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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:

Yours sincerely,

Sydney Cullis (Race Director)

Suicide, sport and medicine: more education and awareness needed for athletes’ mental health

10 Dec, 12 | by Karim Khan

By Dr. Kerry Lang

I was very interested to read Dominic Malcolm and Andrea Scott’s BJSM editorial on suicide, sport and medicine (2012) and agree that more attention should be paid to the psychological welfare of athletes.

I am a doctor, albeit not a psychiatrist, and have also been part of the British triathlon team since 2005. On several occasions I was acutely aware of depression in athletes that has gone apparently undetected. In one particular case, a female athlete was deliberately self-harming in response to her perceived poor performance in training. She had inflicted substantial lacerations to her forearms, which were obviously visible when swimming. I felt a duty of care to report this to her coaches and challenged them on whether or not they had noticed the wounds. The response from the first coach was they had not noticed and from the other coach was that they had noticed but felt inadequately qualified to address the issue.

This is just one example of where education is needed to identify warning signs and hopefully prevent catastrophic consequences. Not only the sports physician, but the whole support team needs to be aware of signs and symptoms for mental health issues.

Treatment for athletes is available. Education in what services are available is the key to providing mental health resources. There are sports psychologists who work closely with teams and individual athletes, general practitioners and team doctors with mental health training may also be useful and in more serious cases tertiary referral to a psychiatrist. Cognitive behavioral therapy and antidepressants are currently used with good effect. There is also an important role for preventative medicine in identifying “at risk” individuals and implementing early intervention.

Screening may be useful. Some simple signs for the performance team to look out for are: changes in appetite and weight, withdrawal from other team members or friends, crying, tiredness, indecision, anxiety, moodiness, loss of enthusiasm, feelings of sadness, lack of concentration and anger.

Formal screening can be done with the Beck Depression Inventory, the Hamilton Rating Scale for Depression (Ham-D), or the Montgomery-Asberg Depression Rating Scale.

A simple tool that, as far as I know, is not widely used but may be helpful in a coach-athlete setting is a self reported “vigor” score. Ask athletes to rate their level of vigor from 1-10 on any particular day. Scores consistently of less than 5 may merit further investigation.

In the case I describe in this blog, a sports psychologist became involved and with counseling the individual went on to perform internationally at a high level. Good mental health will ultimately lead to better athletic performance and is as important as good physical health.


1. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J (June 1961). “An inventory for measuring depression”. Arch. Gen. Psychiatry 4 (6): 561–71. doi:10.1001/archpsyc.1961.01710120031004. PMID 13688369
2. Hedlund JL, Viewig BW (1979) The Hamilton rating scale for depression: a comprehensive review. Journal of Operational Psychiatry 10:149-165
3. Williams, J. B. W.; Kobak, K. A. (2008). “Development and reliability of a structured interview guide for the Montgomery-Asberg Depression Rating Scale (SIGMA)”. The British Journal of Psychiatry 192 (1): 52–58. doi:10.1192/bjp.bp.106.032532. PMID 18174510


Kerry Lang MBChB, MRCS (Glas)

Concussion management in England’s FA – better than it appears in new BJSM paper….

10 Oct, 12 | by Karim Khan

E-letter and update by Dr Ian Beasley (FFSEM)

In response to:

Jo Price, Peter Malliaras, Zoe Hudson. 2012. Current practices in determining return to play following head injury in professional football in the UK. Br J Sports Med 2012; 0: 201109068 (Original article). [this paper is Online First and is included in the upcoming November Print Issue of BJSM [BASEM Theme Issue].

There is no doubt that since the first consensus statement on concussion, conceived in Vienna in 2001 (read BJSM summary article here), every sport has raised its game on head injury and concussion management and reviews by the various sports over the years have resulted in updated and improved practice.

Football in this country has been similarly active.  At the behest of the FA medical committee, and as a result of collaboration between an eminent Premier League medical officer, and a Neurosurgeon working in sport, the current FA head injury guidelines were devised.  They were circulated to clubs in November 2009, and have been in use since then.

Since its inception the SCAT 2 form has been included in these guidelines, and is published as part of the head injury guidelines in the FA handbook (1), and on our website (here).

In their study Price et al (2) mention that many club medical officers ‘are not required to demonstrate any expertise in concussion management’.

Medical indemnity providers have insisted for some time that medical practitioners attending sporting events must ensure they are adequately trained to provide appropriate care for their athletes (3).  We would encourage any medical practitioner involved in sport to heed this message.

