We read with interest the recent International Olympic Committee consensus statement: methods for recording and reporting of epidemiological data on injury and illness in sport 2020 (including STROBE Extension for Sport Injury and Illness Surveillance (STROBE-SIIS))”.[1] While helping to clarify aspects associated with recording and reporting epidemiological data, based on the definitions included in the statement, we believe that some of the examples in Table 10 require clarification with regards to the recording of injuries and calculation of time loss.
Consider the example for ‘Delayed’ time loss: Sunday injury, thigh contusion, able to train on Monday and Tuesday but unable to train on Wednesday and returns on Sunday (time loss starts on Wednesday even though the injury was on Sunday). Time loss (days) 3. Given the recommended reported time loss of 3-days, and definition provided whereby “time-loss days should be counted from the day after the onset that the athlete is unable to participate”, we assume Wednesday is considered as the day of onset (day 0), with subsequent impact on Thursday, Friday and Saturday resulting in a 3-day time-loss (days). When considering this example, we were then somewhat confused by the example for, ‘Intermittent’ time loss: boy with Osgood-Schlatter disease that gets reported at the start of a training camp on Monday. The player may train fully on Monday, Tuesday and Thursday, but miss training on Wednesday and Friday (time loss co...
We read with interest the recent International Olympic Committee consensus statement: methods for recording and reporting of epidemiological data on injury and illness in sport 2020 (including STROBE Extension for Sport Injury and Illness Surveillance (STROBE-SIIS))”.[1] While helping to clarify aspects associated with recording and reporting epidemiological data, based on the definitions included in the statement, we believe that some of the examples in Table 10 require clarification with regards to the recording of injuries and calculation of time loss.
Consider the example for ‘Delayed’ time loss: Sunday injury, thigh contusion, able to train on Monday and Tuesday but unable to train on Wednesday and returns on Sunday (time loss starts on Wednesday even though the injury was on Sunday). Time loss (days) 3. Given the recommended reported time loss of 3-days, and definition provided whereby “time-loss days should be counted from the day after the onset that the athlete is unable to participate”, we assume Wednesday is considered as the day of onset (day 0), with subsequent impact on Thursday, Friday and Saturday resulting in a 3-day time-loss (days). When considering this example, we were then somewhat confused by the example for, ‘Intermittent’ time loss: boy with Osgood-Schlatter disease that gets reported at the start of a training camp on Monday. The player may train fully on Monday, Tuesday and Thursday, but miss training on Wednesday and Friday (time loss counted as Wednesday and Friday only). Time loss (days) 2. Herein, applying the time-loss definition provided in the consensus statement [1] and the logic applied to the delayed time loss example, should the Wednesday not be considered as the onset of time loss and therefore counted as day 0? Based on the two examples and the time-loss (days) provided for each we feel as if time-loss (days) has been calculated differently and as such wish for the authors to clarify. From our position we agree with recording time-loss from the day after the injury when the injury occurs during training on that day, but if an athlete is unable to participate at all due to injury we feel as if this could be considered day 1 of time-loss.
In relation to the above examples it is also unclear as to why these have been considered as single injury reports (cases) given the definitions provided within the consensus statement, “subsequent injuries to the same location and tissue as the index injury are recurrences if the index injury was healed/fully recovered; they are exacerbations if the index injury was not yet healed/fully recovered”, when healed/fully recovered is when an “athlete is fully available for training and competition”.[1] Herein, for the delayed time loss and intermittent time loss examples we would interpret that the injury examples should be considered as multiple injury reports (cases). For delayed time loss, the first case would open following the initial injury on the Sunday and close when the athlete is considered healed/fully recovered, when they return to full training Monday, before a subsequent recurrence on the Wednesday, second case open, which closes on the Sunday (Figure 1a). Similarly for intermittent time loss, it seems that the initial case opens with the initial injury report Monday, closes when the athlete trained fully Monday, second injury case opens on Wednesday as the athlete is unable to train and closes Thursday upon full return to training, before another case opens on the Friday (Figure 1b).
INSERT FIGURE 1A AND 1B ABOUT HERE
Moreover, if the intermittent time loss example should in fact be considered as multiple injury reports (cases), based on time-loss methods suggested within the paper, both Wednesday and Friday would be considered as the onset of time loss and counted as day 0. Therefore, although the athlete missed two days of training, 0 time loss (days) would be calculated (Figure 1b). As a result such an approach for calculating time loss may lead to underreporting. We feel as if this supports our view that an athlete reporting injured at the start of training (and does not participate at all), incurs the first day of time loss and in this example results in two 1-day time-loss events linked to two subsequent injury reports (cases).
It is not our intention to challenge the authors and indeed the updated consensus statements has provided valuable recommendations for injury surveillance. Additionally, we are pleased to see the inclusion of examples within the paper as in our areas of research such examples are a regular occurrence. However, based on the two examples provided, we feel that there are discrepancies with regards to the calculation of time-loss (days) and a lack of clarity surrounding injury recording, specifically with respect to what keeps an injury report (case) open (delayed and intermittent time loss examples). We therefore ask the authors to consider clarification on each point we raise in this letter.
References
Bahr R, Clarsen B, Derman W, et al. International Olympic Committee consensus statement: methods for recording and reporting of epidemiological data on injury and illness in sport 2020 (including STROBE Extension for Sport Injury and Illness Surveillance (STROBE-SIIS)). Br J Sports Med Published Online First: 18 February 2020. doi: 10.1136/bjsports-2019-101969
Figure Descriptions
Figure 1: Injury examples from the International Olympic Committee consensus statement, with the inclusion of injury cases and associated time loss (days), based on the healed/fully recovered and time loss (days) definitions provided.
Tables and Figures
Figure available upon reasonable request
The Australian Sports Drug Medical Advisory Committee (ASDMAC) and Drug Free Sport New Zealand (DFSNZ) Therapeutic Use Exemption (TUE) committees welcome the recent discussion paper by our esteemed colleague Dr Ken Fitch entitled "Therapeutic Use Exemptions (TUEs) are essential in sport: but there is room for improvement." As the national bodies responsible for TUE assessment and processing in our respective nations, ASDMAC and DFSNZ agree that the integrity of the TUE process is sound and essential, but could be improved through a peer review process.
