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.

REFERENCES

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.

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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

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

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!

References
(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.

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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

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

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 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
Oxford

References

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

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

References

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 [http://bjsm.com/cgi/eletters/43/3/159]

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.

This E-letter is in response to Are there risk factors in alpine skiing? A controlled multicentre survey of 1278 skiers. Abstract | Full article

In general, the answer is: ‘yes, there are internal (e.g. gender, age, fitness, skill level, risk taking) and external (equipment, environment) risk factors’ according to comprehensive model for injury causation by Bahr and Krosshaug (1). However, we would like to comment on the presented data and methods used because some results seem contrary to other studies in this research field.

Firstly, Hasler et al. reported that skiers with new equipment have a higher risk of being injured. However, there seems a mistake in the presented data because in the abstract the Odds Ratio (OR) was 59 with a 95% confidence interval of 0.37-0.93 while in Table 1 the OR was 0.59. If the OR of 0.59 was correct, new equipment would decrease injury risk. In addition, what means new equipment? Did the authors compare carving skiers with traditional skiers as done by Burtscher et al. (2) showing a reduced injury rate since the introduction of carving ski? Where is the cut off between new and old equipment? In the discussion section, Hasler et al. stated that the results might be explained by a mismatch between the abilities of the skier and the equipment. Unfortunately, they did not include skill levels in their questionnaire. Several studies showed higher injury rates in less skilled skiers and snowboarders (3, 4) while more skilled skiers had a higher risk to sustain a more severe injury (5).

Secondly, there seem mistakes concerning the presented data about snow conditions. In Figure 3, artificial snow versus old snow and fresh snow versus powder snow show OR <1 while in Table 1 the same OR are presented vice versa (OR 0.21 for old snow vs. artificial snow and OR 0.31 for old snow vs. fresh snow, respectively). It is the same with slush snow versus powder snow which is not a snow condition but a skiing condition in Figure 3 and powder snow vs. slush snow in Table 1, respectively. In addition, old snow seems to be in contrast to fresh snow. Does fresh snow mean powder snow? However, can old snow not be also old artificial snow? Therefore, it is not clear which snow condition actually increases or decreases injury risk.

Thirdly, seasonal checking of skiing equipment showed a trend to decrease injury risk (OR: 0.46, p = 0.056). In our opinion, seasonal checking of skiing equipment includes primarily an adjustment of the bindings. In accordance, Burtscher et al. (2) showed that female carving skiers with a binding adjustment older than 1 year had a twofold knee injury rate compared to those with newly adjusted bindings. The release of a binding is primarily important in preventing injuries to the lower extremity. Therefore, it would be better to define risk factors with regard to the injured body location.

Fourthly, injured skiers showed a higher readiness for risk taking in this study. In contrast, other studies  reported that injured skiers did not take more risk but were less skilled compared to uninjured skiers (6-8). Therefore, it would make sense to include skill level.

Fifthly, Hasler et al. showed a higher injury risk when skiing under bad weather conditions which is well in accordance with the study by Aschauer et al. (9). However, poor snow and weather conditions may be misjudged by injured skiers because they may look for an explanation as to why the injury occurred. In general, self-report to questions might lead to underreport or overreport of health-risk behaviours affected by cognitive and situational factors (10).

Sixthly, gender has not been found to be a significant risk factor in this study. That might be due to the fact that Hasler et al. did not differentiate between injured parts of the body, e.g. females have a higher knee injury risk (2) and males have a higher head injury risk (11) compared to the other gender.

Seventhly, Hasler et al. calculated that injury risk is higher when warming up. This result contrasts general preventive recommendations (12) and also the findings by Ruedl et al. (13) who demonstrated a twofold injury reduction in a cohort of 36.000 participants of 12 ski schools when warming up.

Eighthly, there seems a mistake concerning the presented data about drug consumption. Figure 3 shows an OR > 1 for abstinence from drugs while inTable 1 drug consumption was presented vice versa. In  addition, in Table 1 an OR of 5.92 was presented while in the discussion the OR was 1.78 for drug consumption.

