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

Dear BJSM,

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

The relevant section from the code is included below:

S2. HORMONES AND RELATED SUBSTANCES

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

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

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

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

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

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

Thank you,

Raph S. Bovard MD

Dear Editors,

Knechtle and Kohler have considered the factors relating to overall performance in triple ironman triathlon. There are however several other considerations which must be made when looking at total race time.

The mental preparation needed for ultra-endurance events may have a significant impact on total race time. This can limit training time and total race time, especially if an individual misjudges their pacing early in the event.

Some consideration needs to be taken of pre-race injuries. Endurance athletes commonly have a number of injuries which limit different aspects of their preparation and race. With a sample size of only 17, these two factors are likely to prevent any true association between anthropomorphic factors and total race time.

The study of triple ironman distance events is unusual as there are few events of this type globally. Comparisons to marathon running, ironman triathlon and cycling are perhaps misguided as these are all sports with large numbers of competitors and a circuit of races for professional athletes.

Subjects in this study trained between only 6 hours each week and up to 55 hours. Skin fold thickness was high indicating a high body fat percentage. Average weight was 85Kg, considerably higher than most professional ironman triathletes. Competitors clearly varied considerably in their preparation. They range between casual competitors and professional athletes. This makes study of the factors needed for low total race time difficult.

The use of performance in individual sections of the race may not be a valid measurement to make alone. Whilst there is a trend towards time in the running section being the best predictor of total race time, this is in fact also a function of both cycling time and swimming time. The energy expended in other sections of the event will take a toll on the later part even with the best athletes. As the last section of the race the run is most likely to show a trend.

Despite the thorough analysis made of the results, currently there is insufficient participation in this type of event for this type of study. As the popularity of ultra-endurance sport grows, the factors necessary for optimum performance may more easily be delineated.

Edward J.C. Dawe, Orthopaedic Trainee, BASEM Member

Dear Editor-in-Chief,

We are concerned with an important confusion about data unit of measurement presented by Girard et al. when evaluating the changes in Lower Limbs Stiffness (LLS) during prolonged tennis playing (1). Evaluation of LLS is of great interest in a sport like tennis where speed and reactivity takes a great part. LLS is an important element of the muscle biomechanical characteristics and the optimal utilization of the stretch-shortening cycle requires some level of stiffness (2). Then an appropriate level of stiffness is necessary for optimal performance and prevention of injury (2). To evaluate LLS, Girard et al. used a standardized procedure proposed by Dalleau et al. (3). This method allows evaluation of LLS (expressed in N/m or in kN/m) in field conditions via the measure of both flight and contact times during a multi-rebound test.

Such a procedure has been previously used in several sport activities and results reported (4-5). However, in the article published by the British Journal of Sports Medicine, the results are presented expressed in N/m/kg while the correct unit is N/m or kN/m, as mentioned above. Comparison with the range of previous LLS data reported in the literature (4-5) confirms the confusion in the choice of unit by Girard et al. and suggests that it should likely be in kN/m. Although not affecting the conclusion of the authors concerning the relative changes in stiffness during prolonged tennis playing, we would like the scientists interested in LLS evaluation to be aware of this mistake in order to avoid a wrong interpretation of the data presented and to permit their use for comparison with other results.

By Sylvain Durand and Abdel Rahmani, Université du Maine, France.

A response to Hancock, Ste-Marie and Young (2008) by Joseph Baker and A. Jane Logan, York University.

We appreciate the thoughtful review of our manuscript by Hancock, Ste -Marie and Young.(1) In this brief response, we reconsider the issues raised in their review and continue the discussion of relative age effects in National Hockey League (NHL) draftees.

REGARDING THE APPROPRIATE USE OF CUTOFF DATES.

Hancock et al. proposed that the more appropriate method for examining relative age effects in NHL draft players was to use the age cutoff criterion established by the NHL (September 16th). Our original analyses (2) utilized the age cutoff from the Hockey Canada and Hockey USA governing bodies (January 1st). Although the cutoff used by Hancock et al. seems reasonable, we submit that our original analyses were more appropriate because the proposed mechanisms of relative age effects are known to originate early in an athlete’s development. (3)

In sport, relative age attainment differentials are proposed to result from physical maturation differences among individuals during growth and development. (4) Specifically, those born shortly after the cut -off date established by sport governing bodies typically display more mature physical characteristics compared to those born later in the year.