Although the World Anti-Doping Agency (WADA) does screen TUEs entered in Anti-Doping Administration and Managements System (ADAMS), the supplementary screening of TUE Committees themselves, including the members, their TUE processes and procedures, as suggested by Dr Fitch would improve the reliability and standardisation of TUEs. In 2018 and 2019, ASDMAC and DFSNZ with the support of the World Anti-Doping Agency (WADA) TUE expert group designed and conducted a TUE Peer Review Audit. This process included the documentation of the proposed audit process, followed by the respective visits of each Chair to the others TUEC meeting. During the visits the Chairs assessed a number of TUE applications and outcomes to ensure that those granted were done so in accordance with the WADA ISTUE and that the WADA Medical Information to Support TUEC decisions had been appropriately interpreted. These visits also includ...
The Australian Sports Drug Medical Advisory Committee (ASDMAC) and Drug Free Sport New Zealand (DFSNZ) Therapeutic Use Exemption (TUE) committees welcome the recent discussion paper by our esteemed colleague Dr Ken Fitch entitled "Therapeutic Use Exemptions (TUEs) are essential in sport: but there is room for improvement." As the national bodies responsible for TUE assessment and processing in our respective nations, ASDMAC and DFSNZ agree that the integrity of the TUE process is sound and essential, but could be improved through a peer review process.
Although the World Anti-Doping Agency (WADA) does screen TUEs entered in Anti-Doping Administration and Managements System (ADAMS), the supplementary screening of TUE Committees themselves, including the members, their TUE processes and procedures, as suggested by Dr Fitch would improve the reliability and standardisation of TUEs. In 2018 and 2019, ASDMAC and DFSNZ with the support of the World Anti-Doping Agency (WADA) TUE expert group designed and conducted a TUE Peer Review Audit. This process included the documentation of the proposed audit process, followed by the respective visits of each Chair to the others TUEC meeting. During the visits the Chairs assessed a number of TUE applications and outcomes to ensure that those granted were done so in accordance with the WADA ISTUE and that the WADA Medical Information to Support TUEC decisions had been appropriately interpreted. These visits also included meetings with other members of the National Anti-Doping Organisation (NADO) such as the TUE Secretariat and other staff in leadership and education roles. The entire process was presented and discussed at the WADA TUE Expert Group meetings.
Having conducted this peer review, ASDMAC and DFSNZ TUEC would commend this process to all NADO and International Federation (IF) TUECs. There is great potential to use this Peer Review process to ensure the quality and transparency in granting elite athlete TUEs around the world and across nations and sports, as well as supporting smaller, less experienced TUECs to establish robust processes in their work as TUE Committees. The universal adoption of a TUEC peer review process would be beneficial to all organisations involved in anti-doping and to athletes and sports to whom the integrity of the TUE process reflects the integrity of sport and performance itself.
In the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries (Figure 1) impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [1-3] and ultimately myocardial infarction (MI) and death.
In recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have taken advantage of the obesity epidemic and focused everyone’s attention on obesity and weight loss. These individuals have not determined the actual impact their diets have on CAD - which would require more than just looking at changes in weight or serum blood tests. It would require measurement of changes occurring within the walls of the coronary arteries themselves – not some other artery - and the resulting change in coronary artery function [1,4].
These individuals, including Dr. Aseem Malhotra [5] support their dietary recommendations by showing weight loss, and occasionally reductions in cholesterol levels – at least initially in some people. Over the years as it has been shown that cholesterol levels fail to fall, and frequently increase on such diets, their argument has changed and has been replaced with “...
In the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries (Figure 1) impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [1-3] and ultimately myocardial infarction (MI) and death.
In recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have taken advantage of the obesity epidemic and focused everyone’s attention on obesity and weight loss. These individuals have not determined the actual impact their diets have on CAD - which would require more than just looking at changes in weight or serum blood tests. It would require measurement of changes occurring within the walls of the coronary arteries themselves – not some other artery - and the resulting change in coronary artery function [1,4].
These individuals, including Dr. Aseem Malhotra [5] support their dietary recommendations by showing weight loss, and occasionally reductions in cholesterol levels – at least initially in some people. Over the years as it has been shown that cholesterol levels fail to fall, and frequently increase on such diets, their argument has changed and has been replaced with “saturated fat does not clog the (coronary or other) arteries” [5].
We argue that the claim by Malhotra, and others -- that saturated fat and LDL-cholesterol have nothing to do with the development of inflammatory CAD – demonstrates a complete failure to understand the “Inflammation and Heart Disease” Theory [3,6] as shown in Figure 1 and therefore cannot be taken seriously.
Their claims introduce yet another major misconception into the discussion of CAD. Specifically, the process of “clogging of the coronary arteries.” The narrowing or “clogging” of the coronary artery lumen – where the blood flows - so frequently referred to as CAD, is actually a late process in the development of the inflammatory changes that are CAD [7-13].
CAD begins with the inflammatory process first distending the wall of the artery outward away from the lumen – impairing the function of the artery - and only later encroaching upon the lumen itself [1,3,7]. Recognition that the rupture of this inflammatory process may occur following minimal or no coronary lumen narrowing [1,3,7] has resulted in the recent acknowledgement by the Cardiology community that infarction of myocardium may occur with (Type I) or without (TYPE II) coronary lumen obstruction.
Fleming and Harrington’s work – published in 2008 [14] - demonstrated that the relationship between weight loss, and changes in lipids and other blood tests reflecting inflammatory processes [3], are only mildly-to-moderately correlated (Figure 2) with actual changes occurring within the coronary arteries themselves. Thus further exposing the erroneous statement - using the results of blood tests - declaring that saturated fat and cholesterol are not involved in CAD.
To understand the impact LowCarb-Keto diets - or for that matter any diet - has on CAD, one needs to measure what is happening to the coronary arteries themselves [15-17] by using FMTVDM.
To state that Saturated fat and LDL-cholesterol has nothing to do with CAD and do not result in the “clogging” of coronary arteries, and then to state that CAD is a chronic inflammatory condition - raises serious concerns about the motivation of their arguments. It also raises serious questions about their actual understanding of the ”Inflammation and Heart Disease” Theory. To which we acknowledge, “we can teach it to you but we cannot understand it for you.”
Acknowledged potential COI: FMTVDM (The Fleming Method for Tissue and Vascular Differentiation and Metabolism) [4] is issued to the first author. The first author authored the Inflammation and Heart Disease and Angina Theories.
RM Fleming and Matthew R Fleming, FHHI-OI-Camelot
TK Chaudhuri, Eastern Virginia Medical School.
Figures available upon reasonable request:
Figure 1. Fleming Inflammation and Heart Disease Theory first introduced in the 1990s [3].
