.

[5] Brain Res Rev. 2009 Apr;60(1):149-70. Epub 2008 Dec 31.Chloride regulation in the pain pathway. Price TJ, Cervero F, Gold MS, Hammond DL, Prescott SA.
University of Arizona, Department of Pharmacology, USA.

[6] Curr Pain Headache Rep. 2008 Jan;12(1):28-31. Peripheral nerve stimulation for chronic pain.Henderson JM.Stereotactic and Functional Neurosurgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Building/R-227, Stanford, CA 94305, USA.



[7] Schmerz. 2007 Aug;21(4):307-10, 312-7. From Descartes to fMRI. Pain theories and pain concepts.Handwerker HO.Institut fur Physiologie und Pathophysiologie, Universitat Erlangen/Nurnberg, Deutschland.



[8] Pain Physician. 2002 Apr;5(2):156-66. Spinal cord stimulation.
Stojanovic MP, Abdi S.Interventional Pain Program, MGH Pain Center, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School,
Cambridge, MA 02135, USA.


[9] J Bone Joint Surg Am. 2006 Apr;88 Suppl 2:58-62.Basic science of pain.
DeLeo JA. Dartmouth-Hitchcock Medical Center, Dartmouth Medical School, Neuroscience
Center at Dartmouth, Department of Anesthesiology, Lebanon, NH 03756, USA.

[10] Pain. 2005 May;115(1-2):152-60. Segmental noxious versus innocuous electrical stimulation for chronic pain relief and the effect of fading sensation during treatment. Defrin R, Ariel E, Peretz C. Department of Physical Therapy, School of Allied Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, 69978 Ramat Aviv, Israel.

[11] Annu Rev Neurosci. 2003;26:1-30. Epub 2003 Mar 6. Pain mechanisms: labeled lines versus convergence in central processing. Craig AD. Atkinson Pain Research Laboratory, Barrow Neurological Institute, 350 W.Thomas Road, Phoenix, AZ 85013, USA.

[12] Sports Med. 2002;32(4):251-67. Return-to-work interventions for low back pain: a descriptive review of contents and concepts of working mechanisms. Staal JB, Hlobil H, van Tulder MW, K?ke AJ, Smid T, van Mechelen W.Department of Social Medicine and Research Centre on Work, Physical Activity and Health, VU University Medical Center, Van der Boechorststraat 7, Amsterdam, The Netherlands.


[13] Curr Pain Headache Rep. 2001 Apr;5(2):130-7.Stimulation methods for neuropathic pain control. Stojanovic MP. MGH Pain Center, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA 02114, USA.



[14] Curr Rev Pain. 1999;3(6):419-426. Spinal Cord Stimulation: Indications, Mechanism of Action, and Efficacy. Krames E. Pacific Pain Treatment Centers, 2000 Van Ness Avenue, Suite 402, San Francisco, CA 94109, USA.

[15] Ann Pharm Fr. 2000 Mar;58(2):77-83. Pain and its main transmitters.Costentin J.Unite de Neuropsychopharmacologie Experimentale, ESA 6036 CNRS, Institut Federatif de Recherches Multidisciplinaires sur les Peptides=IFR 23, Faculte de Medecine et Pharmacie, 22, bd Gambetta, F 76000 Rouen.

[16] Neurol Res. 2000 Apr;22(3):285-92.Mechanisms of spinal cord stimulation in neuropathic pain. Meyerson BA, Linderoth B. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.


[17] Pain. 1999 Aug;Suppl 6:S149-52.Regulation of spinal nociceptive processing: where we went when we wandered onto the path marked by the gate. Yaksh TL.Department of Anesthesiology, University of California, San Diego, USA.

[18] Pain. 1999 Aug;Suppl 6:S121-6. From the gate to the neuromatrix. Melzack R. Department of Psychology, McGill University, Montreal, Quebec, Canada.


[19] J Clin Neurophysiol. 1997 Jan;14(1):46-62. Stimulation of the central and peripheral nervous system for the control of pain. Stanton-Hicks M, Salamon J. Anaesthesia Pain Management Center, Cleveland Clinic Foundation, OH 44195, USA.

[20] Percept Psychophys. 1996 Jul;58(5):693-703. An investigation of the gate control theory of pain using the experimental pain stimulus of potassium iontophoresis.
Humphries SA, Johnson MH, Long NR. Department of Psychology, Massey University, Palmerston North, New Zealand.