Greater height, strength, speed and power not only relate to maturity, but also provide physical attributes that underpin performance in many sports. As a result, earlier-born, more mature individuals are more likely to dominate youth sport, be identified as ‘outstanding’ and be selected by scouts and coaches for representative sport competition. (4)

More competitive levels of sport participation are associated with dramatic changes in the practice environment. Here, selected athletes access practice more frequently and dedicate an increasingly significant proportion of weekly time to training with more highly qualified and specialized coaches to facilitate continued development. Thus selection and access to quality practice propagate relative age effects well into the senior years, explaining why discrepancies in birth date tendencies have been reported repeatedly across professional sports.(4) Interestingly, a recent meta-analysis by our research team found that relative age effects were strongest in adolescence and diminished in adulthood. (4)

In summary, the cutoff dates associated with early development drive relative age effects, not the cutoff date used for the NHL draft. Altering the cutoff date as we saw from Hancock et al. should have little influence on the overall effect. Their re-analysis indicates the largest representation was in birth quarter two followed by birth quarter three, which, as they showed, corresponds better to a relative age effect originating from the Hockey Canada and Hockey USA cutoff date of January 1st than September 1st.

REGARDING THE USE OF ALL DRAFT ROUNDS

Hancock et al criticized our choice to use all seven rounds of the draft for our relative age analyses on the basis that later rounds are made up of lower quality players. This seems like splitting hairs to us, as this rationale could also be used to justify using only round one instead of rounds two to four or the first 10 players of round one versus the remaining 20 players in round one. Moreover, our paper was written to demonstrate that the relative age effect explained some of the results for the NHL draft, not the performance of the draftees after they had entered the NHL. We defend our original choice on the basis that any selection in the NHL represents a reasonable level of expertise to examine the relative age effect in this population. Furthermore, and perhaps more interesting, an additional analysis of our data comparing relative age distributions for rounds one to four with rounds five to nine (up to 2005 the NHL draft had nine rounds), noted a slightly stronger relative age effect in later rounds than earlier rounds (Cramér’s V = 0.08 for rounds 1-4 and 0.13 for rounds 5-9).

REGARDING DRAFT VERSUS OVERALL SELECTION FOR SPEARMAN CORRELATION

The rationale for using an athlete’s overall selection in the draft versus round number is reasonable, as it adds additional depth to the selection variable. However, coaches, athletes and spectators rarely talk about athletes in terms of what their overall selection was - more often the overall draft round number is the characteristic of interest. Teams often have differing strategies for how they choose players in the draft (e.g., drafting to win the Stanley Cup vs. drafting for team development).

As a result, players ranked highly by one team might not be considered at all by another. Removing draft round number assumes a) that each team uses the same strategy for how they choose their draft picks and b) that players can be easily rank-ordered and are equivalent from team to team.
We defend our original analysis as being perhaps more relevant to the specific practices used by each team during the draft, although we appreciate the additional statistical depth that might be added by Hancock et al.’s method. The lack of consistency between our analyses and theirs is cause for concern, however, and we encourage future research in the area to elucidate these contradictory findings.

In summary, these studies continue to highlight the effects of secondary factors on long-term athlete development.

References

1. Hancock, D. J., Ste-Marie, D. M., Young, B. W. Birth date and birth place effects in National Hockey League draftees 2000-2005: Comments on Baker and Logan (2007). Br J Sports Med 2008; 42: 948-949.

2. Baker, J. Logan, A. J. Developmental contexts and sporting success: Birthdate and birthplace effects in NHL draftees 2000-2005. Br J Sports Med 2007; 41: 515-517.

3. Barnsley, R. H., Thompson, A. H. Birthdate and success in minor hockey: The key to the NHL. Can J Behav Sci 1988; 20 167-176.

4. Cobley, S., Baker, J., Wattie, N. McKenna, J. Annual age grouping and athlete development: A meta- analytical review of relative age effects in sport. Sports Med 2009; 39 235-256.

5. Sherar LB, Baxter-Jones ADG, Faulkner RA, et al. Does physical maturity and birth date predict talent in male youth ice hockey players? J Sports Sci 2007; 25: 879-86

By Justin A Paoloni

I read with interest the Consensus Statement on Concussion, and believe this worthwhile in furthering scientific knowledge on concussion in sport. However, I have concerns about definitive comments in the consensus statement, given the lack of supporting scientific evidence. Whilst this consensus document is only “a guide and is of a general nature consistent with the reasonable practice of a healthcare professional”, it is also “reflects the current state of knowledge”. This comment does not accurately represent the documents’ contents with definitive statements not evidenced based.

