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Peer Review

What the BJSM editors look for in a paper – clinical relevance

1 Mar, 11 | by Karim Khan

BJSM is transparent about its peer-review process. We receive 1000 papers a year and can only publish about 10% of them. So 60% of papers are returned to authors after the editorial team has reviewed them. Who’s the editorial team? It’s Karim Khan, Babette Pluim and Jill Cook. So these are called ‘rejected without external review’. This should happen within a week of submission so the good news is that if the paper doesn’t look like having a chance to get into BJSM, authors have it back without delay.

Today, I’ll focus on what it takes to get through that first hurdle – to have a paper sent for external review. BJSM’s mission is to provide clinically useful material for clinicians the world over. Our summary slogan could be ‘clinically-relevant’ and ‘global/international’. Will your paper influence practice or policy in sport and exercise medicine? There are many ways to do that so we have a broad scope. Our member societies include BASEM, AMSSM, ECOSEP and the Swiss Sports Physiotherapy Association so papers should be of interest to those readers.

We are also endorsed by sports and exercise medicine societies in South Africa (SASMA), Australia and New Zealand (ACSP) so BJSM has wide reach. Our plan to focus on clinical relevance came after consultation with folks from all our member societies. We are executing a strategy which has us aiming to provide multimedia value to clinicians as they practice every day and work with active individuals in various settings. (Hence the videos and podcasts on the home page).

Sports clinicians are involved in public health so papers about physical activity and health are clearly relevant. Papers that will influence decision-makers in the field of exercise and health are also important. Data that will help teams perform better in relation to health issues are grist for the mill. But if you have a new ‘play’ in basketball that would fit better in a coaching or coaching science journals.

If you are interested in the peer-review process, see the BMJ ‘Head to Head’ (two articles, one for, one against ‘open’ peer review). Also, BJSM has a take on innovation and the problems that researchers have in challenging conventional thinking.

I’ll clarify this more about BJSM’s process in the next few days among our other blog topics. Feel free to ask questions or to comment.

Letter to the Editor: Does exercise training during pregnancy affect gestational age?

10 Sep, 08 | by Karim Khan

pregnant yoga bjsm

By Adriana Suely de Oliveira Melo, MD, MSc et al.

Barakat et al. 1 have presented us with a paper of excellent methodological quality, following all the steps recommended in the Consolidated Standards of Reporting Trials (CONSORT) and dealing with a question that never fails to generate controversy with respect to the practice of physical activity during pregnancy: prematurity. nother strong point of the paper is the fact that the physical exercise was systematized and monitored, guaranteeing that the pregnant woman indeed followed the prescribed program.

Various controversies continue to surround the topic of physical exercise and pregnancy and the real effects of exercise on the conceptus remain to be clarified. The spectrum of these effects ranges from fetal growth to the duration of the pregnancy, with some studies associating prematurity and growth restriction with the practice of physical exercise 2-4. Despite these speculations, until recently no randomized clinical trials (RCT) with adequate sample sizes had been identified in which pregnant women were systematically followed up for a period encompassing the second and third trimesters.

The excellent quality of this paper prompted us to examine it in detail in an attempt to understand some points that we would now like to put to the authors. Since the objective of the RCT was to evaluate the risk of premature labor, would it not have been better to have excluded all the pregnant women with a history of premature labor in view of the fact that the results show that one of the cases of prematurity in the intervention group was precisely due to a prior history of prematurity?

Another point that drew our attention concerns the exclusions in both groups, which were the result of various situations that may have affected the outcome “gestational age”, such as bleeding, pregnancy-induced hypertension and threatened preterm labor. In our opinion, these women should have continued in the study and an intent-to-treat analysis should have been carried out. We were also intrigued by the fact that one patient was excluded because her pregnancy was a twin pregnancy. Was a single pregnancy not one of the inclusion criteria?

It may perhaps have been interesting NOT to have included women with a history of premature delivery. Although the inclusion criteria accepted the possibility of the participants having had at the most one previous premature delivery, this may have had an effect on the mean gestational age reported in the present study.

We were unable to identify in the paper any description of the parameters used to calculate sample size to determine whether the final number of participants included was sufficient to demonstrate any
differences between the groups. Could a type II statistical error have occurred?

Another minor question we would like to pose is whether the intensity of the prescribed exercise was light-to-moderate or moderate, since it is described in different ways in the various sections of the manuscript and it is known that some outcomes are dependent on the intensity of exercise.