Figure 2. Changes in weight loss and serum markers of lipids and other inflammatory blood tests correlate only mildly-to-moderately with actual measured changes in coronary artery disease [14].
References:
1. Fleming RM. Chapter 29. Atherosclerosis: Understanding the relationship between coronary artery disease and stenosis flow reserve. Textbook of Angiology. John C. Chang Editor, Springer-Verlag, New York, NY. 1999. pp. 381-387.
2. Fleming RM. Chapter 30. Cholesterol, Triglycerides and the treatment of hyperlipidemias. Textbook of Angiology. John C. Chang Editor, Springer-Verlag, New York, NY. 1999, pp. 388-396.
3. Fleming RM. Chapter 64. The Pathogenesis of Vascular Disease. Textbook of Angiology. John C. Chang Editor, Springer-Verlag New York, NY. 1999, pp. 787-798.
4. The Fleming Method for Tissue and Vascular Differentiation and Metabolism (FMTVDM) using same state single or sequential quantification comparisons. Patent Number 9566037. Issued 02/14/2017.
5. Malhotra A, Redberg R, Meier P. Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions. British J Sports Med 2017;51:1111-1112.
6. 20/20 Segment on Heart Disease and Inflammation. https://www.youtube.com/watch?v=Hvb_Ced7KyA&t=22s
7. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316(22):1371-1375.
8. Fleming RM., Kirkeeide RL, Smalling RW, Gould KL. Patterns in Visual Interpretation of Coronary Arteriograms as Detected by Quantitative Coronary Arteriography. J Am Coll. Cardiol. 1991;18:945- 951.
9. Fleming RM, Harrington GM. Quantitative Coronary Arteriography and its Assessment of Atherosclerosis. Part 1. Examining the Independent Variables. Angiology 1994;45(10):829-833.
10. Fleming RM, Harrington GM. Quantitative Coronary Arteriography and its Assessment of Atherosclerosis. Part 2. Calculating Stenosis Flow Reserve Directly from Percent Diameter Stenosis. Angiology 1994;45(10):835-840.
11. Fleming RM. Shortcomings of coronary angiography. Letter to the Editor. Cleve Clin J Med 2000;67:450.
12. Fleming RM. Coronary Artery Disease is More than Just Coronary Lumen Disease. Amer J Card 2001;88:599-600.
13. Fleming RM, Harrington GM. TAM-A.7 Sestamibi redistribution measurement defines ischemic coronary artery lumen disease. 56th Annual Meeting of the Health Physics Society. (American Conference of Radiological Safety) West Palm Beach, FL, USA, 30 June 2011. http://hpschapters.org/2011AM/program/singlesession.php3?sessid=TAM-A
14. Fleming RM, Harrington GM. What is the Relationship between Myocardial Perfusion Imaging and Coronary Artery Disease Risk Factors and Markers of Inflammation? Angiology 2008;59:16-25.
15. Fleming RM, Fleming MR, Chaudhuri TK. Replacing Cardiovascular Risk Factors with True AI and Absolute Quantifiable Measurement (FMTVDM) of Coronary Artery Disease. Inter J Res Studies Med & Health Sci. 2019;4(11):11- 13. ISSN:2456-6373.
16. Fleming RM, Fleming MR, Chaudhuri TK. Are we prescribing the right diets and drugs for CAD, T2D, Cancer and Obesity? Int J Nuclear Med Radioactive Subs 2019;2(2):000115.
17. Fleming RM, Fleming MR, Chaudhuri TK, Harrington GM. Cardiovascular Outcomes of Diet Counseling. Edel J Biomed Res Rev. 2019;1(1):20-29.
We read the referenced article by Chisholm et al.1 with keen interest. Concussions present a significant injury burden on the athletic community, especially among youth athletes who are more susceptible to potential long-term consequences.3,7,9 Concussion diagnosis and treatment are important, but prevention is key. Chisholm and colleagues present data on young athletes that supports a reduction in the risk of concussion with the use of a mouthguard. However, the authors admit that the current literature on mouthguards has methodological limitations and high risk of bias. The primary objective of their study was to examine the association between concussion and mouthguard use in youth ice hockey.
We agree with the benefit players derive from wearing mouthguards to protect dentition and possibly reduce the incidence and/or severity of concussion during contact sports. However, we question the statistical methodology performed and the resultant conclusions of the manuscript. The authors utilized a nested case-control design to determine the risk of concussion with mouthguard use. Due to this design utilization, the results potentially present a high risk of bias that the authors were attempting to avoid. A nested case-control design compares incident cases nested in a cohort study with controls drawn at random from the rest of the cohort.2,6 Further, a nested case-control is useful for summarizing the trends observed in a large population when study of the e...
We read the referenced article by Chisholm et al.1 with keen interest. Concussions present a significant injury burden on the athletic community, especially among youth athletes who are more susceptible to potential long-term consequences.3,7,9 Concussion diagnosis and treatment are important, but prevention is key. Chisholm and colleagues present data on young athletes that supports a reduction in the risk of concussion with the use of a mouthguard. However, the authors admit that the current literature on mouthguards has methodological limitations and high risk of bias. The primary objective of their study was to examine the association between concussion and mouthguard use in youth ice hockey.
We agree with the benefit players derive from wearing mouthguards to protect dentition and possibly reduce the incidence and/or severity of concussion during contact sports. However, we question the statistical methodology performed and the resultant conclusions of the manuscript. The authors utilized a nested case-control design to determine the risk of concussion with mouthguard use. Due to this design utilization, the results potentially present a high risk of bias that the authors were attempting to avoid. A nested case-control design compares incident cases nested in a cohort study with controls drawn at random from the rest of the cohort.2,6 Further, a nested case-control is useful for summarizing the trends observed in a large population when study of the entire population would be too expensive or burdensome with relatively minor loss in statistical efficiency.6
The authors utilized two databases that total 2,355 youth hockey players. Based on a relatively small cohort, a complete case-control study would have been more appropriate than a nested case-control study. Table 1 shows that only n=270 players were used as controls and n=315 were used as cases. This represents only 25% of the cohort, since 1,770 players were excluded. The authors stated, “Cases were defined as those who sustained a suspected concussion during a game or practice. Controls were players who sustained a non-concussion (e.g. trunk or extremity orthopaedic) injury.” Consequently, this selection criteria of the non-concussion group biased the study as a random sample was not selected from the remaining cohort (n=2,040). In effect, the authors eliminated from the analysis all non-injured players who wore mouthguards. These non-injured controls are a factor in the non-concussed group, regardless of whether they wore a mouthguard. Thus, the reported odds ratio is very favorable (64% less likely). Although the primary objective was to examine the association between concussion and mouthguard use, the analysis compared concussion to other orthopaedic injuries. It did not properly compare the incidence of concussion between wearers or non-wearers of mouthguards. Clearly, many of the excluded participants (n=1,770) wore a mouthguard who did not suffer a concussion or any other orthopaedic injury. Consequently, there is likely significant error in the results reported. Furthermore, common practice with controls in a case-control or even a nested case-control is to use a subject ratio of 2:1 or 4:12,5 to allow for adequate statistical power and elimination of bias. The study in question did not adhere to these ratio paradigms.