I agree with the preamble; “management and return to play decisions remain in the realm of clinical judgement on an individualized basis”, as scant high level evidence is available on concussion management. However, Section 2.2 states that “a player with diagnosed concussion should not be allowed to return to play on the day of injury. Occasionally, in adult athletes, there may be a return to play on the same day of injury (see Section 4.2)”, which follows with “adult athletes, in some settings, where there are team physicians experienced in concussion management and sufficient resources…return to play may be more rapid.” These statements have multiple qualifiers, but do not represent the management of concussion in sport. More than “occasionally” do athletes return to play on the same day after medical assessment and symptom resolution, and this appears safe and effective. The return to play decision does not require the “sufficient resources” mentioned, but does require a physician experienced in concussion management. Certainly, there are no scientific studies, and no comparison studies, with high enough level of evidence to definitively support either approach.

Section 11 states that “the consensus statement is intended to serve as the scientific record of the conference”. Thus, these definitive statements on concussion management, from an expert panel, require supporting scientific evidence and appropriate referencing, as for any scientific paper. To make these statements without quoting relevant high level evidence is not scientific. There are potential legal ramifications for medical practitioners who do not follow these concussion management guidelines.

By Maxintosh.

Dear Editor,

I read with interest the recent article published on this journal about the left-handedness in boxing and the proclivity to success (1). As Gursoy quotes in his paper, the rate of left-handedness in the general population ranges between 1 and 30% in different studies, but the body of medical sports literature on this topic is very small. If we consider the actual World Boxing Council (WBC) title-holders in the 17 weight categories, for example, we find that 6 boxers (35.3%) fight using a southpaw stance and that rate is identical (12/34) when we take into account all the athletes (both champions and contenders) engaged in the last title matches. This figure is very similar to that reported by Gursoy (36.4%), and it is questionable whether a higher rate of left-handed subjects in respect to general population is typical of boxing or whether southpaw boxers are really more successful than right-handed athletes, as Gursoy stated. However, this paper has some points that need a more careful evaluation:

The sample size (22 boxers) of investigated subjects is very small and, consequently, the power of the statistical analysis is not so high. More questions, moreover, arise when examining this sample and the statistics adopted. A parametric test was used to compare the boxing records of right- and left-handed athletes but inspection of the range of disputed (and won/lost) matches, it is quite unlikely that these variables have a Gaussian distribution.

The competitive level of this group of “semi-professional” boxers seems to be very wide. It is possible that different subgroups of athletes have been investigated in the same group (amateurs and professionals, winners and losers, etc.).

All the boxers were recruited from a single boxing club. Boxing, as other open skill disciplines, is a sport where emulation is very frequent. If, in a boxing club, a southpaw champion is present, or the coach is left-handed, it is more likely that a higher rate of left-handed boxers come out from this gym.

In conclusion, this paper addresses an important topic in boxing and in sport in general. However, the investigated population and the adopted statistical methods have some gaps. In future, greater and more homogenous samples are advisable, possible analyzing subjects from several clubs. A national survey and analysis of boxers’ handedness could be very interesting, trying to full the scientific holes present on this topic.

References
Gursoy R. Effects of left- or right-hand preference on the success of boxers in Turkey. Br J Sports Med. 2009; 43:142-144.

–
Dr. Massimiliano Bianco
Sports Medicine Department
Catholic University
Rome - Italy

By Sarmax.

In many practical situations such as the treatment of hypertension, it is important to determine whether an improvement of condition following exercise prescription is due to an increase in aerobic fitness, or whether it simply reflects a reduction in body fat content (1) A previous review of 61 studies of training-induced changes in resting blood pressure (2) concluded that any reduction in resting pressures could not be attributed to concomitant weight loss, since the changes in systolic and diastolic readings showed very small and statistically non-significant correlations with changes in body mass.