[21] J Peripher Nerv Syst. 1996;1(3):189-98. Pain relief by various kinds of interference stimulation applied to the peripheral skin in humans: pain-related brain potentials following CO2 laser stimulation. Kakigi R, Watanabe S. Department of Integrative Physiology, National Institute for Physiological Sciences, Okazaki, Japan.


[22] Nurs Stand. 1993 Jul 28-Aug 3;7(45):25-7. Pain: opening up the gate control theory. Davis P.


[23] Bull Acad Natl Med. 1989 Oct;173(7):855-60; discussion 860-1.Gate control of the nociceptive message: applications to the treatment of pain. Cambier J.


[24] Brain Res. 1983 Dec 5;280(2):217-31. Thalamic nucleus ventro-postero-lateralis inhibits nucleus parafascicularis response to noxious stimuli through a non-opioid pathway. Benabid AL, Henriksen SJ, McGinty JF, Bloom FE.

[25] Psychosom Med. 1979 Mar;41(2):101-8. A signal detection analysis of the effects of transcutaneous stimulation on pain. Malow RM, Dougher MJ.

[26] GATE CONTROL OF ION FLUX IN AXONS. GOLDMAN DE. J Gen Physiol. 1965 May;48:SUPPL:75-7.

Conflict of Interest: None declared

Fitness and health of children through sport: the context for action – Guest Blog Caroline Finch

20 Oct, 11 | by Karim Khan

(follow Caroline Finch on Twitter — @CarolineFinch)

This relates to:

Micheli, L, Mountjoy, M, and Engebretsen, L et al. 2011. Fitness and health of children through sport: the context for action. BJSM. 45:931-936

photo: owenfinn16 via Flickr cc

I read, with great interest, the paper by Micheli et al [1]in the September Injury Prevention and Health Promotion issue of the BJSM,because it outlined  different policy contexts for action.  These contexts are generally consistent with the ecological levels of sports delivery we outlined in the Sports Setting Matrix as a framework for the implementation and evaluation of programs delivered through sport.[2]  It is also consistent with our previous argument that the sports delivery and policy contexts need to be more aligned for global sports safety.[3]

Given that injury is one of the major barriers towards participating in sport,[4] it is surprising that no international policy link for addressing this key factor in children’s sports participation was named in the article.  Many of the organisations named in the paper (e.g. the World Health Organization) have divisions that are concerned with injury prevention as well as NCD (non-communicable disease) prevention, for example. A major way forward to ensuring lifelong participation in sport would surely be to bring together the policy bodies for physical activity/sport promotion together with those concerned with reducing or removing injury risk in such activities.

Whilst there is no doubt that having global policy is a key driver of action and priority attention given to health issues, it is largely practitioners at a more local level who need to implement those policies and to translate them into appropriate acceptable and sustainable programs.  In the sports injury context, we have found a mismatch between what the policy makers want and what the practitioners or implementers need.[5] Moreover, just because there is an international policy/guideline/directive one cannot assume that the desired practice or action at the grass roots level of participation, even at a low level, is achieved.[6]  No matter how much evidence-base there is for a new policy, the end-users will have their own perspectives that will directly influence their readiness to act according to the desired policy result.[7]

Having global, national and local policy responses to fitness and health (including injury prevention) will be crucial for ensuring lifelong participation in sport well into the future.  But not less so than also ensuring both an adequate informed workforce of practitioners to deliver associated programs and end users who are fully receptive to the messages that have been appropriately targeted to reach them.

References

1.         Micheli L, Mountjoy M, Engebretsen L, et al. Fitness and health of children through sport: the context for action. Br J Sports Med. 2011;45:931-6.

2.         Finch CF, Donaldson A. A sports setting matrix for understanding the implementation context for community sport. Br J Sports Med 2010;44:973-8.

3.         Timpka T, Finch CF, Goulet C, et al. Meeting the global demand of sports safety – the role of the science and policy intersection for sports safety. Sports Med. 2008;39:795-805.

4.         Siesmaa E, Blitvich J, Finch CF. Chapter 1. A systematic review of the factors that are most influential in children’s decisions to drop out of organised sport.  In: Farelli A, editor. Sport participation: health benefits, injuries, and psychological effects: Nova Science Publishers Ltd; 2011. p. 1-45.