The initial questionnaires in this study (2) were sent to clubs before the availability of current guidelines. By the time the second batch of questionnaires were sent out, all clubs were in receipt of the current guidelines from the FA.  Hence, by the time conclusions were drawn in this study, they were not contemporary. They do not reflect current practice within professional football.  Nor do they represent the stance of the FA in dealing with this important issue.

In my experience, governing bodies and their medical officers will always be of help when trying to obtain up to date information regarding practice and policy within their respective sports if asked.

1. The FA Handbook, Rules and Regulations of The Association, season 2012-13.
2.  Current practices in determining return to play following head injury in professional football in the UK. Price, J., Malliaras, P., Hudson, Z.  Br J Sports Med 2012;0:1-5
3. MPS issues advice to doctors assisting at sporting events :  07 Jul, 2006. 

Editor’s note – link to the most current consensus document here – the Zurich (3rd) concussion guidelines (>47,00o page views as of October 8th, 2012).

Dr Ian Beasley MBBS, MRCGP, MSc, DIP.Sports Med, FFSEM (UK) is Head of Medical Services Club England Division The FA Group Wembley Stadium, Wembley, London, HA9 0WS

Good News: Tweaks to commuting behaviour may improve activity levels

25 Jun, 12 | by Karim Khan

By Tony H. Reinhardt-Rutland

Guest Blog

Charles R Ratzlaff. 2012. Good news, bad news: sports matter but occupational and household activity really matter – sport and recreation unlikely to be a panacea for public health Br J Sports Med. bjsports-2011-090800 (Editorial) Published Online First: 12 March 2012 

Ratzlaff (1) outlines broad categories in assessing societal activity-levels: occupational and household. While the latter was traditionally the greater source of activity, particularly for men, the nature of work has become steadily more sedentary. However, the same may be less true for household tasks. One conclusion is that women today, as the gender likely to undertake most household tasks, may well be more active than their male counterparts. The gender imbalance may only be partly diminished by the fact that males are more likely – at least at younger ages – to obtain a third category of activity in the voluntary participation in energetic sports.

My concern here is with another category of exercise that entails both occupational and sports elements: the commute to the work-place. Choices of commuting-mode are dependent on distance to be travelled. Short home-to-work distances may render walking predominant. Distances beyond a few kilometres may render powered transport – cars, buses and trains – compulsory, so the scope for exercise may seem limited. The steady increase in the UK of park-and-ride facilities attempts to reduce traffic in major centres such as cities: commuters drive to a strategically located car-park away from the city-centre and continue by public transport. This would not of course alter the conclusion that long- distance commuting does not entail significant activity-levels.

However, multi-modal commuting can include substantial elements of walking, cycling or running; this particularly applies to journeys entailing public transport, where pick-up points for public transport (bus -stops and railway stations) may be at some distance from home. As many would attest, the disadvantages of walking, cycling and running concern poor weather conditions and build-up of sweat, perhaps requiring change of clothing at the work-place. Probably of most importance for all commuters is the issue of conflicts and potential collision with motor traffic.

Despite these problems, the incorporation of exercise into commuting is receiving some official support in the UK. For example, at least one public-transport provider now promotes exercise as a valuable “add-on” to travel by public transport (2) – far removed from the days when exercise- free travel was regarded as a major feature supporting the preference for the private car (3). Furthermore, there are also now governmental schemes to provide grants for the purchase of bikes to access the work-place (4).

To pursue the issues, if the problems with petroleum price and availability continue towards the levels that characterised the 1970s, the private motorcar may come to have a more restricted presence on the road. At that stage, walking, cycling and running could become generally prominent in commuting – in a way that has applied particularly to cycling in the Netherlands for many years. However, for this scenario to continue in the UK beyond the present age of economic downturn requires a societal change in attitude that eschews a thoughtless dependence on the car. That most certainly did not happen after the petroleum crises of the 1970s had passed (5). Perhaps the lessons will be learned this time.

See also the relevant paper by Lawrence Frank relating to how the built environment and physical activity promotion.


1. Ratzlaff CR, Good news, bad news: sports matter but occupational and household activity really matter – sport and recreation unlikely to be a panacea for public health. Br J Sports Med 2012 (10.1136/bjsports-2011- 090800).

2. (accessed 25/4/12).

3. www.bike2workscheme (accessed 25/4/12).