In their recent paper, Barrone et al. (1) wished to test whether the same was true of exercise hypertension, and in support of such a conclusion they claim to have demonstrated independent correlations of delta fitness and delta fat with changes of pressure through the use of generalized estimating equations. A variety of valid measures of body fatness were obtained on their subjects, but unfortunately an inappropriate measure of aerobic fitness was chosen for the analysis. The outcome is reported as a change in peak oxygen transport, expressed in ml/kg/min. This is dimensionally incorrect, but let us assume that the authors intended to indicate a relative change of oxygen transport, expressed in ml/[kg.min]. Aerobic fitness is in fact the overall ability of the cardio-respiratory system to transport litres of oxygen to the working tissues. Any accumulation of body fat reduces the utility of this transport in terms of daily activities (including treadmill running). To take a practical example, a man with a body mass of 70 kg and an aerobic fitness of 3.5 l/min has a relative VO2max of 50ml/[kg.min]. If that same person accumulates an extra 14 kg of body fat, the aerobic fitness may remain at 3.5 l/min. but the relative VO2max decreases to 41.7 ml/[kg.min]. Plainly, the relative units of oxygen transport confound the influence of fitness and fatness, and cannot be used to distinguish the importance of changes in fitness relative to changes in fatness.

The authors must have the data to make a more convincing independent analysis of the two variables, and I would encourage them to do so.

REFERENCES.

1. Barone BB, Wong N-Y, Bacher AC et al. Decreased exercise blood presure in older adults after exercise training: contributions of
increased fitness and decreased fatness. Br J Sports Med 2009; 43: 52-56.

2. Hagberg JM, Park J-J, Brown MD. The role of exercie training in the treatment of hypertension. An Update. Sports Med 2000; 30: 193-206.

Photo by Lisa Bettany.

By Nicola Maffulli, Umile Giuseppe Longo, Vincenzo Denaro, Consultant Trauma and Orthopaedic Surgeon, University Hospital of North Staffordshire, Keele University School of Medicine

We read with interest the Review Article “Rotator cuff tendinopathy: A review”, by Lewis.

This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.

We investigated supraspinatus tendon samples obtained from patients undergoing arthroscopic repair of a rotator cuff tear to examine the distribution of tendinopathic changes associated with this condition. At arthroscopy, a full thickness supraspinatus tendon biopsy was harvested close to the tear edge. We found more frequent tendon changes on the articular side of the rotator cuff 4.

We found more cartilage-like changes in patients affected by rotator cuff tears, but not in our control group.Recent biomechanical data suggest that the stress-shielded and transversely-compressed side of the enthesis has a distinct tendency to develop cartilage-like or atrophic changes in response to the lack of tensile load 2,7,9,10. Over a long period, this process may develop into a primary degenerative lesion in that area of the tendon. This may explain why the tendinopathy is not always clearly activity related, and can be strongly correlated with age. In this manner, it could almost be considered an ”underuse” injury rather than an overuse injury as a result of stress-shielding 7,9,10. The formation of cartilage-like changes in the enthesis in many ways can be considered a physiological adaptation to the compressive loads 12-14. It may not allow the tendon to maintain its ability to withstand high tensile loads in that region of the tendon.

As the stress-shielding may have led to tensile weakening over time, an injury may occur more easily in this region. In this manner, insertional tendinopathy could be considered an overuse injury, but predisposed by pre -existing weakening of the tendon 12-14.

In another study 3 to evaluate the histopathological features of macroscopic intact tendon portion of patients with rotator cuff tears, we demonstrated that the supraspinatus tendons of patients undergoing arthroscopic repair for a rupture show profound histopathologic changes, while the tendons of aged persons with no known tendon abnormalities have, as a group, little histological evidence of pathological changes.

Moreover, tendon changes are not only localized at the site of rupture, but also in the macroscopic intact tendon portion.

Several centres are undertaking studies on tendinopathy 11,16,17, and the individual studies are unlikely to be large enough to result in adequate power for reliable evaluation. Therefore, combining the data from those studies with a similar study design will be essential. Consistent high- quality pathology data are thus remarkably important for the success of the studies. Two scoring systems can be used for classification of the histopathological findings of tendinopathy: the Movin score 15 and its validated modifications 4,6,12, and the Bonar score 1. We performed a study to answer the question whether these two scores of abnormal tendon tissue were comparable 8. In our hands, Movin and Bonar scores assess the same characteristics of tendon pathology.

In an frequency-matched case-control study we determined the plasma glucose levels in non diabetic patients with rotator cuff tear 5. We found that normal, but in the high range of normal, increasing plasma glucose levels may be a risk factor for rotator cuff tear.