Finally, we would like to know whether the authors have data on other gestational or perinatal outcomes, since such a well-conducted RCT as this one should have generated interesting results that deserve to be published.

1. Barakat R, Stirling JR, Lucia A. Does exercise training during pregnancy affect gestational age? A randomised controlled trial. Br J Sports Med 2008; 42(8):674-8.

2. De Ver Dye T, Fernandez ID, Rains A, Fershteyn Z. Recent studies in the epidemiologic assessment of physical activity, fetal growth, and preterm delivery: a narrative review. Clin Obstet Gynecol 2003; 46(2):415-22.

3. Grisso JA, Main DM, Chiu G, Synder ES, Holmes JH. Effects of physical activity and life-style factors on uterine contraction frequency. Am J Perinatol 1992; 9(5-6):489-92.

4. Misra DP, Strobino DM, Stashinko EE, Nagey DA, Nanda J. Effects of physical activity on preterm birth. Am J Epidemiol 1998; 147(7):628-35.

Hot Topic: Current Anti-Doping Policies

7 Aug, 08 | by Karim Khan

legs bjsm

A recent editorial by Babette Pluim entitled, “A doping sinner is not always a cheat” [excerpt below], has created some fiery discussion amongst BJSM editors and readers this month.

The doping rules these days are really tough. The basic principle is: first offense gets a 2 year ban, second offence a lifetime ban. Everyone seems to agree that doping is cheating, and those who cheat should be sanctioned, so if an athlete provides a positive sample in any sporting situation, the inference must be that they are cheating. Unfortunately, both for the athlete and the anti-doping system, that is not always the case.

Here is a selection of BJSM editors’ & readers’ reactions:

“Drug cheats – or are they?”
By Dr Tim Wood, Chief medical officer for the Australian Open Tennis Championship and a member of Tennis Australia’s Anti-Doping Review Board

With the formation of the World Anti-Doping Agency (WADA) and the universal harmonization in the fight against the drug cheats in the late 90s everyone applauded. What we didn’t realize at the time was how many ’innocent’ victims would be caught up in the new rules and regulations. I therefore applaud Dr Babette Pluim’s BJSM editorial which reviews the positive doping cases recorded by the International Tennis Federation from 2001-07. She found that the majority of so-called ‘positive’ tests are no more than innocent mistakes by players and officials alike. Nevertheless, the trauma suffered and the tainting of these players is irreversible.

Having been involved in professional tennis for the last 7 years, I also experience frustration at the paperwork required to allow player with genuine medical conditions to take legitimate, scientifically proven drugs that certainly do not enhance performance. The most recent ‘crazy redtape’ is the requirement for a full Therapeutic Use Exemption (TUE) to allow an athlete to have intravenous fluid during elective surgery (Babette has some stories about that!).

Fortunately, it would appear that sanity may be about to prevail on at least three fronts. First, abbreviated TUEs (ATUES for those in the know, even though it sounds like a sneeze) that are currently required for intra-articular cortisone injections will be changed to notification via ADAMS (WADA’s web-based anti-doping management system). Second, ATUEs for beta-2 agonists will be valid for four years instead of needing to be renewed annually but this will come with more stringent proof of the player’s asthmatic status. And finally, many of us hope that the intravenous rule will revert to the 2007 ruling ‘… except for genuine medical situations’.

Everyone involved in professional sport strongly supports WADA and their efforts to catch the cheats but the rules shouldn’t catch innocent athletes, particularly those with genuine medical conditions.

swimmer bjsm

“WADA is on the verge of losing the plot”
By John Orchard, Sports Physician

The idea to create the World Anti-Doping Agency (WADA) was a good one, particularly for international sports. It meant that rogue states like the USA, which had a track record of going soft on their own athletes who tested positive, could be forced to implement universal sanctions.

The big problem with WADA is that it is a monopoly. And it is being run increasingly like one, currently under the Presidency of our own ex-politician John Fahey. WADA’s aim should be to stamp out cheating in sport. This is quite difficult to do, as the cheats are usually very clever. WADA instead is trying to maximise scalps of athletes who “test positive for drugs”, without apparent concern for whether they are actually cheating. Instead of concentrating only on the genuinely performance-enhancing (and usually difficult-to-detect) drugs, the WADA banned list is ever-expanding. It now includes commonly used medications which are much easier to detect and “might conceivably” be used for performance-enhancing in rare circumstances. Whether these rare circumstances exist when an athlete tests positive don’t seem faze WADA, as there is a presumption of guilt rather than innocence.