Perhaps the authors did not have accurate data on the cohort of non-injured players (n= 1,770) that did or did not wear a mouthguard, especially due to the retrospective study design. However, it may be possible to estimate mouthguard compliance among youth players and use the estimated trends for all control subjects. This adds an additional limitation to the study, but would permit a sampling of the entire population (n=2,355) and more appropriately address the original objective of the manuscript.
To properly establish evidence of causality (in this case, wearing a mouthguard to reduce concussion incidence), results from various study designs must demonstrate: 1) consistency, 2) strength of association, and 3) biologic plausibility.6 Based on the results (biased in our opinion), the authors suggested three potential mechanisms of how mouthguards could reduce concussion incidence among young hockey players to establish biologic plausibility. Two of three mechanisms involve mandibular impacts. Although impacts to the mandible occur, they are not the most common mechanism of injury for concussion.3,4,8,10–12 Even a video analysis of Taekwondo (in which mandibular contact would be more common), only 12.1% of concussions were caused from contact to the mandible.8 Chisholm et al. stated that biomechanical modelling research is needed to better inform the mechanism by which mouthguards protect players from concussion, but the authors subsequently cited an article that used an instrumented artificial mandible skull model tested with and without a mouthguard that demonstrated no differences in head injury criterion.13 Thus, the theory they posited for mandible directed impacts is not sufficiently supported with consistency or biologic plausibility.
We ask the authors, who are recognized leaders in epidemiology of injury research, to address the significant bias inherent in their current nested case-control. A corrigendum would be appropriate which performs a full case-control analysis on the data to include the remaining n=1,770 individuals. A report of these outcomes on the full, unbiased cohort would be ideal for the published literature.
REFERENCES
1. Chisholm DA, Black AM, Palacios-Derflingher L, et al. Mouthguard use in youth ice hockey and the risk of concussion: Nested case-control study of 315 cases. Br J Sports Med. 2020:1-6. doi:10.1136/bjsports-2019-101011.
2. Ernster VL. Nested Case-Control Studies. Prev Med (Baltim). 1994;23(5):587-590. doi:10.1006/pmed.1994.1093.
3. Haarbauer-Krupa J, Arbogast KB, Metzger KB, et al. Variations in Mechanisms of Injury for Children with Concussion. J Pediatr. 2018;197:241-248.e1. doi:10.1016/j.jpeds.2018.01.075.
4. Hendricks S, O’Connor S, Lambert M, et al. Video analysis of concussion injury mechanism in under-18 rugby. BMJ Open Sport Exerc Med. 2016;2(1):e000053. doi:10.1136/bmjsem-2015-000053.
5. Hennessy S, Bilker WB, Berlin JA, Strom BL. Factors influencing the optimal control-to-case ratio in matched case- control studies. Am J Epidemiol. 1999;149(2):195-197.
6. Hulley SB, Commings SR, Browner WS, Grady DG, Newman TB. Designing Clinical Research. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2013.
7. Kamins J, Bigler E, Covassin T, et al. What is the physiological time to recovery after concussion? A systematic review. Br J Sports Med. 2017;51(12):935-940. doi:10.1136/bjsports-2016-097464.
8. Koh JO, Watkinson EJ, Yoon YJ. Video analysis of head blows leading to concussion in competition Taekwondo. Brain Inj. 2004;18(12):1287-1296. doi:10.1080/02699050410001719907.
9. Langlois, Jean A. Scd M, Wesley Rytland-Brown M, Marlena M Wald, MLS M. The Epidemiology and Impact of Traumatic Brain Injury. J Head Trauma Rehabil. 2006;21(5):375-378.
10. McIntosh AS, McCrory P, Comerford J. The dynamics of concussive head impacts in rugby and Australian rules football. Med Sci Sports Exerc. 2000;32(12):1980-1984. doi:10.1097/00005768-200012000-00002.
11. Rowson S, Duma SM, Stemper BD, et al. Correlation of Concussion Symptom Profile with Head Impact Biomechanics: A Case for Individual-Specific Injury Tolerance. J Neurotrauma. 2018;35(4):681-690. doi:10.1089/neu.2017.5169.
12. Sobin L, Kopp R, Walsh R, Kellman RM, Harris T. Incidence of concussion in patients with isolated mandible fractures. JAMA Facial Plast Surg. 2016;18(1):15-18. doi:10.1001/jamafacial.2015.1339.
13. Viano DC, Withnall C, Wonnacott M. Effect of mouthguards on head responses and mandible forces in football helmet impacts. Ann Biomed Eng. 2012;40(1):47-69. doi:10.1007/s10439-011-0399-x.
As part of this excellent summary editorial, you mentioned how important it is to tailor your education to the needs and preferences of the patient. Therapists also have these diverse needs so it would be an excellent resource to have this in a graphical format that could be displayed openly in any department, whether it be in Outpatients or in physiotherapy for example as a visual reminder to clinicians but also visible for patients to interrogate so that they can have an understanding of what is to be expected in their consultation and by creating these expectations, will help to drive forward better, more holistic assessment and care of patients.
We congratulate O’Keeffe et al. [1] for their research on the comparative efficacy of Cognitive Functional Therapy (CFT) and physiotherapist-delivered group-based exercise and education for individuals with chronic low back pain (CLBP). Their study shows that “CFT can reduce disability, but not pain, at 6 months compared with the group-based exercise and education intervention”. The CFT approach is very promising and has caught the attention and interest of a number of clinicians worldwide in the management of non‐specific disabling CLBP. The study by O’Keeffe et al. [1] has methodological strengths compared to a previous clinical trial by Vibe Fersum et al. [2,3] such as a higher sample size which means it is less vulnerable to type-II error. Nonetheless, some shortcomings threaten substantially the risk of bias and type I error that are worthy of further discussion.