5.         Poulos R, Donaldson A, Finch C. Towards evidence informed sports safety policy for NSW, Australia: assessing the readiness of the sector. Inj Prev. 2010;16:127-31.

6.         Hollis S, Stevenson M, McIntosh A, et al. Compliance with return-to-play regulations following mild traumatic brain injury in Australian schoolboy and community rugby union players. 2011;On line First, published on June 24, 2011 as 10.1136/bjsm.2011.085332.

7.         Donaldson A, Leggett S, Finch CF. Community perceptions of a draft policy and training structure for Australian football sports trainers at the community level: a qualitative analysis. 2011;In press. Published online 16 September 2011 as DOI: 10.1177/1012690211422009.

*************************************************************

Caroline Finch is an injury prevention researcher specialising in implementation and dissemination science applications for sports injury prevention.  She is the Senior Associate Editor for Implementation & Dissemination for the British Journal of Sports Medicine and a member of the Editorial Board of Injury Prevention; both journals are published by the BMJ Group.  Caroline can be followed on Twitter @CarolineFinch

Letter to the editor: Chronic Exertional Compartment Syndrome articles – clarification needed!

20 Sep, 11 | by Karim Khan

September 19, 2011

The Editor

British Journal of Sports Medicine

Dear Prof Khan

Re: Chronic Exertional Compartment Syndrome articles

I was very excited to receive the September issue of your journal and observe that there were a number of articles on chronic exertional compartment syndrome. As Hutchinson quite rightly states in Chronic exertional compartment syndrome: “key questions remain regarding the specific protocol a clinician should undergo when performing intracompartmental pressure testing.”

Although one can not be 100% sure of the diagnosis by only performing a thorough history and clinical examination, it is quite a painful and invasive procedure. I am therefore quite reluctant to do the procedure as suggested by Hutchinson i.e. both legs, pre- and post exertional, and all four compartments. Much to my surprise the next article by Hislop and Batt advised the exact opposite, i.e. one leg should suffice, resting pressures can be misleading and it is not necessary to test asymptomatic compartments.

I am now more confused than before reading these articles and would really appreciate guidance.

Kind regards,

DR DC JANSE VAN RENSBURG

HEAD: SECTION SPORTS MEDICINE

DEPARTMENT OF ORTHOPAEDICS

UNIVERSITY OF PRETORIA

**********************************************************

What are your thoughts on this topic? Leave your comments below

Or email: karim.khan@familymed.ubc.ca

Or tweet your response and we’ll retweet: @bjsm_bmj

Debating weight change and performance in marathon runners: Armstrong, Johnson, and Munoz guest blog (e-letter)

21 Feb, 11 | by Karim Khan

We write to present alternative interpretations of the data published by Zouhal and colleagues, in the BJSM article: Inverse relationship between percentage body weight change and finishing time in 643 forty-two-kilometre marathon runners

The Abstract states that "... these  data are not compatible with laboratory-derived data suggesting that BW [body weight] loss greater than 2% during exercise impairs athletic performance."  We agree, but not for the reason proposed in this paper.

Figure 2, which is critical to the findings of this publication, presents an intra-individual group relationship; laboratory studies regarding the influence of dehydration on exercise performance utilize an individual as his/her own control.  The cross-sectional trend in Figure 2, which arose from a single field study, should not be equated with a randomized, controlled, repeated measures experimental design.

On the basis of Figure 2, the text states, "... lesser degrees of body weight loss were associated with longer race finishing times..." and the discussion section implies cause-and-effect. However, statistical correlation neither implies causation nor warrants a principle.  Figure 2 also includes noteworthy exceptions.  Three runners (upper left quadrant) lost approximately 4 - 7% of body weight (i.e., 2.9 - 5.1 kg, based on a prerace body weight of 72.2 kg) but finished with times >300 min; and three runners (lower right quadrant) gained 2 - 3% of body weight (i.e., 1.4 - 2.2 kg) but finished with times approximating 180 min.