4. Wolmar C. Fire and steam: a new history of the railways in Britain. London: Atlantic.

5. Transport statistics Great Britain. 2001. London: Department for Transport.


Tony Reinhardt-Rutland is Reader in Psychology at University of Ulster at Coleraine. His research interests include visual perception of motion and space, and the safety of road travel. 

Conflict of Interest: None declared


Review: The development of a walkability index: application to the Neighborhood Quality of Life Study. L D Frank, J F Sallis,B E Saelens, L Leary,K Cain,T L Conway, P M Hess.  Br J Sports Med 2010;44:13 924-933 Published Online First: 29 April 2009 doi:10.1136/bjsm.2009.058701 


‘Cool it!’… So is thermal perception a controller of exercise intensity during heat stress?

28 Apr, 12 | by Karim Khan

By  Drs. Zachary J. Schlader &  Toby Mündel 


In response to:  Barwood MJ, Corbett J, White D, et al. Early change in thermal perception is not a driver of anticipatory exercise pacing in the heat. Br J Sports Med 2011


Dear Editor,

We read with great interest the study by Barwood and colleagues published recently within BJSM  [1].  In this study, the authors aimed to explore the relationships between body temperature(s), thermal perception, and the voluntary control of exercise intensity in the heat.  For this they should be commended for although this area is quite topical, our understanding of these relationships remains virtually unknown.  By chemically activating peripheral cold thermo-sensors with menthol, Barwood et al. [1] have demonstrated that improvements in thermal comfort and reductions in sensations of warmth, independent of changes in skin temperature, both prior to, and during, the initial stages of self-paced exercise in the heat did not influence the selection of exercise intensity.  Although the conclusions drawn appear appropriate, we would like to further discuss their results in the context of others to explore this topic and perhaps allow a better understanding of our current base of knowledge.

As part of the rationale for conducting their study, Barwood et al. [1] state “It is presently unknown whether altered pacing strategy is regulated as part of behavioral thermoregulation driven by a conscious awareness of thermal state or if a central and subconscious homeostatic mechanism is activated when skin temperature rises above a threshold rate”. Furthermore, Barwood et al. [1] conclude that “This study addresses an as-yet unanswered question of whether the fatiguing mechanisms during exercise in the heat are primarily consciously or subconsciously mediated”.  Firstly, we would like to draw the authors’ attention to our recent work testing the hypothesis that voluntary reductions in exercise intensity in the heat are thermoregulatory behaviors [2].  Our results demonstrated that the observed reductions in power output during exercise in ~40°C compared to ~20°C were, at least in part, due to a conscious action that was inversely related to total heat body storage and thermal discomfort, and improved heat exchange [2].  Secondly, it is unfortunate that it was not possible to discuss two of our recent studies demonstrating that skin temperature and/or the perceptions of this temperature play a large role in the initial selection of [3] or sustained decrease in [4] exercise intensity.  Perhaps in “addressing [only] two current viewpoints on how exercise pacing is driven in hot conditions” Barwood et al. have unintentionally overlooked this recent evidence?

This notwithstanding, the results put forward by Barwood and colleagues [1] appear to be in stark contrast to those we obtained utilizing a similar methodology whereby menthol and skin cooling was used to independently alter thermal perception and skin temperature during exercise at a fixed rating of perceived exertion (RPE) [5]. These results showed that an improved thermal comfort and reduced sensations of warmth with menthol enhanced the capacity to maintain exercise intensity.  Thus, we concluded that thermal perception is a capable modulator of exercise intensity independent of any change in skin temperature [5]; so why, then, such opposing views?

As supported by Barwood et al. [1], it is becoming increasingly clear that RPE is perhaps the most dependable criterion dictating the voluntary selection of exercise intensity [6].  In such circumstances, it appears as though, independent of perturbation (e.g. hypoxia, heating, cooling etc.), the exerciser compares how they feel to how they expect themselves to feel at that moment in time and adjust their exercise intensity accordingly [6].  Thus, although the RPE response during self-paced exercise appears to be tightly controlled, the effect of a given perturbation is found in changes in the selection of exercise intensity (or pacing strategy).  Therefore, the sole manner in which pacing strategy can be altered is if the perturbation is large enough in magnitude to alter RPE.  Herein lies the difference between our studies.  It is unlikely that the cooling modalities (either skin cooling or menthol) utilized by Barwood et al. [1] were sufficiently sustained or large enough in magnitude to alter RPE.  In contrast, by utilizing a significantly different experimental design to address the same question, we were successful in altering RPE.