The first is the choice of three physiotherapists for delivering both interventions in this trial. This aspect was considered by O’Keeffe et al. [1] as a strength of the study because it arguably minimized differences in clinicians’ expertise and communication style. Notwithstanding, this fact could also have decreased the treatment effect on the control group. It is important to remember that the trial was performed by the research group that not only developed CFT but also has trained the physiotherapists on such an approach, and thus the enthusiasm and motivation to apply the intervention on the CFT...
We congratulate O’Keeffe et al. [1] for their research on the comparative efficacy of Cognitive Functional Therapy (CFT) and physiotherapist-delivered group-based exercise and education for individuals with chronic low back pain (CLBP). Their study shows that “CFT can reduce disability, but not pain, at 6 months compared with the group-based exercise and education intervention”. The CFT approach is very promising and has caught the attention and interest of a number of clinicians worldwide in the management of non‐specific disabling CLBP. The study by O’Keeffe et al. [1] has methodological strengths compared to a previous clinical trial by Vibe Fersum et al. [2,3] such as a higher sample size which means it is less vulnerable to type-II error. Nonetheless, some shortcomings threaten substantially the risk of bias and type I error that are worthy of further discussion.
The first is the choice of three physiotherapists for delivering both interventions in this trial. This aspect was considered by O’Keeffe et al. [1] as a strength of the study because it arguably minimized differences in clinicians’ expertise and communication style. Notwithstanding, this fact could also have decreased the treatment effect on the control group. It is important to remember that the trial was performed by the research group that not only developed CFT but also has trained the physiotherapists on such an approach, and thus the enthusiasm and motivation to apply the intervention on the CFT group could have been considerably greater. Likewise, if the physiotherapists providing the group-based exercise were not involved in any kind of CFT training and had a strong belief in their intervention, one can argue that the performance of the latter group could have been better. Also, the CFT group received the intervention for an average (SD) of 13.7 (10.9) weeks, while the comparison group received treatment for just 4.4 (2.4) weeks. The same therapist applying both interventions combined with the longer period of the CFT group treatment may have generated performance bias.
The second is the unblinded assessment of the outcomes immediately postintervention. Since CFT therapists had more one-to-one time with each patient and therefore had more opportunities to enhance the therapeutic alliance, this could have influenced patients’ behavior when filling the outcome assessment questionnaires in their presence, arguably not only in the postintervention assessment but also in the blinded follow up periods at 6 and 12-months.
Third, apparently, the authors were not concerned with the multiple primary outcomes (n = 2; pain and disability) and endpoints (n = 4; at 8-14 weeks; 6, 12 and 36 months). The problem of multiple testing is that the overall type-I (false positive) error is much greater than 5%. Assuming a true null hypothesis for all the 6 (independent) effects being tested, the probability that no false positives occur in 6 tests equals (0.95)^6 and hence the probability that at least one false positive occurs is 1–(0.95)^6 = 0.26. This also highlights a discrepancy regarding the primary outcomes between the pre-registered trial protocol on ClinicalTrial.gov (https://clinicaltrials.gov/ct2/show/NCT02145728) and the published protocol by the same authors in 2015 [4]. Notably, O’Keeffe et al. [1] gave up on the postintervention follow up results, which was a primary outcome according to the pre-registered protocol. Therefore, it is mandatory to discuss this aspect and to reduce the number of primary outcomes in future studies, if possible, to 1; in this case, disability at 6 months after randomization would have been recommended.
Finally, 37% of the participants were lost to follow up in the first primary outcome endpoint (postintervention), 28% of loss of follow up on the second primary outcome endpoint (6 months), and 31% on the third (12 months). Although the unmeasured bias was recognized by O’Keeffe et al. [1], it seems that there is a systematic high loss of follow up in CFT clinical trials conducted by the research group of the developers of the method. Similarly to the first trial of Vibe Fersum et al. [2], this trial did not provide high quality evidence about the efficacy of CFT and should be considered as an exploratory study, not confirmatory enough to generate recommendation. Therefore, the next CFT trials should focus on improving the methodological quality. It is recommended that future studies avoid a loss of follow up higher than 15%, blind the assessors, establish up to 2 primary outcomes, and special attention be paid to the quality and duration of the treatment provided to the comparison group.
References
1 O’Keeffe M, O’Sullivan P, Purtill H, et al. Cognitive functional therapy compared with a group-based exercise and education intervention for chronic low back pain: a multicentre randomised controlled trial (RCT). Br J Sports Med 2019;:bjsports-2019-100780. doi:10.1136/bjsports-2019-100780
2 Vibe Fersum K, O’Sullivan P, Skouen JS, et al. Efficacy of classification-based cognitive functional therapy in patients with non-specific chronic low back pain: a randomized controlled trial. Eur J Pain 2013;17:916–28. doi:10.1002/j.1532-2149.2012.00252.x
3 Fersum KV, Smith A, Kvåle A, et al. Cognitive Functional Therapy in patients with Non Specific Chronic Low Back Pain A randomized controlled trial 3-year follow up. Eur J Pain 2019;:ejp.1399. doi:10.1002/ejp.1399
4 O’Keeffe M, Purtill H, Kennedy N, et al. Individualised cognitive functional therapy compared with a combined exercise and pain education class for patients with non-specific chronic low back pain: study protocol for a multicentre randomised controlled trial. BMJ Open 2015;5:e007156. doi:10.1136/bmjopen-2014-007156
Here is my simple response to this absurd proposal. If drugs help those who are not as genetically advantaged to be more competitive with those who are, shall we prohibit the genetically advantaged from taking them? Otherwise, you create the situation where all athletes must take these drugs just to maintain the status quo. Athletes who prefer not to use drugs would suffer the most. Since drug use monitoring will be required anyway for safety, let's prohibit their use as much as possible. Allowing their use only benefits the pharmaceutical companies who sell the drugs. Sports would becomes less about athletic ability and more about who can come up with the best drug formula for competitive success.
Dear editor,
We have read with great interest the article by Wheeler et al1 showing distinct effects of exercise with and without breaks in sitting on cognition. In this study, they also demonstrated that both activity conditions increase serum brain-derived neurotrophic growth factor (BDNF) levels. Although we highly appreciate the efforts of the authors to explore potential mechanisms, we suggest that the followings need to be addressed.