Banned medications now include asthma puffers and cortisone injections, which are generally considered by doctors and scientists to not be performing-enhancing. Intravenous fluids, including those given for an anaesthetic as part of surgery, are now also banned as of 2008. The status quo is now the farcical situation that the vast majority of athletes are breaking the WADA code whenever they go in for elective surgery. In theory, the only thing stopping these athletes from being suspended is that drug testers aren’t (yet) following them into hospitals.

An editorial just published in the British Journal of Sports Medicine found that in the last 5 years of drug testing in tennis, it was accepted that 68% of the players who were banned for positive drug tests were not actually cheating. They were banned presumably because WADA wanted to increase their tally of convictions. They include cases such as known asthmatics taking puffers such as Ventolin for asthma attacks, but whose ‘permits’ to treat their asthma with appropriate medication had either recently expired or been faxed to the wrong number. In 2009, WADA has plans that asthmatics should apply to a panel to ‘prove’ they have asthma, or else they will be banned from sport for using their puffers. The Howard government basically held the funding gun to the head of all Australian sports in 2005 and forced them to sign up to WADA, despite many sports fearing the situation we are now in. This being that the universal drug code has become draconian and the sports have signed away all rights to do anything about it.

runner bjsm

“Accidental cheating?”
By Giuseppe Lippi, Associate Professor of Clinical Biochemistry, Università di Verona

In an overview of the 40 most recent cases of doping in tennis, Babette Pluim highlighted that in only 13 of the cases (32%) was a prohibited substance taken to enhance performance, whereas most frequently banned substances were taken with no intent to enhance performance or without (significant) fault or negligence.1

I definitely agree that products that are on the list of prohibited substances should be critically reviewed, but I also emphasize that the current anti-doping policy is essentially a costly, repressive, zero tolerance approach, which seems only partly successful.2 It is also to mention, however, that there may be additional explanations to justify adverse findings on antidoping testing, which have little to do with cheating.

The use of dietary supplements is commonplace in sports, most elite athletes using some form of licit supplementation to burst athletic performance and improve recovery after training or competition. Nevertheless, there is widespread evidence that some of these legitimate products, especially those sold on the “black market”, contain banned substances that are not claimed as a result of poor manufacturing practice or adulteration.

Contaminants mostly include anabolic androgenic steroids, hormones, ephedrine and caffeine.3,4 Indeed, in some cases the adverse findings might be the consequence of deliberate cheating. However, we should still consider the possibility that some positive tests might arise from unintentional consumption of prohibited substances, contaminating dietary supplements. In this respect, not only antidoping agencies should focus on products that are truly harmful and performance-enhancing, but they should also issue a clear regulation on the use of nutritional supplements and establish appropriate bans for inadvertent use of banned molecules. Doping is always to blame, especially when the athletes use illicit methodsor substances that might produce a serious risk for their health. However, as different sanctions are imposed when crimes are intentional or preterintentional, bans should also be clearly differentiated from deliberate and unintentional positivity to banned substances.

References

1. Pluim B. A doping sinner is not always a cheat. Br J Sports Med 2008;42:549-50.

2. Kayser B, Smith AC. Globalisation of anti-doping: the reverse side of the medal. BMJ 2008 Jul 4;337:a584. doi: 10.1136/bmj.a584.

3. Maughan RJ. Contamination of dietary supplements and positive drug tests in sport. J Sports Sci 2005;23:883-9.

4. Linksvan der Merwe PJ, Grobbelaar E. Unintentional doping through the use of contaminated nutritional supplements. S Afr Med J 2005;95:510- 1.

Does an ECG screening programme for sudden cardiac death in the young result in a long term increase in cardiac mortality in the screened population?

25 Apr, 08 | by Karim Khan

A special theme issue of BJSM guest edited by Jon Drezner and Babette Pluim on the topic of sudden cardiac death in young athletes is scheduled for June 2009.

A letter from Dr. Thamindu Wedatilake, Hope Hospital, Salford, UK, related to this serious sports medicine condition:

I have read in interest the article by Wilson et al regarding their support for using an ECG in screening for sudden cardiac death in the young. Furthermore I note that there is considerable support from many sporting governing bodies for the above recommendation.

I note the comments of Dr Richard Page where he argued that in the USA alone, mass ECG screening of young athletes would exclude 2000 children from sport for every life saved.

Dr. Page’s comments have concerned me. By trying to save one life in an issue that is highly media motivated for the obvious dramatic nature of sudden cardiac death, we prison a further 2000 children to a potentially life threatening sedentary life style. Hence, ironically we may increase their risk of death from a cardiac cause later in life.