The reason for this is likely four-fold, but certainly other rationale cannot be discounted.  Firstly, in contrast to the entire skin surface we chose to manipulate the skin of the face, an area that is both of high thermal sensitivity during heat stress [7] and an area that has been directly demonstrated to modulate exercise duration [8].   Secondarily, we used a greater concentration of menthol (8% vs. 0.05%) which, together with the facial manipulation, likely elicited a larger change in thermal perception.  Thirdly, we chose to use fit but untrained subjects, as trained individuals have an altered perception of their physiological thermal strain during exercise [9].   Thus, our subjects were likely more sensitive to changes in thermal perception.  The fourth, and perhaps final reason for the observed differences between these two studies likely stems from the exercise protocols used, i.e. fixed-RPE vs. time trial.  For instance, anecdotal observations from our laboratory suggest that the fixed-RPE protocol may be more sensitive to a given thermal stimulus than a time trial; although to our knowledge there is no formal data suggesting this arrangement.  Other rationale that should probably also be considered include the heat stress compensability and modality, exercise duration, and suitable subject blinding to the experimental conditions, amongst others.

In conclusion, we would like to commend Barwood and colleagues for their study and the data it adds to the literature.  However, we would urge caution before readers draw conclusions based on this study alone.  As it currently stands, the relationships between temperature, thermal perception, and exercise intensity remain uncertain and further research is required before conclusions can and should be drawn.  The differences between our study [5] and that of Barwood et al. [1] further highlight that the choice of experimental methodology may greatly influence a study’s outcome(s).  Issues pertaining to methodology are not specific to perception and exercise.  For instance, this journal recently highlighted another (equally debated) area, i.e. exercise and fluid replacement, which suffers from similar methodological concerns [10, 11].  Nevertheless, these studies [1, 5] endorse (and encourage) the use of menthol and other chemicals capable of affecting thermal perception without changing skin temperature in providing a useful paradigm to study the interactions between thermal perception and the voluntary control of exercise intensity.  Finally, as is the case with nearly all areas of research, we would encourage further studies in this area to ensure a better understanding and therefore, perhaps, a resolution to this interesting and topical area.



1.         Barwood MJ, Corbett J, White D, et al. Early change in thermal perception is not a driver of anticipatory exercise pacing in the heat. Br J Sports Med 2011.

2.         Schlader ZJ, Stannard SR, Mundel T. Evidence for thermoregulatory behavior during self-paced exercise in the heat. J Therm Biol 2011;36:390-6.

3.         Schlader ZJ, Simmons SE, Stannard SR, et al. Skin temperature as a thermal controller of exercise intensity. Eur J Appl Physiol 2011;11:1631-9.

4.         Schlader ZJ, Stannard SR, Mundel T. Is peak oxygen uptake a determinant of moderate-duration self-paced exercise performance in the heat? Appl Physiol Nutr Metab 2011;36:863-72.

5.         Schlader ZJ, Simmons SE, Stannard SR, et al. The independent roles of temperature and thermal perception in the control of human thermoregulatory behavior. Physiol Behav 2011;103:217-24.

6.         Schlader ZJ, Stannard SR, Mundel T. Human thermoregulatory behavior during rest and exercise – a prospective review. Physiol Behav 2010;99:269-75.

7.         Cotter JD, Taylor NA. The distribution of cutaneous sudomotor and alliesthesial thermosensitivity in mildly heat-stressed humans: an open-loop approach. J Physiol 2005;565:335-45.

8.         Ansley L, Marvin G, Sharma A, et al. The effects of head cooling on endurance and neuroendocrine reponses to exericse in warm conditions. Physiol Res 2008;57:863-72.

9.         Tikuisis P, McLellan TM, Selkirk G. Perceptual versus physiological heat strain during exercise-heat stress. Med Sci Sports Exerc 2002;34:1454-61.

10.       Mundel T. To drink or not to drink? Explaining “contradictory findings” in fluid replacement and exercise performance: evidence from a more valid model for real-life competition. Br J Sports Med 2011;45:2.

11.       Goulet ED. Effect of exercise-induced dehydration on time-trial exercise performance: a meta-analysis. Br J Sports Med 2011;45:1149-56.


Zachary J. Schlader, PhD, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, TX, USA

 Toby Mündel, PhD, School of Sport and Exercise, Massey University, Palmerston North, New Zealand


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.