BDNF is an important member of the neurotrophic factors family which enhances neuronal development and plasticity. It is synthesized as the N-glycosylated precursor (brain-derived neurotrophic factor precursor, proBDNF), and secreted into cell matrix processed by Golgi complex. Additionally, BDNF is a novel kind of myokines produced by skeletal muscle after the muscle contraction immediately. Hayashi and coworkers2 observed that both exercise and electrical muscle stimulation could increase the mRNA and protein expression of BDNF in skeletal muscle of rats. In addition, exercise could also enhance gene expression of BDNF and other neuroprotective factors in hippocampus via peroxisome proliferator-activated receptor gamma coactivator-1α-fibronectin type III domain-containing protein 5/irisin (PGC-1α-FNDC5/irisin) pathway.3
BDNF has been reported to play a pivotal role in the improvement of learning and memory function, which might be associated with the phosphorylation of tropomyosin-related kinase B (TrkB) in cognitive-...
Dear editor,
We have read with great interest the article by Wheeler et al1 showing distinct effects of exercise with and without breaks in sitting on cognition. In this study, they also demonstrated that both activity conditions increase serum brain-derived neurotrophic growth factor (BDNF) levels. Although we highly appreciate the efforts of the authors to explore potential mechanisms, we suggest that the followings need to be addressed.
BDNF is an important member of the neurotrophic factors family which enhances neuronal development and plasticity. It is synthesized as the N-glycosylated precursor (brain-derived neurotrophic factor precursor, proBDNF), and secreted into cell matrix processed by Golgi complex. Additionally, BDNF is a novel kind of myokines produced by skeletal muscle after the muscle contraction immediately. Hayashi and coworkers2 observed that both exercise and electrical muscle stimulation could increase the mRNA and protein expression of BDNF in skeletal muscle of rats. In addition, exercise could also enhance gene expression of BDNF and other neuroprotective factors in hippocampus via peroxisome proliferator-activated receptor gamma coactivator-1α-fibronectin type III domain-containing protein 5/irisin (PGC-1α-FNDC5/irisin) pathway.3
BDNF has been reported to play a pivotal role in the improvement of learning and memory function, which might be associated with the phosphorylation of tropomyosin-related kinase B (TrkB) in cognitive-related brain regions. BDNF and its specific receptor TrkB are widely expressed in the animal neural tissues. After binding to TrkB, BDNF could activate mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K), and phospholipase C-γ (PLC-γ), thereby eliciting a protective effect on neurons.4 Moreover, BDNF could also enhance long-term potentiation (LTP) via regulating synaptic transmission,4 and the lack or dysfunction of BDNF would be accompanied by severe impairments in learning and memory function.
Very recently, proBDNF, previously considered as a transitional form, could be directly secreted into cell matrix without being cleaved, possessing physiologic functions that are distinct from mature BDNF.5 ProBDNF could specifically bind to p75 neurotrophin receptor (p75NTR), a member of tumor necrosis factor receptor superfamily, and activate c-Jun amino terminal kinase (JNK) pathway to up-regulate p53 expression, finally leading to apoptosis.5 Importantly, proBDNF could also impair the learning and memory function by affecting neurotransmitter release and inhibiting axonal outgrowth.5 However, further studies have indicated that the major pro-apoptotic signal stimulated by proBDNF-p75NTR would be largely suppressed by activation of BDNF-TrkB and the downstream signaling.4 More interestingly, p75NTR could promote the efficacy of BDNF-TrkB signaling, thus improving neuronal survival.4 A study by Luo et al6 suggested that aerobic exercise could increase BDNF/proBDNF ratio, and relatively inhibit the proBDNF-p75NTR pathway, which exerts a protective action against apoptosis.
Taken together, exercise could activate BDNF expression not only in skeletal muscle but also in brain, which might be conducive to enhance BDNF-trkB-mediated neuroprotective pathways and inhibit proBDNF-p75NTR-mediated pro-apoptotic response, finally improving cognitive function. Further detailed studies on this field are greatly needed.
Competing interests
None declared.
Contributions
All the authors conceived the scientific ideas, critically reviewed, approved the final version.
Provenance and peer review
Not commissioned; externally peer reviewed.
Finding sources
This work was supported by grants from the Program of Bureau of Science and Technology Foundation of Changzhou (CJ20179028), Major Science and Technology Project of Changzhou Municipal Commission of Health and Family Planning (ZD201407, ZD201505, ZD201601) and "333 Project" (BRA2016122) of Jiangsu Province.
REFERENCES
1 Wheeler MJ, Green DJ, Ellis KA, et al. Distinct effects of acute exercise and breaks in sitting on working memory and executive function in older adults: a three-arm, randomised cross-over trial to evaluate the effects of exercise with and without breaks in sitting on cognition. Br J Sports Med 2019.
2 Hayashi N, Himi N, Nakamura-Maruyama E, et al. Improvement of motor function induced by skeletal muscle contraction in spinal cord-injured rats. Spine J 2019;19:1094-105.
3 Wrann CD. FNDC5/irisin - their role in the nervous system and as a mediator for beneficial effects of exercise on the brain. Brain Plast 2015;1:55-61.
4 Kowianski P, Lietzau G, Czuba E, et al. BDNF: A Key Factor with Multipotent Impact on Brain Signaling and Synaptic Plasticity. Cell Mol Neurobiol 2018;38:579-93.
5 Chen J, Zhang T, Jiao S, et al. proBDNF Accelerates Brain Amyloid-beta Deposition and Learning and Memory Impairment in APPswePS1dE9 Transgenic Mice. J Alzheimers Dis 2017;59:941-9.
6 Luo L, Li C, Du X, et al. Effect of aerobic exercise on BDNF/proBDNF expression in the ischemic hippocampus and depression recovery of rats after stroke. Behav Brain Res 2019;362:323-31.
The BJSM recently rejected our request of retraction or errata corrige of the editorials by Blanch and Gabbett(1) and Gabbett (2) presenting the relation between the Acute:Chronic Workload Ratio (ACWR) and likelihood of injuries. The preprint and a list of some of the errors presented in that figure can be found here: https://osf.io/preprints/sportrxiv/gs8yu/. In challenging our request, it was underlined several times by the Editor in Chief of BJSM that the “model” was presented as illustrative only, and this seems to make errors acceptable like if the editorials are a “safe zone” where for illustrative purposes it is possible to bend and even break scientific rules and methods, presenting models using unpublished and uncontrollable data.