Are we really doing whats best for these children or are we dancing to the tune of the media? Have we thought about the long term repercussions that such a screening programme may have on our childrens’ physical and psychological wellbeing?

Yours/your colleagues thoughts are appreciated.

Jon Drezner replies:

Dr. Wedatilake,

You make an excellent point which was also raised by Dr. Page. Interestingly, I just gave a pro/con ECG screening Grand Rounds with Dr. Page and we looked at this question together.

The number of disqualifications and the downstream effect of limiting exercise in a subset of kids (with identified cardiovascular disease) but who may never suffer SCA is a question that needs to be investigated. I would agree that disqualifying 2000 to save 1 life may not be acceptable. What number of disqualifications is acceptable? 1000? 100? 10? I think the number of disqualifications calculated to save one life is hugely affected by 3 things: the incidence of SCD, prevalence of asymptomatic disease, and total positive (and false positive) rate of ECG screening. If you begin with traditional reported estimates (1:200,000 incidence and 15% false positive) you get about 2000 disqualifications. If you use statistics from more recent studies (1:50,000 incidence and 2-5% total positive rate), you get about 30-50 disqualifications to save a life. Unfortunately, these are all just calculations and until we have large scale studies with follow-up of those disqualified, the long-term effects will just be speculative.

BJSM Peer Review: “There is a “biologically plausible explanation” for lower supramaximal oxygen uptake”

24 Apr, 08 | by Karim Khan

BJSM peer review of Noakes’ paper, “How did A.V. Hill understand the VO2max and the “plateau phenomenon”? Still no clarity?” by Mark Burnley, Department of Sport and Exercise Science, Aberystwyth University, Wales, UK.

“There is a “biologically plausible explanation” for lower supramaximal oxygen uptake”

I read with concern the recent review of Noakes[1] accepted for publication in the journal. Noakes suggests that there is no “biologically plausible explanation” for the observation of lower oxygen uptake (VO2) values in supramaximal exercise compared to incremental exercise.[2] Noakes further argues that those supramaximal data are therefore questionable and should be excluded, thus resulting in the conclusions of the original authors being disproved. Noakes’ first assertion (biological implausibility) is incorrect. His second assertion is at best biased, and at worst could be viewed as endorsing unethical practices.

The observation of lower VO2 values at exhaustion during supramaximal exercise could be attributed to normal biological variation (random error). However, the kinetics of VO2 dictates the rate at which VO2 rises to meet the energetic demand. In situations where exhaustion occurs before the kinetics drive VO2 to the maximum (so-called “extreme intensity exercise”[3]), VO2 will be lower than that measured in an incremental test performed to exhaustion. The boundary between “severe intensity exercise” (wherein VO2 reaches VO2max before exercise termination) and “extreme exercise” has been estimated to be ~110-135% VO2max,[3,4] providing the “biologically plausible explanation” Noakes wishes to deny.

To argue exclusion of the supramaximal data is ethically troubling.

Such exclusion, in this case solely for the purpose of interpretation, results in grossly biased conclusions. For any scientist, particularly one as influential as Noakes, to adopt such an approach does a disservice to students of exercise science. It would be tragic indeed
if these impressionable proto-scientists use Noakes’ precedence to endorse unethical data manipulation techniques to promote their own subjective opinions. Accordingly, I call upon Noakes to retract these statements to prevent further misleading interpretations from entering the literature.

References

1. Noakes TD. Peer review/fair review: How did A.V. Hill understand the VO2max and the “plateau phenomenon”? Still no clarity? Brit J Sports Med, in press. DOI: 10.1136/bjsm.2008.046771.

2. Hawkins MN, Raven PD, Snell PG, Stray-Gundersen J, Levine BD. Maximal oxygen uptake as a parametric parameter of cardiorespiratory capacity. Med Sci Sports Exerc. 2007;39:103-107.

3. Hill DW, Poole DC, Stevens JC. The relationship between power and the time to achieve VO2max. Med Sci Sports Exerc. 2002;34:709-714.

4. Wilkerson DP, Koppo K, Barstow TJ, Jones AM. Effect of work rate on the functional ‘gain’ of Phase II pulmonary O2 uptake response to exercise. Respir Physiol Neurobiol. 2004;142: 211-223.

Noakes response to Dr Burnley.

Dr Mark Burnley makes an important point. He is correct. No one has the right selectively to analyze data. Whilst I appreciate that this is how what I wrote can be interpreted, that was never my meaning (as should be apparent from the general gist of my argument).