Since a case control design was used, the amount of exposure to the suggested risk factors was unknown which should be taken into account when interpreting the results (14). In the study by Hasler et al. the controls were interviewed when coming off slopes after skiing. This implies that controls skied probably more than 3 hours although other studies showed that most injuries to the lower extremity occurred within the first 2 or 3 hours of skiing (15, 16). A total of 782 patients were recruited over a period of 5 and a half month and 496 controls were interviewed in six different ski resorts. This means an average of about 83 controls per ski resort and an average of 15 uninjured skiers per month, respectively. However, Hasler et al. (2009) did not specify when controls have been recruited, e.g. every second day. A continuous recruitment of controls seems of utmost importance to compare prospectively potential external risk factors like snow, weather and slope conditions. In general, a prospective study design concerning internal and external risk factors in relation to gender and type of injury should be used. However, at least a case-control-design should be applied matching controls according to gender, age and skill level.

Gerhard Ruedl & Martin Burtscher
Department of Sport Science
University of Innsbruck, Austria

References

1. Bahr R, Krosshaug T. Understanding injury mechanisms: a key component of preventing injuries in sport. Br J Sports Med 2005; 39: 324-329.
2. Burtscher M, Gatterer H, Flatz M et al. Effects of modern ski equipment on the overall injury rate and the pattern of injury location in Alpine skiing. Clin J Sport Med 2008; 18:355-357.
3. Langran M, Selvaraj S. Increased injury risk among first-day skiers, snowboarders, and skiboarders. Am J Sports Med 2004;32:96-103.
4. Hagel B. Skiing and snowboarding injuries. Caine DJ, Maffulli (eds.): Epidemiology of Pediatric Sports Injuries. Individual Sports. Med Sport Sci. Basel. Karger,2005;48:74-119.
5. Goulet C, Hagel BE, Hamel D, et al. Self-reported skill level and injury severity in skiers and snowboarders. J Sci Med Sport 2008; doi: 10.1016/j.jsams.10.002
6. Bouter LM, Knipschild PG, Feij JA, et al. Sensation seeking and injury risk in downhill skiing. Person. Individ. Diff. 1988;9:667-73.
7. Cherpitel CJ, Meyers AR, Perrine MW. Alcohol consumption, sensation seeking and ski injury: a case-control study. Journal of Studies on Alcohol 1998;59:216-21.
8. Goulet C, Regnier G, Valois P, et al. Injuries and risk taking in alpine skiing. ASTM STP 1397, Skiing Trauma and Safety: Thirteenth Volume, RJ Johnson, P Zucco, JE Shealy (eds.), ASTM International, West Conshohocken, PA, 2000:139-46.
9. Aschauer E, Ritter E, Resch H et al. Injuries and injury risk in skiing and snowboarding. Unfallchirug 2007; 110: 301 306. (in German)
10. Brenner ND, Billy JOG, Grady WR. Assessment of factors affecting the validity of self-reported health-risk behavior among adolescents: evidence from the scientific literature. J Adolesc Health 2003;33:436-457.
11. Mueller BA, Cummings P, Rivara FP, et al. Injuries of the head, face, and neck in relation to ski helmet use. Epidemiology 2008;19:270-76.
12. Koehle MS, Lloyd-Smith R, Taunton JE. Alpine ski injuries and their prevention. Sports Med 2002; 32 (12): 785-793.
13. Ruedl G, Sommersacher R, Woldrich T et al. A structured warm-up program to prevent injury in recreational skiers. Senner V, Fastenbauer V, Boehm H (eds.): Book of Abstracts of the 18th Congress of the International Society for Skiing Safety, Garmisch-Partenkirchen, Germany, April 26 to May 02 2009, 77.
14. Vandenbroucke JP, von Elm E, Altman DG et al. Strengthening the reporting of observational studies in epidemiology (STROBE): explanation and elaboration. Epidemiology 2007;18 (6): 805-835.
15. Ungerholm S, Engkvist O, Gierup J et al. Skiing injuries in children and adults: a comparative study from a 8-year period. Int J Sports 16. Ruedl G, Schranz A, Fink C et al. Are ACL injuries related to perceived fatigue in female skiers? ASTM International 2010; 7 (4), Paper ID JAI102747