Lastly, although it is likely that the histopathology of tendinopathy is similar, of not the same, regardless of its location, this has only been shown in a formal fashion in the Achilles and patellar tendons 12: we were slightly surprised of the fact that a number of papers dealing with pathology of other tendons (i.e., patellar tendon, Achilles Tendon, and extensor carpi radialis brevis tendon (tennis elbow) are quoted referring to rotator cuff tendinopathy (references n°23,24,25,26,81,94,96,97,98, 147,148).

References
1. Cook, J.; Feller, J.; Bonar, S.; and Khan, K. Abnormal tenocyte morphology is more prevalent than collagen disruption in asymptomatic athletes’ patellar tendons. J Orthop Res 2004;22:334-338.
2. Gardner, K.; Arnoczky, S. P.; Caballero, O.; and Lavagnino, M. The effect of stress-deprivation and cyclic loading on the TIMP/MMP ratio in tendon cells: An in vitro experimental study. Disabil Rehabil 2008:1-7.
3. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Rabitti, C.; Morini, S.; Maffulli, N.; and Denaro, V. Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med 2008;36:533-8.
4. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Rabitti, C.; Morini, S.; Maffulli, N.; Forriol, F.; and Denaro, V. Light microscopic histology of supraspinatus tendon ruptures. Knee Surg Sports Traumatol Arthrosc 2007;15:1390-4.
5. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Spiezia, F.; Maffulli, N.; and Denaro, V. Higher fasting plasma glucose levels within the normoglycemic range and rotator cuff tears. Br J Sports Med 2008;
6. Maffulli, N.; Barrass, V.; and Ewen, S. W. Light microscopic histology of achilles tendon ruptures. A comparison with unruptured tendons. Am J Sports Med 2000;28:857-63.
7. Maffulli, N.; Khan, K. M.; and Puddu, G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy 1998;14:840-3.
8. Maffulli, N.; Longo, U. G.; Franceschi, F.; Rabitti, C.; and Denaro, V. Movin and Bonar scores assess the same characteristics of tendon histology. Clin Orthop Relat Res 2008;466:1605-11.
9. Maffulli, N.; Reaper, J.; Ewen, S. W.; Waterston, S. W.; and Barrass, V. Chondral metaplasia in calcific insertional tendinopathy of the Achilles tendon. Clin J Sport Med 2006;16:329-34.
10. Maffulli, N.; Sharma, P.; and Luscombe, K. L. Achilles tendinopathy: aetiology and management. J R Soc Med 2004;97:472-6.
11. Maffulli, N.; Testa, V.; Capasso, G.; Bifulco, G.; and Binfield, P. M. Results of percutaneous longitudinal tenotomy for Achilles tendinopathy in middle- and long-distance runners. Am J Sports Med 1997;25:835-40.
12. Maffulli, N.; Testa, V.; Capasso, G.; Ewen, S. W.; Sullo, A.; Benazzo, F.; and King, J. B. Similar histopathological picture in males with Achilles and patellar tendinopathy. Med Sci Sports Exerc 2004;36:1470-5.
13. Maffulli, N.; Waterston, S. W.; and Ewen, S. W. Ruptured Achilles tendons show increased lectin stainability. Med Sci Sports Exerc 2002;34:1057-64.
14. Maffulli, N.; Wong, J.; and Almekinders, L. C. Types and epidemiology of tendinopathy. Clin Sports Med 2003;22:675-92.
15. Movin, T.; Gad, A.; Reinholt, F.; and Rolf, C. Tendon pathology in long-standing achillodynia. Biopsy findings in 40 patients. Acta Orthop Scand 1997;68:170-5.
16. Murrell, G. A. Oxygen free radicals and tendon healing. J Shoulder Elbow Surg 2007;16:S208-14.
17. Murrell, G. A. Using nitric oxide to treat tendinopathy. Br J Sports Med 2007;41:227-31.

By Fergus Joseph Dignan, Civilian Medical Practitioner, MOD

I very much enjoyed reading the ‘warm up’ article by Steven N Blair in the January edition of BJSM. The first study that he quoted on attributable fractions for all cause deaths was a real eye popper!

I was very surprised to see that low cardiorespiratory fitness was a greater attributable risk factor (in both sexes) than obesity, smoking, high cholesterol, and diabetes, as well as hypertension in women.