[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

Injury surveillance on young elite athletes participating in the 1st Winter Youth Olympic Games in Innsbruck/Austria

27 Dec, 11 | by Karim Khan

BJSM e-letter by:

Gerhard Ruedl and Wolfgang Schobersberger

E-letter for: Kathrin Steffen, Lars Engebretsen. The Youth Olympic Games and a new awakening for sports and exercise medicine. BJSM. 2011; 45: 1251-1252 (Warm up)

Photo courtesy of IYOGOC

Do we really want to see our young promising talents go through a major injury at one stage into their career?

Definitely no!

However, in competitive alpine skiing, snowboarding and freestyle, the risk to get major head and anterior cruciate ligament injuries is indeed high [1-4]. Therefore, training focussing on injury prevention should start at an early age and should go along with the athletes’ career. To implement evidence based preventive measures, however, it is of utmost importance to investigate first of all data on occurrence and severity of injuries according to the 4-step model of injury prevention research [5].

At this point of time, there is little data available concerning the injury risk of youth elite athletes competing in winter sports [6, 7]. Therefore, we will conduct a systematic injury and illness surveillance on young elite athletes participating in the 1st Winter Youth Olympic Games in Innsbruck/Austria in January 2012.  Let us work together to get meaningful data as a basis for further research on injury risk factors and injury mechanisms and finally on injury prevention strategies among young elite winter sport athletes.

We are glad to welcome you in Innsbruck!

(1) Pujol N, Blanchi MP, Chambat P. The incidence of anterior cruciate ligament injuries among competitive alpine skiers.  Am J Sports Med 2007; 35: 1070-4.
(2) Florenes TW, Bere T, Nordsletten L et al. Injuries among male and female World Cup alpine skiers. Br J Sports Med 2009; 43: 973-8.
(3) Florenes TW, Nordsletten L, Heir S et al. Injuries among World Cup freestyle skiers. Br J Sports Med 2010; 44: 803-8.
(4) Florenes TW, Nordsletten L, Heir S et al. Injuries among World Cup ski and snowboard atlethes. Scand J Med Sci Sports. 2010 Jun 18 [Epub ahead of print].
(5) Bahr R, Krosshaug T. Understanding injury mechanisms: a key component of preventing injuries in sport. Br J Sports Med 2005; 39: 324-9.
(6) Steffen K, Engebretsen L. The Youth Olympic Games and a new awakening for sports and exercise medicine. Br J Sports Med 2011; 45: 1251-52.
(7) Steffen K, Engebretsen L. More data needed on injury risk among young elite athletes. Br J Sports Med 2010; 44: 485-9.


Gerhard Ruedl is a Senior Researcher at the Department of Sport Science, University of Innsbruck, Austria

Wolfgang Schobersberger is the Chief Medical Officer of Winter Youth Olympic Games in Innsbruck; Institute for Sports Medicine, Alpine Medicine & Health Tourism Innsbruck/Austria

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.


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

E-letter: Are we ready for GGPAQ?

7 Oct, 10 | by Karim Khan

The following E-letter is a response to Physical activity in the UK: a unique crossroad (Br J Sports Med 2010; 44: 912-914). The original article can be read here.

I was delighted to read Dr Weilers editorial which eloquently presents many of the issues currently faced in exercise medicine. It is so important to debate this subject-particularly as we are in a unique position in the U.K to effect permanent change.

I was interested in Dr Weilers’ view that the introduction of the GGPAQ into QOF would be a valuable place to start what will have to be a process of cultural change. I would like to debate this opinion further. It has been clearly established in the literature that changes in physical activity levels in the long term are not easy to effect. The most successful interventions involve patient centred, long term, well supported, behaviourally based interventions delivered by highly motivated and well trained medical professionals. I do not agree with your statement that ‘brief interventions (3-10min) can lead to substantial increases in physical activity level (by around 30%)’. I am not aware of any evidence to substantiate this claim, particularly in the long term. The studies which have shown these sorts of results have used of a much more intense intervention, not sustainable within the NHS, and most do not show significant long term results (greater than 3 months).(1,2)

I agree that physical activity promotion to ‘healthy’ populations can only be delivered by primary care. I feel, however, that we are not yet ready for GGPAQ. The effect of creating another ‘box to tick’ in an already target driven culture, I feel, at this stage would be counterproductive. We have a long way to go in the process of educating G.P’s and practice nurses about the evidence base for the benefits of and the delivery of exercise prescription. It will, rightly, take convincing evidence of effectiveness to persuade G.P’s to engage in this process. There is, currently, no evidence that could possibly lead us to suppose that the introduction of GGPAQ would lead to significant and sustained changes in physical activity levels ?1million , to introduce a QOF point does not seem an enormous amount of money until you consider that with that sum, per year, you could employ 10 SEM consultants. I feel this would be a very much more effective way of spending the limited resources available at this stage. A single SEM consultant could provide a comprehensive education programme from medical school to primary and secondary care, could lead good quality, translational research into cost effective ways of delivering exercise interventions and could coordinate existing services for exercise in chronic disease which are often non-existent or ineffective and poorly evaluated. They could assess local needs, building on strengths of existing structures and working on the weaknesses. They could improve links with the fitness industry which in many cases are poorly supported and therefore less effective.