Further, percent body weight change accounted for only 4.7% of the variance in race time (r2 = 0.047).  We believe that this relationship is weak because endurance exercise performance is influenced by training, diet, psychological state, years of experience, age, and numerous other factors which interact in complex ways 2.  Further, the 2009 Mont Saint-Michel marathon was run in air temperatures ranging from 9 to 16?C (Table 1).  In a hot environment, runners who drink less (i.e., 6% of runners lost 6 - 8% body weight loss, see Fig. 1) increase their risk of exertional heat exhaustion and heatstroke 4.  This medical advice is noticeably absent, as a qualification to the concept that "the fastest runners lost the most weight."

Three other factors likely complicated the relationship between body weight change (%) and race time (min).  Firstly, approximately 78% of the 643 runners lost weight.  Sweat loss, of course, was part of their total body water deficits, but was not considered in the interpretation of
Figure 2.  Similarly, we note that pre-race excretion is not mentioned. This would amplify reported body weight changes because runners void bladder and bowl as the race start nears.  Body weight was measured between 90 and 60 min before the race, and thus weight loss due to pre-race elimination of urine and feces was unknown in Figure 2.  Thirdly, we examined numerous online photos of competitors in the 2009 Mont Saint-Michel marathon.  On the basis of our previous experiences at marathon events, we expected that front runners would wear less clothing than slow runners.  This trend was evident.  Thus sweat-soaked clothing, which had been dry at the starting line, represented an additional unmeasured component of the body weight variance in Figure 2.

Much text concerns drinking, biological signals and thirst, however none of these variables were measured during the present study.  Thus it is invalid and speculative to state, "... athletes will not wilfully (sic) ignore their thirst when fluid is available in excess...", or to state, "... the only conclusion can be that these 'dehydrated' athletes were drinking according to their innate biological signals..."  What evidence supports these statements besides a range of body weight change?  It is widely appreciated that athletes ignore innate biological signals (e.g., pain, fatigue, perceived exertion) during competition, to optimize performance.  This issue is further complicated by the fact that thirst sensation and drinking behavior are influenced by numerous host factors (e.g., stomach distention, plasma osmolality, oropharyngeal reflexes), the environment, and fluid characteristics (e.g., saltiness, sweetness) 3.
Therefore it is impossible, from the data of Zouhal et al. 1, to formulate substantiated conclusions about the relationship between body weight change and thirst, or between performance and thirst.

Fluid overload and illness are considered in the Introduction and Discussion sections.  However, these concepts are misplaced, in that neither symptomatic exertional hyponatremia (EHS) nor fluid intake were reported for any of these 643 runners, including those who gained 3 - 4%
of body weight (2.2 - 2.9 kg, Fig. 2).  Because the data of this paper focus on performance, not illness, and because > 90% of participants did not gain weight, we believe that the following question is more relevant to competitors, "Is finish time faster or slower when a runner is
mildly dehydrated (1 - 2% body weight loss) than when she/he is severely dehydrated (>5% body weight loss)?"  It is impossible for group trends (Fig. 2, Tables 3 and 4) to answer this question.

Finally, the interpretations of Tables 3 and 4 (which present the same concept, in reverse order) fail to consider differences between the fastest and slowest runners.  Exercise intensity and duration affect the volume of fluid consumed during a race.  Front runners (i.e., those who
finish 42.1 km in 160 min) experience a high ventilation rate (e.g., >120 L/min) that precludes consuming water, out of concern for inhalation and coughing; they also are conscious of time spent at aid stations.  In contrast, back-of-the-pack runners typically spend more time
at aid stations, drink more often, walk during part of the race, and have a greater requirement for exogenous carbohydrate (i.e., 30 - 60 g*h-1, mostly in fluids 5) because they are on the course for more than 5 h. Thus, we believe that an alternative interpretation (i.e., "During a marathon, fast runners drink less than slow runners.") is superior to the published conclusion, "body weight loss during a marathon race may be ergogenic".

Lawrence E. Armstrong, Ph.D., FACSM
Evan C. Johnson, M.A.
Colleen X. Munoz, M.S.

REFERENCES

1.  Zouhal H, Groussard C, Minter G, et al. Inverse relationship between percentage body weight change and finishing time in 643 forty-two kilometere marathon runners. Br J Sports Med, published online December 15, 2010 as 10.1136/bjsm.2010.074641.

2.  Leyk D, Erley O, Gorges W, et al.  Performance, training and lifestyle parameters of marathon runners aged 20-80 years: Results of the PACE-study. Int J Sports Med 2009;30:360-365.