This E-letter is in response to Daily energy expenditure and cardiovascular risk in Masai, rural and urban Bantu Tanzanians Abstract | Full Article

Mbalilaki and associates have reported very high daily energy expenditures for a sample of Masai pastoralists and farmers (56% of whom were women)(1). The stated average of 10.7 MJ/day (2565 kcal/day) appears to be a gross value for that part of the day when the subjects were physically active, although this is not specifically indicated in their paper. The expenditure is suggested as equivalent to 19 km of walking, which would occupy a total of some 4 hours. The remaining 20 hours would contribute at least a further 6 MJ of resting energy expenditure, for a daily total of some 16.7 MJ or 4010 kcal. One earlier Kofranyi-Michaelis respirometer study of traditional male Inuit did observe daily expenditures ranging from 10.5 to 18.5 MJ/day for different categories of hunting in a harsh arctic environment (2). However, the figure of 16.7 MJ/day proposed for the Masai sample is somewhat surprising on several counts, including the low average body mass of the subjects (56.8 kg), the relatively low physical working capacity seen in a previous Masai sample (3) and the conclusions from at least one energy input-output analysis that food requirements in this environment could be satisfied by working only two days per week (4).

One potential issue is the method adopted when determining energy expenditures. Mbalilaki and associates (1) apparently based their estimate on an interviewer-administered North American  questionnaire (5), translated into Swahili and slightly adjusted for Tanzanian conditions. The nature of these slight adjustments and their possible impact on test validity are not discussed, but there are clearly important limitations to the absolute accuracy of information obtained from most physical activity questionnaires (including the instrument of Paffenbarger and associates, 5) even in an urban North American environment (6),and many of the items listed in the published version of the instrument of Paffenbarger et al.(5) would have little relevance to the Masai sample.

Given the importance of understanding physical activity patterns in populations that have a low prevalence of cardiovascular risk factors, I hope that Mbalilaki and associates will soon find opportunity to replicate their interesting observations, using currently available and relatively inexpensive objective physical activity monitors.

Roy J. Shepard
Professor Emeritus
University of Toronto

References

1. Mbalilaki JA, Msesa Z, Stromme SB et al. Daily energy expenditure and cardiovascular risk in Masai, rural and urban Bantu Tanzanians. Br J Sports Med 2010; 44: 121-126.

2. Godin G, Shephard RJ. Activity patterns in the Canadian Eskimo.  In: Edholm O, Gunderson EK, eds. Polar Human Biology, London, UK:  Heinemann, 1973.

3. Wyndham CH, Strydom NB, Morrison JF et al. Differences between ethnic groups in physical working capacity.  J Appl Physiol 1963; 18: 361- 366.

4. Lee RB. Kung bushmen subsistence: An input-output analysis. In:  Vayda AP. Environment and cultural behavior. New York, NY: Natural History Press.

5. Paffenbarger RS, Blair SN, Lee IM et al. Measuring physical activity to assess health effects in free-living populations. Med Sci Sports Exerc 1993; 25: 60-70.

6. Shephard RJ. Limits to the measurement of habitual physical activity by questionnaires. Br J Sports Med 2003; 37: 197-206.

This E-lettter is in response to Setting standards for the prevention and management of travellers’ diarrhoea in elite athletes: an audit of one team during the Youth Commonwealth Games in India Abstract | Full Article

The article by Tillett and Loosemore describes guidelines for the prevention and management of travellers’ diarrhoea (TD) based on their experience with the elite athletes and noncompeting members of Team England during the 2008 Youth Commonwealth Games in India. The authors recommended that all team members receive oral and written advice regarding prevention of TD, that all team members are issued alcohol hand gel and instruction for its use, and that all noncompeting team members receive ciprofloxacin for TD prophylaxis. As ciprofloxacin use in elite athletes is considered controversial because of a possible association with tendon rupture, the authors recommended that elite athletes consider the nonabsorbable antibiotic rifaximin as a prophylactic for TD. However, none of the elite athletes on Team England actually received rifaximin as a prophylactic therapy for TD. Further, the authors stopped short of recommending rifaximin for the treatment of TD, simply recommending treatment with empiric antibiotics per local advice and the results of stool culture.