I agree, clinical research is essential at this stage and funding is not easy to come by. The N.H.S needs to address this through its own research organisations. Partnerships with the tremendously powerful fitness industry may also help to fund translational research as might charitable foundations for chronic disease research. Overall, I agree with much of the editorial, but feel that in the current economic climate , we need to think very carefully before rolling out blanket schemes which are open to criticism from the very people we are hoping will deliver them.

Natasha S. Jones
ST6 in SEM


1.Eakin EG, Glasgow RE, Riley KM. Review of primary care-based
physical activity intervention studies: effectiveness and implications for
practice and future research. J Fam Pract. 2000; 49: 158-168.

2. Lawlor D.A The Effect of physical activity advice given in primary care
consultations-a review. Journal of public Health Medicine.2001; 23:219-226

E-Letter: Performance anomalies in running shoe design: Psychological factors?

16 Jul, 10 | by Karim Khan

The following E-Letter is a response to The effect of three different levels of footwear stability on pain outcomes in women runners: a randomised control trial . Abstract | Full article

Ryan et al (1) provide empirical evidence that standards for running shoes in relation to foot posture are far from convincing. In particular, a sophisticated and expensive motion-control design intended for highly pronated feet was less effective than more basic shoes in minimizing injuries and pain to all categories of foot. This outcome echoes Richards et al’s (2) recent negative review regarding the role of shoe design in reducing injury.

I wrote a rapid response (3) to the latter paper suggesting that the origin of the conundrum may not reside only in biomechanics, but rather there may be a psychological element concerning the individual’s interpretation of risk. The extreme form of this conceptualisation is “risk homeostasis”, whereby it is argued that the individual “targets” a fixed level of perceived risk to govern his/her performance on any given activity (4,5). The psycholigical mechanisms by which risk is perceived and affects behaviour remain speculative; one model is based on low-level learning of the outcomes of competing tendencies in beviour (6). The typical activity to which the conceptualisation is applied has been road- travel and reflects the observation that may safety features do not maintain their benefit over time: drivers squander safety benefits in less careful driving, as reflected for example in greater and more erratic speeds. Two examples concern seat-belts and ABS brakes (5,6,7).

As applied to running, the implication is that greater sophistication in shoe design reduces the perceived likelihood of potential injury; however, the consequence may be an increase in risky running behaviour. For example, the runner may pay more attention to uneven surfaces when wearing a less sophisticated design of shoe, but determine that a more sophisticated design deals adequately in equivalent circumstances; if this is not the case then more pain and injuries will result from the more sophisticated design.

Tony H. Reinhardt-Rutland
Reader in Psychology
University of Ulster


1. Ryan MB, Valiant GA, McDonald K, Taunton JE. The effect of three different levels of footwear stability on pain outcomes in women runners: a randomised control trial. Br J Sports Med doi:10.1136/bjsm.2009.069849.

2. Richards CE, Magin PJ, Callister R. Is your prescription of distance running shoes evidence-based? Br J Sports Med 2009; 43: 159-162.

3. Reinhardt-Rutland AH. Negating the safety advantage in running shoe design: perceived risk affecting performance? Br J Sports Med 2009 []

4. Wilde GJS, Robertson LS, Pless IB. Does risk homeostasis theory have implications for road safety? BMJ 2002; 324: 1149-1152.

5. Adams JGU. Risk. London: UCL, 1995.

6. Reinhardt-rutland AH. Seat-belts and behavioural adaptation: the loss of looming as a negative reinforcer. Safety Sci 2001; 39: 145-155.

7. Aschenbrenner M, Biehl B. Improved safety through improved technical measures? Empirical studies regarding risk compensation processes in relation to anti-lock brake systems. In RM Trimpop, GJS Wilde (eds). Changes in accident prevention: The issue of risk compensation. Groningen: Styx, 1994.

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