3.  Johnson AK. The Sensory Psychobiology of Thirst and Salt Appetite. Med Sci Sports Exerc 2007;39:1388-1400.

4.  Armstrong LE, Casa DJ, Millard-Stafford M, et al.  American College of Sports Medicine position stand: Exertional heat illness during training and competition.  Med Sci Sports Exerc 2007;39:556-572.

5.  Coyle EF. (1999). Physiological determinants of endurance exercise performance. J Sci Med Sport 1999;2:181-189.

Conflict of Interest: None declared

Response to Ian Shrier

30 Nov, 10 | by Karim Khan

We agree with Ian Shrier that the finding of an effect of stretching on risk of muscle, ligament and tendon injuries should be interpreted with caution. That is why we wrote “The finding of an effect of stretching on muscle, ligament and tendon injury risk needs to be considered cautiously because muscle, ligament and tendon injury risk was a secondary outcome, and there was no evidence of an effect of stretching on the primary outcome of all-injury risk. If stretching had reduced the risk of muscle, ligament and tendon injuries without increasing the risk of other injuries, we would expect a reduction in all-injury risk.” Nonetheless, after a prolonged discussion of this issue we decided that the finding could not be totally dismissed. We believe that it was appropriate to report the observed effect on muscle, ligament and tendon injuries with an explicit acknowledgement of the uncertainty associated with this finding.

Regardless of whether one accepts the finding that stretching reduces risk of muscle, tendon and ligament injuries, the implications would appear to be the same. Even if the effect is real, it is quite small in absolute terms (even in this population, at quite a high risk of injury, only “one injury to muscle, ligament or tendon was prevented for every 20 people who stretched for 12 weeks”). For this reason the data from this study do not appear to provide support for the practice of stretching, at least in so far as the aim is to reduce injury risk. The stronger justification for stretching, though still a marginal one in our view, is provided by the clear evidence of a very small effect of stretching on soreness. For other outcomes, such as performance or range of motion our study did not provide any data.

It is not yet known whether stretching is best carried out before exercise, after exercise, or both before and after exercise. We were surprised, when planning this study, to learn that most Australian stretch before exercise but not after, and most Norwegians stretch after exercise but not before! It was for that reason we designed a trial in which participants stretched both before and after exercise. We do not agree with Ian Shrier’s suggestion to conduct an unplanned post-hoc comparison of the non-randomised subgroups that chose to stretch only before, only after, or both before and after exercise. Such an analysis would almost certainly be seriously confounded and would probably be uninterpretable; at any rate it hardly seems consistent with his disapproval of our much more disciplined pre-planned secondary comparison between randomised groups. The only truly satisfactory way to resolve the issue of whether it is better to stretch before or after exercise is to conduct a further randomised trial in which participants are randomised to those two conditions.

Conflict of Interest: None declared

Research in Stretching- A Letter to the Editor

16 Nov, 10 | by Karim Khan

Editor,

I recently read the article Jamtvedt et al on whether pre and post stretching prevents injury (1) with interest. I commend the authors for their well-conducted study and would like to comment on two particular issues.

First, the authors correctly point out that there was no difference in the primary outcome of all injuries, and that the analysis showing an absolute 22% reduction in muscle, ligament and tendon injuries with stretching should be interpreted cautiously. However, they then continue to say “Nonetheless, it is plausible that stretching reduces muscle, ligament and tendon injuries, and it may be implausible that stretching increases other injuries”. Moreover, in the conclusion, they only mention the “probable reduction in muscle, ligament and tendon injuries” and omit the absence of an effect on the primary outcome of overall injuries. This type of thinking appears to be gaining popularity. For example, Small et al (cited by the current article) emphasized the decrease in musculotendinous injuries they observed in their review of stretching and discounted the associated increase in stress fractures and “shin splints” (2).

In other areas of medicine, we have already learned the difficult lesson that “all- cause mortality” is generally a much more important outcome compared to “disease- specific mortality” because interventions can cause damage through unrecognized mechanisms. It would be a pity if the sport medicine world has to go through the same lessons. Plausible reasons why stretching would increase some types of injuries are already available from a review of basic science evidence (3). Because Jamtvedt et al do not actually detail the non muscle-tendon-ligament injuries, I will use the example from Small et al. related to stress fractures and “shin splints” (not defined, but presumably periostitis and compartment syndrome). An acute bout of stretching causes weakness, (4) which is expected to lead to 1) an increased force transmission to the bone (5), (6), which would lead to increased stress reaction and stress fractures and 2) a possible increase in compensatory muscle use, which could theoretically cause shin splints of any cause. Further, stretching-induced weakness would theoretically also decrease proprioception, although this remains to be studied. Authors who decide to report sub-group analyses need to show the same analyses for all the sub-groups created by the categorization.