The second study was almost equally as fascinating. This illustrated that the risk of cardiovascular mortality in Type 2 diabetes in the obese category who took moderate to high levels of exercise, was half that of diabetics in the normal weight category who took no exercise. There was one thing that puzzled me and that was the histograms illustrated that for the type 2 diabetics who took low levels of exercise the cardiovascular risk was the same for those in the obese category as in the normal weight group.

This article will certainly alter the way that I communicate health promotion to my patients, and I would like to congratulate Steven Blair for such a stimulating article.

By Samuele M Marcora, Senior Lecturer in Exercise Physiology School of Sport, Health and Exercise Sciences, Bangor University, Wales

To the Editor: I agree with Professor Tim Noakes that the presence of an end-spurt cannot be explained by either the traditional peripheral fatigue model, or the more recent negative feedback model proposed by Amann and Dempsey (1, 4). However, I think that the presence of an end-spurt is also at odds with Noakes’ central governor model.

In fact, a subconscious intelligent system capable of regulating in anticipation the central neural drive to the locomotor muscles on the basis of a known end-point and afferent feedback from a variety of intero- and extero-receptors should not allow for an end-spurt. On the contrary, it should choose from the very start the maximum speed that can be sustained over 4 miles without dangerous homeostatic failure and, in stable environmental conditions, provide very small but frequent adjustments in central motor command/speed during the race in relation to unpredictable small changes in the physiological conditions of the body. This is the typical functioning of subconscious physiological control systems of homeostasis, and this principle should apply to the central governor as well.

On the other hand, the end-spurt is perfectly compatible with an effort-based decision-making model of exercise performance. When the exercise task is simple (constant-workload or incremental exercise tests to exhaustion), the goal is to last for as long as possible and the conscious decision to take is simple: do I keep going or do I stop? In these testing conditions anticipation is not necessary, and time to exhaustion is determined by two psychological factors: i) potential motivation (the maximum effort a person is willing to exert in order to satisfy a motive) and ii) perceived exertion (2-3, 5).

When the exercise task is more complex (time trials in the lab or actual endurance competitions such as the 4-mile races analysed by Noakes), the conscious decision to take is also more complex: at which speed do I run at the beginning, middle, and end* of the race? Again potential motivation and perception of effort play a major role. However, we need additional conscious information to allow for such complex decision-making process. These conscious information are iii) memory of perception of effort during previous exercise bouts of different intensities and duration, and in different environmental conditions, iv) knowledge of total distance to cover, v) knowledge of distance covered/remaining. Precise knowledge of running speed (or, in the field, running time over a certain distance) certainly helps conscious regulation of pacing, but it is not crucial because our kinaesthetic sense gives us good enough information. Conveniently, we also exclude tactical considerations and we assume that the goal (as in time trials) is to finish the race in the shortest time possible.

Because precise conscious anticipation of perceived exertion and running speed at the end of the race is not possible (and because finishing the race is paramount), athletes usually choose a slightly conservative pace for most of the race. Near the end of the race, when the information provided by the conscious sensation of effort at a certain running speed is more reliable, most “conservative” athletes realise that they can significantly increase running speed without reaching exhaustion before the finishing line, and decide to go for an end-spurt. No additional subconscious intelligent system needed, just our conscious brain.

* such simplistic tripartite subdivision is for illustration purposes only. Decisions about running speed may vary in frequency depending on tactical considerations and other factors

References

1. Marcora S. Is peripheral locomotor muscle fatigue during endurance exercise a variable carefully regulated by a negative feedback system? J Physiol. 2008; 586(7): 2027-8.

2. Marcora SM. Do we really need a central governor to explain brain regulation of exercise performance? Eur J Appl Physiol. 2008; DOI: 10.1007 s00421-008-0818-3.

3. Marcora SM, Bosio A, de Morree HM. Locomotor muscle fatigue increases cardiorespiratory responses and reduces performance during intense cycling exercise independently from metabolic stress. Am J Physiol Regul Integr Comp Physiol. 2008; 294(3): R874-83.

4. Noakes TD, Marino FE. Arterial oxygenation, central motor output and exercise performance in humans. J Physiol. 2007; 585(Pt 3): 919-21.

5. Wright RA. Refining the Prediction of Effort: Brehm’s Distinction between Potential Motivation and Motivation Intensity. Soc Pers Psychol Compass. 2008; 2(2): 682-701.