The point I repeatedly make is that the “truth” in exercise science is so often model-dependant since few people actually bother to measure all the variables that comprise their particular model. Thus the basis for the Hill model (which I believe to be incorrect) is the use of oxygen consumption, measured at the mouth, as a surrogate measure of cardiac output and the state of muscle oxygenation during exercise. This model predicts that when the cardiac output reaches its maximum value, (“anaerobic”) conditions develop in the muscle which then cause the termination of exercise. If this is the case, then the cardiac output and hence the oxygen consumption and the state of muscle oxygenation must always be IDENTICAL at exhaustion. If this is not the case, then the model does not explain what is actually causing exhaustion.

So my argument is that if the oxygen consumption is not always exactly the same at exhaustion during maximum exercise testing, then the model has to be rather more complex than is this simple explanation we have inherited from Hill. Better stated, my point was that “submaximal” VO2max values must, according to the Hill model, indicate that exercise terminated before the maximal cardiac output and maximum levels of muscle de-oxygenation were achieved. But since this cannot happen according to the Hill model (since it is these two variables which cause exhaustion), the data are not compatible with his model and thus disprove it. In this sense it is my argument that those data cannot LOGICALLY be included in the analysis if their inclusion modifies the data suffficiently to “prove” a theory with which those specific data are actually incompatible. It was in this sense that I argued that the data should be LOGICALLY excluded from analysis since their inclusion led to the incorrect conclusion. Of course anyone wedded to the Hill model will find it difficult to follow this logic.

Dr Burnley may be one such person for he believes that exhaustion at submaximal VO2 values occurs before the “kinetics drive the VO2 to its maximum’. But how does the Hill model explain such exhaustion? Stating that it occurs because limiting “anaerobic” conditions develop in muscle even before the cardiac output reaches its maximum value is convenient but is ultimately unsatisfactory since it is again a model-dependant explanation. Would it not be better if defenders of this interpretation actually measured cardiac output and skeletal muscle oxygenation and not just their model-dependant surrogate – oxygen consumption at the mouth? The simulaneous measurement of muscle activation would be essential in my view if one wishes to test the alternate (central governor) theory that maximal exercise always terminates before there is 100% activation of all the available motor units in the exercising limbs.

However I am relieved that Dr Burnley does not find fault with the remainder of this quite long review. Does this mean that he accepts the logic of my argument that the regulation of maximal exercise performance must reside in the central nervous system?

Or what does he mean by the loaded phrase “further misleading interpretations from entering the literature”? To which other “misleading interpretations” does he refer?

Mark Burnley’s RESPONSE to Dr Noakes:

I now better appreciate Prof. Noakes’ reasons for using the words he used following his response to my eletter posted on the BJSM Blog, and consider the issue of “data exclusion” settled. However, I would like to make the following points to clarify my position and respond to Noakes’ interpretation of the physiology:

1. I do not consider myself “wedded to the Hill model” because the “Hill model” as presented by Noakes bears no relationship to my understanding of the physiological response to exercise. It is my contention that the “Hill model” is an erroneous caricature of the physiology of exercise that Noakes uses as a straw man in contrast to his central governor model. Few scientists are likely to defend the view that cardiac output and VO2 must always be identical at exhaustion, for the evidence against this proposition is overwhelming! In short, the “Hill model” is not a contemporary model of exercise physiology, it is a vehicle invented by Noakes.

2. “Oxygen consumption” or, more correctly, pulmonary oxygen uptake, is not a “surrogate measure of cardiac output and the state of muscle oxygenation”. To claim this indicates a misunderstanding or misrepresentation of basic physiological measurements. Pulmonary VO2 is useful because in both the non-steady state and the steady state it closely reflects muscle VO2, which itself reflects energetic events occurring in the cell. If one accepts that the rate of energy transfer is an important consideration during exercise, then measuring the most quantitatively significant energy transfer process is worthwhile. Furthermore, the phrase “state of muscle oxygenation” is hopelessly vague. Does Noakes mean “muscle O2 extraction”, “arterio-venous oxygen difference” or “intracellular [or mitochondrial] PO2”? The first two measures are difficult to make, whilst the latter is currently impossible to make during whole-body exercise.