However, the reason of this communication is to warn the members of the consensus (and readers) that the ACWR model published in the IOC consensus(3) as a validated model has in fact not been validated at all: [page 1034] “The model has currently been validated through data from three different sports (Australian football, cricket and rugby league)(187)”. The reference 187 is one of the two editorials(1) for which we asked the retraction. So on one side the Editor in Chief insists that it is just an illustrative (flawed) model, but on the other side the same Editor in Chief, co-author (with one of the proponents of the model) of the IOC consensus wrote and published that it...
The BJSM recently rejected our request of retraction or errata corrige of the editorials by Blanch and Gabbett(1) and Gabbett (2) presenting the relation between the Acute:Chronic Workload Ratio (ACWR) and likelihood of injuries. The preprint and a list of some of the errors presented in that figure can be found here: https://osf.io/preprints/sportrxiv/gs8yu/. In challenging our request, it was underlined several times by the Editor in Chief of BJSM that the “model” was presented as illustrative only, and this seems to make errors acceptable like if the editorials are a “safe zone” where for illustrative purposes it is possible to bend and even break scientific rules and methods, presenting models using unpublished and uncontrollable data.
However, the reason of this communication is to warn the members of the consensus (and readers) that the ACWR model published in the IOC consensus(3) as a validated model has in fact not been validated at all: [page 1034] “The model has currently been validated through data from three different sports (Australian football, cricket and rugby league)(187)”. The reference 187 is one of the two editorials(1) for which we asked the retraction. So on one side the Editor in Chief insists that it is just an illustrative (flawed) model, but on the other side the same Editor in Chief, co-author (with one of the proponents of the model) of the IOC consensus wrote and published that it was a validated model. There is something of great concern here. The publication of this figure in your consensus has given that model the credit it does not deserve. Other than not being validated, the errors in developing that figure are evident and I am sure the members can easily realize this by reading the original editorials proposing the model in the first place or by reading the problems in our request of retraction or errata. I believe that the consensus members gave too much credit to some participants involved in the consensus that proposed the model as validated. I further underline that the ACWR model you have presented also shows that if you taper before a competition or you complete a recovery week (i.e. you are outside the “sweet spot”), you are at higher risk of injuries. This is, unfortunately, an exemplificative “practical” translation of one part of the model you have contributed (unknowingly) to be popularized through including it in a consensus statement. The problem is that the metric (ACWR) is also deceptive and the members probably did not realize the meaning and hence interpretation of the ratio and figure. Furthermore, the ACWR-injury relation it is not established and in the literature various and contrasting relations can be found. Clearly more studies, hopefully with lower risk of bias, are needed. Therefore, since I value your contribution to better science and evidence-based recommendations, it would be appreciated to know whether at least the IOC panel will acknowledge and advise the reader the fact that the model has not been validated and potentially misleading.
References
1. Blanch P, Gabbett TJ. Has the athlete trained enough to return to play safely? The acute:chronic workload ratio permits clinicians to quantify a player's risk of subsequent injury. Br J Sports Med 2016;50(8):471-5. doi: 10.1136/bjsports-2015-095445
2. Gabbett TJ. The training-injury prevention paradox: should athletes be training smarter and harder? Br J Sports Med 2016;50(5):273-80. doi: 10.1136/bjsports-2015-095788
3. Soligard T, Schwellnus M, Alonso JM, et al. How much is too much? (Part 1) International Olympic Committee consensus statement on load in sport and risk of injury. Br J Sports Med 2016;50(17):1030-41. doi: 10.1136/bjsports-2016-096581
Thank you for your thorough response to my initial comment.
I am wondering if you could help me understand the new AE-level as-treated analysis you have done in response to Point 2. This accounts for all non-compliant AEs among all athletes, correct? If I understood you correctly, there were somewhat more than the 711 non-compliant AEs reported in the paper and which you reported in your response to Point 4, correct?
What would be very helpful to see is a.) the number of AEs and b.) the number of SRCs that occurred during those AEs for each of the following groups when considering any non-compliant AE, not just ones from athletes who suffered an SRC while non-compliant or were non-compliant >50% of the time:
Assigned HG/Did Not Wear:
Assigned HG/Did Wear:
Assigned No HG/Did Not Wear:
Assigned No HG/Did Wear:
We read with interest the recent International Olympic Committee consensus statement: methods for recording and reporting of epidemiological data on injury and illness in sport 2020 (including STROBE Extension for Sport Injury and Illness Surveillance (STROBE-SIIS))”.[1] While helping to clarify aspects associated with recording and reporting epidemiological data, based on the definitions included in the statement, we believe that some of the examples in Table 10 require clarification with regards to the recording of injuries and calculation of time loss.
Consider the example for ‘Delayed’ time loss: Sunday injury, thigh contusion, able to train on Monday and Tuesday but unable to train on Wednesday and returns on Sunday (time loss starts on Wednesday even though the injury was on Sunday). Time loss (days) 3. Given the recommended reported time loss of 3-days, and definition provided whereby “time-loss days should be counted from the day after the onset that the athlete is unable to participate”, we assume Wednesday is considered as the day of onset (day 0), with subsequent impact on Thursday, Friday and Saturday resulting in a 3-day time-loss (days). When considering this example, we were then somewhat confused by the example for, ‘Intermittent’ time loss: boy with Osgood-Schlatter disease that gets reported at the start of a training camp on Monday. The player may train fully on Monday, Tuesday and Thursday, but miss training on Wednesday and Friday (time loss co...
Show MoreThe Australian Sports Drug Medical Advisory Committee (ASDMAC) and Drug Free Sport New Zealand (DFSNZ) Therapeutic Use Exemption (TUE) committees welcome the recent discussion paper by our esteemed colleague Dr Ken Fitch entitled "Therapeutic Use Exemptions (TUEs) are essential in sport: but there is room for improvement." As the national bodies responsible for TUE assessment and processing in our respective nations, ASDMAC and DFSNZ agree that the integrity of the TUE process is sound and essential, but could be improved through a peer review process.
Although the World Anti-Doping Agency (WADA) does screen TUEs entered in Anti-Doping Administration and Managements System (ADAMS), the supplementary screening of TUE Committees themselves, including the members, their TUE processes and procedures, as suggested by Dr Fitch would improve the reliability and standardisation of TUEs. In 2018 and 2019, ASDMAC and DFSNZ with the support of the World Anti-Doping Agency (WADA) TUE expert group designed and conducted a TUE Peer Review Audit. This process included the documentation of the proposed audit process, followed by the respective visits of each Chair to the others TUEC meeting. During the visits the Chairs assessed a number of TUE applications and outcomes to ensure that those granted were done so in accordance with the WADA ISTUE and that the WADA Medical Information to Support TUEC decisions had been appropriately interpreted. These visits also includ...