Second, “stretching” as an intervention is intricately related to the timing of the stretch, and one expects different results from stretching before exercise compared to stretching at other times (7). In their conclusion, Jamtvedt et al suggest that “the results of this trial support the decision to stretch” (1), with no mention of the timing; reviews by Small et al (2), and Thacker et al (8) (cited by the current article) made the same error. In brief, the effects of “stretching” are similar to those of “weight lifting”. An acute bout of weight lifting or stretching will cause an immediate decrease in strength, power and endurance 4. However, if one weight lifts or stretches for weeks, there is an increase in strength, power and endurance (4). Based on this, one would expect that stretching before every exercise session would increase the risk of injury due the acute effects, but there would also be an expected decrease in injury risk as the body adapts and strengthens over time. If the two effects were relatively balanced, one would expect no effect on overall injury rate. However, if one stretched regularly but not before exercise, then one would expect only the benefits, with a decrease in overall injury rate. Indeed, there have been three randomized trials prior to this study and a meta-analysis of these (one study had subjects stretch before and after exercise as in the current study (9)) suggests regular stretching not before exercise reduces injury risk [OR=0.68 (95%CI: 0.52, 0.88)] (7).

Given these previous studies, it would be interesting for the authors to conduct a post-hoc analysis (with the appropriate cautious interpretation) comparing the injury risk among those who stretched only before exercise, those that stretched only after exercise, and those that stretched both before and after exercise.

In summary, there should be little controversy about 1) post-exercise stretching reducing acute muscle soreness, just as it reduces any chronic musculoskeletal pain (10), presumably due to its well-studied effects on stretch-tolerance (a form of analgesia) (11, 12), and 2) stretching not before exercise reducing injury risk given that both basic science and clinical science provide consistent evidence, although a couple more confirmatory studies could be helpful.

Future research priorities should focus on questions where there is little to no evidence such as 1) whether post-exercise stretching is as beneficial as stretching at other times, 2) what are the effects for high intensity sports, 3) the effects of stretching on rehabilitation of injuries, and 4) the effects on the performance in injured athletes (all published studies examined healthy subjects) (13).

Ian Shrier MD, PhD, Dip Sport Med, FACSM Centre for Clinical Epidemiology and Community Studies SMBD-Jewish General Hospital 3755 Cote Ste-Catherine Rd Montreal, Qc H3T 1E2 Tel: 514-340-7563

Fax: 514-340-7564

References

1. Jamtvedt G, Herbert RD, Flottorp S, et al. A pragmatic randomised trial of stretching before and after physical activity to prevent injury and soreness. Br J Sports Med. 2010;44:1002-1009.

2. Small K, McNaughton L, Matthews M. A systematic review into the efficacy of static stretching as part of a warm-up for the prevention of exercise-related injury. Res Sports Med. 2008;16:213-231.

3. Shrier I. Does stretching help prevent injuries? In: MacAuley D, Best T, eds. Evidence-based sports medicine. London: BMJ Publishing Group; 2007.

4. Shrier I. Does stretching improve performance: A systematic and critical review of the literature. Clin J Sport Med. 2004;14:267-273.

5. Mizrahi J, Verbitsky O, Isakov E. Fatigue-related loading imbalance on the shank in running: a possible factor in stress fractures. Ann Biomed Eng. 2000;28:463- 469.

6. Christina KA, White SC, Gilchrist LA. Effect of localized muscle fatigue on vertical ground reaction forces and ankle joint motion during running. Hum Mov Sci. 2001;20:257-276.

7. Shrier I. Meta-analysis on preexercise stretching. Med Sci Sports Exerc. 2004;36:1832-1832.

8. Thacker SB, Gilchrist J, Stroup DF, et al. The impact of stretching on sports injury risk: a systematic review of the literature. Med Sci Sports Exerc. 2004;36:371-378.

9. Amako M, Oda T, Masuoka K, et al. Effect of static stretching on prevention of injuries for military recruits. Mil Med. 2003;168:442-446.