3. I do not “believe” that exhaustion occurs before VO2max is attained during “extreme” exercise, it is an experimental fact: exercise is terminated whilst VO2 is still rising in a futile attempt to meet the energetic demand.[1] Exercise under these conditions is terminated because the subject is no longer able to sustain the power requirements of the task (in my experience not because the subject is unwilling), but this says little of the mechanism. Classic works on the aetiology of muscle fatigue acknowledge that fatigue processes occur at a number of sites within the neuromuscular system,[2,3] and I certainly embrace this. Exhaustion at these “extreme” work rates is attended by falling [PCr] and pH and rising [Pi] and [ADP], amongst other derangements known to cause a fall in tension produced by the myocyte.[4] However, measurements of these processes in whole-body exercise are presently too spatially or temporally crude to be definitive – but that is certainly not a reason to reject the periphery as a plausible or even pivotal contributor to task failure (exhaustion). Note also that the identification of metabolites involved in substrate-level phosphorylation does not imply that the conditions within the cell are “anaerobic”: the concentrations of these metabolites will change progressively during exercise above the so-called “critical power”[5] irrespective of cellular PO2.[6]

4. Noakes argues that the “simulaneous [sic] measurement of muscle activation” is required to test the alternate (central governor) theory “that maximal exercise always terminates before there is 100% activation of all the available motor units in the exercising limbs”. However, this is impossible to verify with current technology. Even if electromyographic recordings are taken from the surface of a large number of muscles and normalised to some measure of maximal voluntary muscle function (such as an MVC), this will not provide an estimate of the fractional number of motor units that are active. The EMG signal is determined, in part, by the number of active muscle fibres in the region of interrogation, their firing frequency, and the conductivity of the tissues between the fibres and the electrodes, not simply by the number of active motor units. A method of determining the total number of active motor units during whole-body exercise would be very useful but does not currently exist.

The processes leading to additional motor unit recruitment during rhythmic whole-body exercise are far from understood. However, it is logical that in conditions where the rate of O2 delivery is maximal (i.e., when cardiac output is maximal) the recruitment of additional motor units will lead to worsening metabolic conditions within the exercising muscles, as those newly recruited fibres will also extract O2 from the microvasculature. The consequent fall in microvascular PO2 will make the appropriate matching of O2 demand and supply (essential for the continuance of exercise) increasingly difficult. Additional motor unit recruitment is thus likely to yield diminishing returns in terms of sustaining the required power output. In this scenario, task failure will occur before all motor units are activated even in the absence of a “governor”.

In summary, Prof. Noakes’ representation of the physiology of exercise could be charitably described as inaccurate. The “Hill model” is not one that any physiologist is “wedded” to because it does not exist. Therein lay the “misleading interpretations” to which I referred in my first letter. One final point needs to be made:

If the “absence of any such catastrophe [myocardial ischaemia or rigor during exercise] suggests the presence of an anticipatory, complex, regulatory control system”[7], then surely the presence of myocardial ischaemia during exercise[8] suggests the absence of an anticipatory, complex regulatory control system? How long can the central governor theory survive with this elephant in the room?

“It does not make any difference how beautiful your guess is. It does not make any difference how smart you are, who made the guess, or what his name is – if it disagrees with experiment it’s wrong. That’s all there is to it.” Richard P. Feynman.

References

1. Hill DW, Poole DC, Stevens JC. The relationship between power and the time to achieve VO2max. Med Sci Sports Exerc. 2002;34:709-714

2. Bigland-Ritchie B, Woods JJ. Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle Nerve. 1984;7:691-699.

3. Gandevia SC. Spinal and supraspinal factors in human muscle fatigue. Physiol Rev. 2001;81:1725-1789.

4. Fitts RH. The cross-bridge cycle and skeletal muscle fatigue. J Appl Physiol. 2008;104:551-558.

5. Jones AM, Wilkerson DP, DiMenna F, Fulford J, Poole DC. Muscle metabolic responses to exercise above and below the “critical power” assessed using 31-PMRS. Am J Physiol Regul Integr Comp Physiol. 2008;294:R585-R593.

6. Richardson RS, Newcomer SC, Noyszewski EA. Skeletal muscle intracellular PO2 assessed by myoglobin desaturation: response to graded exercise. J Appl Physiol. 2001;91:2679-2685.

7. Noakes TD. Peer review/fair review: How did A.V. Hill understand the VO2max and the “plateau phenomenon”? Still no clarity? Brit J Sports Med, in press. DOI: 10.1136/bjsm.2008.046771.

8. Bogaty P, Poirier P, Boyer L, Jobin J, Dagenais GR. What induces the warm-up ischemia/angina phenomenon: exercise or myocardial ischemia? Circulation. 2003;107:1858-1863.

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