We report here that, in 2008, some elite athletes from the United States received rifaximin either for the prophylaxis or treatment of TD while in Beijing, China. In this small sample of elite athletes, rifaximin was safe and well tolerated, and no adverse events were reported. Rifaximin has been found safe, well tolerated, and effective for both the prophylaxis and treatment of TD in other populations1-8. Based on our experience and the excellent safety profile of rifaximin for the treatment of TD, the use of rifaximin as an antibiotic therapy for the treatment of TD in elite athletes deserves further consideration.

Bradley Connor and Scott Rodeo

References

1.           DuPont HL, Ericsson CD, de la Cabada FJ, et al. Prevention of travelers’ diarrhea with rifaximin- a phase 3 randomized double-blind placebo-controlled trial in U.S. students in Mexico [abstract]. Am J Gastroenterol. 2006;101(suppl):S197-S198.

2.           DuPont HL, Ericsson CD, Mathewson JJ, et al. Rifaximin: a nonabsorbed antimicrobial in the therapy of travelers’ diarrhea. Digestion. 1998;59(6):708-714.

3.           DuPont HL, Haake R, Taylor DN, et al. Rifaximin treatment of pathogen- negative travelers’ diarrhea. J Travel Med. 2007;14:16-19.

4.           DuPont HL, Jiang ZD, Ericsson CD, et al. Rifaximin versus ciprofloxacin for the treatment of traveler’s diarrhea: a randomized, double-blind clinical trial. Clin Infect Dis. 2001;33(11):1807-1815.

5.           DuPont HL, Jiang Z-D, Belkind-Gerson J, et al. Treatment of travelers’ diarrhea: randomized trial comparing rifaximin, rifaximin plus loperamide, and loperamide alone. Clin Gastroenterol Hepatol. 2007;5:451-456.

6.           DuPont HL, Jiang Z-D, Okhuysen PC, et al. A randomized, double-blind,
placebo-controlled trial of rifaximin to prevent travelers’ diarrhea.
Ann
Intern Med. 2005;142(10):805-812.

7.           Steffen R, Sack DA, Riopel L, et al. Therapy of travelers’ diarrhea with rifaximin on various continents. Am J Gastroenterol. 2003;98:1073- 1078.

8.           Taylor DN, Bourgeois AL, Ericsson CD, et al. A randomized, double- blind, multicenter study of rifaximin compared with placebo and with ciprofloxacin in the treatment of travelers’ diarrhea. Am J Trop Med Hyg. 2006;74:1060-1066.

Conflict of Interest

Dr Connor has received grant support from and is a consultant for Salix Pharmaceuticals, Inc.
Dr Rodeo has nothing to disclose.

This E-letter is in response to ECG As A Part of the Pre-Participation Screening Programme: An Old an Still Present International Dilemma (Abstract)

Pre-participation screening in competitive athletes in Portugal has been compulsory for more than 40 years. Yearly ECG was introduced in the screening at about the same time as in Italy, for all athletes evaluated at the Sports Medicine Centres in Portugal. The very rare cases of sudden cardiovascular death that have ocurred in the past 25 years in Portugal were not screened at the Centres or had further cardiovascular evaluation pending, and threfore were not qualified for practice. Several athletes have been disqualified from sports participation for cardiovascular reasons, most of them were further investigated because of rest ECG changes findings. We strongly favour the use of 12 lead ECG in the pre- participation screening process. Presently, we routinely screen about 20.000 athletes per year in the 3 Sports Medicine Centres in Portugal.

Marcos A. Miranda
Sports Medicine Specialist
Lisbon Sports Medicine Centre