10. Law RY, Harvey LA, Nicholas MK, et al. Stretch exercises increase tolerance to stretch in patients with chronic musculoskeletal pain: a randomized controlled trial. Phys Ther. 2009;89:1016-1026.

11. Magnusson SP, Simonsen EB, Aagaard P, et al. Mechanical and physiological responses to stretching with and without preisometric contraction in human skeletal muscle. Arch Phys Med Rehabil. 1996;77:373-378.

12. Halbertsma JPK, Mulder I, Goeken LNH, et al. Repeated passive stretching: acute effect on the passive muscle moment and extensibility of short hamstrings. Arch Phys Med Rehabil. 1999;80:407-414.

13. Shrier I. Stretching perspectives. Curr Sports Med Rep. 2005;4:237-238.



E-letter: Question regarding the use of autologous PRP injections for tendinopathies

23 Jul, 09 | by Karim Khan

The following is a letter to BJSM from Ralph S. Bovard MD:

Dear BJSM,

I have a question regarding the use of autologous platelet rich plasma (PRP) injections for tendinopathies of various sorts.  This procedure has been gaining favor with sports medicine clinicians for use in athletes with tendon injuries that are slow to respond or resistant to conservative therapies.  Despite the fact that it would appear to be a seemingly innocent matter of re-injecting one’s own spun down blood products, the World Anti-Doping Agency (WADA) most recent 2009 Prohibited List, if taken literally, would make it an illegal procedure for international competition or national competition under any NGB’s who endorse WADA.  The culprit substances in this case would be growth hormone (GH), Insulin-like Growth Factors (IGF-1), and Mechano Growth Factors (MGF’s).

The relevant section from the code is included below:

S2. HORMONES AND RELATED SUBSTANCES

The following substances and their releasing factors, are prohibited:
1. Erythropoiesis-Stimulating Agents (e.g. erythropoietin (EPO), darbepoietin (dEPO), hematide);
2. Growth Hormone (GH), Insulin-like Growth Factors (e.g. IGF-1), Mechano Growth Factors (MGFs);
3. Chorionic Gonadotrophin (CG) and Luteinizing Hormone (LH) in males;
4. Insulins;
5. Corticotrophins;
and other substances with similar chemical structure or similar biological effect(s).

[Comment to class S2:
Unless the Athlete can demonstrate that the concentration was due to a physiological or pathological condition, a Sample will be deemed to contain a Prohibited Substance (as listed above) where the concentration of the Prohibited Substance or its metabolites and/or relevant ratios or markers in the Athlete’s Sample satisfies positivity criteria established by WADA or otherwise so exceeds the range of values normally found in humans that it is unlikely to be consistent with normal endogenous production.

If a laboratory reports, using a reliable analytical method, that the Prohibited Substance is of exogenous origin, the Sample will be deemed to contain a Prohibited Substance and shall be reported as an Adverse Analytical Finding.] The Prohibited List 2009 20 September 2008

It would thus seem that PRP is banned under “Class S2: Hormones and Related Substances”, rather than under “M1: Blood Doping”.  The re-delivery of blood is prohibited under blood doping; regardless of whether it is endogenous or exogenous.  There is no mention or attempt to discriminate between blood products that are re-injected immediately into soft tissues versus those that are shelved and re-infused by IV weeks or months later in the typical manner of “blood doping”.

The argument is made that while PRP indeed delivers  the athletes own growth factors to a musculoskeletal site, the platelets are concentrated to a level not normally achieved physiologically, and they are activated either chemically (via calcium addition) or mechanically (centrifugation) and thus degranulate  rapidly and deliver a bolus of factors never “normally” or physiologically achieved.

Given this stance it would seem that the use of platelet rich plasma injections is clearly prohibited.   Tendinopathies are not life threatening or otherwise serious medical conditions and as such the rational of applying for a therapeutic use exemption (TUE) would seem a difficult argument.   Yet how would PRP injections be detected other than by admission?  What is the opinion of the BJSM readership regarding this topic?

Thank you,

Raph S. Bovard MD

BJSM blog homepage

BJSM

A peer review journal for health professionals and researchers in sport and exercise medicine. Visit site



Creative Comms logo

Latest from British Journal of Sports Medicine

Latest from British Journal of Sports Medicine