Show MoreIn the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries (Figure 1) impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [1-3] and ultimately myocardial infarction (MI) and death.
Show MoreIn recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have taken advantage of the obesity epidemic and focused everyone’s attention on obesity and weight loss. These individuals have not determined the actual impact their diets have on CAD - which would require more than just looking at changes in weight or serum blood tests. It would require measurement of changes occurring within the walls of the coronary arteries themselves – not some other artery - and the resulting change in coronary artery function [1,4].
These individuals, including Dr. Aseem Malhotra [5] support their dietary recommendations by showing weight loss, and occasionally reductions in cholesterol levels – at least initially in some people. Over the years as it has been shown that cholesterol levels fail to fall, and frequently increase on such diets, their argument has changed and has been replaced with “...
We read the referenced article by Chisholm et al.1 with keen interest. Concussions present a significant injury burden on the athletic community, especially among youth athletes who are more susceptible to potential long-term consequences.3,7,9 Concussion diagnosis and treatment are important, but prevention is key. Chisholm and colleagues present data on young athletes that supports a reduction in the risk of concussion with the use of a mouthguard. However, the authors admit that the current literature on mouthguards has methodological limitations and high risk of bias. The primary objective of their study was to examine the association between concussion and mouthguard use in youth ice hockey.
We agree with the benefit players derive from wearing mouthguards to protect dentition and possibly reduce the incidence and/or severity of concussion during contact sports. However, we question the statistical methodology performed and the resultant conclusions of the manuscript. The authors utilized a nested case-control design to determine the risk of concussion with mouthguard use. Due to this design utilization, the results potentially present a high risk of bias that the authors were attempting to avoid. A nested case-control design compares incident cases nested in a cohort study with controls drawn at random from the rest of the cohort.2,6 Further, a nested case-control is useful for summarizing the trends observed in a large population when study of the e...
Show MoreAs part of this excellent summary editorial, you mentioned how important it is to tailor your education to the needs and preferences of the patient. Therapists also have these diverse needs so it would be an excellent resource to have this in a graphical format that could be displayed openly in any department, whether it be in Outpatients or in physiotherapy for example as a visual reminder to clinicians but also visible for patients to interrogate so that they can have an understanding of what is to be expected in their consultation and by creating these expectations, will help to drive forward better, more holistic assessment and care of patients.
We congratulate O’Keeffe et al. [1] for their research on the comparative efficacy of Cognitive Functional Therapy (CFT) and physiotherapist-delivered group-based exercise and education for individuals with chronic low back pain (CLBP). Their study shows that “CFT can reduce disability, but not pain, at 6 months compared with the group-based exercise and education intervention”. The CFT approach is very promising and has caught the attention and interest of a number of clinicians worldwide in the management of non‐specific disabling CLBP. The study by O’Keeffe et al. [1] has methodological strengths compared to a previous clinical trial by Vibe Fersum et al. [2,3] such as a higher sample size which means it is less vulnerable to type-II error. Nonetheless, some shortcomings threaten substantially the risk of bias and type I error that are worthy of further discussion.
The first is the choice of three physiotherapists for delivering both interventions in this trial. This aspect was considered by O’Keeffe et al. [1] as a strength of the study because it arguably minimized differences in clinicians’ expertise and communication style. Notwithstanding, this fact could also have decreased the treatment effect on the control group. It is important to remember that the trial was performed by the research group that not only developed CFT but also has trained the physiotherapists on such an approach, and thus the enthusiasm and motivation to apply the intervention on the CFT...
Show MoreHere is my simple response to this absurd proposal. If drugs help those who are not as genetically advantaged to be more competitive with those who are, shall we prohibit the genetically advantaged from taking them? Otherwise, you create the situation where all athletes must take these drugs just to maintain the status quo. Athletes who prefer not to use drugs would suffer the most. Since drug use monitoring will be required anyway for safety, let's prohibit their use as much as possible. Allowing their use only benefits the pharmaceutical companies who sell the drugs. Sports would becomes less about athletic ability and more about who can come up with the best drug formula for competitive success.
Dear editor,
Show MoreWe have read with great interest the article by Wheeler et al1 showing distinct effects of exercise with and without breaks in sitting on cognition. In this study, they also demonstrated that both activity conditions increase serum brain-derived neurotrophic growth factor (BDNF) levels. Although we highly appreciate the efforts of the authors to explore potential mechanisms, we suggest that the followings need to be addressed.
BDNF is an important member of the neurotrophic factors family which enhances neuronal development and plasticity. It is synthesized as the N-glycosylated precursor (brain-derived neurotrophic factor precursor, proBDNF), and secreted into cell matrix processed by Golgi complex. Additionally, BDNF is a novel kind of myokines produced by skeletal muscle after the muscle contraction immediately. Hayashi and coworkers2 observed that both exercise and electrical muscle stimulation could increase the mRNA and protein expression of BDNF in skeletal muscle of rats. In addition, exercise could also enhance gene expression of BDNF and other neuroprotective factors in hippocampus via peroxisome proliferator-activated receptor gamma coactivator-1α-fibronectin type III domain-containing protein 5/irisin (PGC-1α-FNDC5/irisin) pathway.3
BDNF has been reported to play a pivotal role in the improvement of learning and memory function, which might be associated with the phosphorylation of tropomyosin-related kinase B (TrkB) in cognitive-...
The BJSM recently rejected our request of retraction or errata corrige of the editorials by Blanch and Gabbett(1) and Gabbett (2) presenting the relation between the Acute:Chronic Workload Ratio (ACWR) and likelihood of injuries. The preprint and a list of some of the errors presented in that figure can be found here: https://osf.io/preprints/sportrxiv/gs8yu/. In challenging our request, it was underlined several times by the Editor in Chief of BJSM that the “model” was presented as illustrative only, and this seems to make errors acceptable like if the editorials are a “safe zone” where for illustrative purposes it is possible to bend and even break scientific rules and methods, presenting models using unpublished and uncontrollable data.
However, the reason of this communication is to warn the members of the consensus (and readers) that the ACWR model published in the IOC consensus(3) as a validated model has in fact not been validated at all: [page 1034] “The model has currently been validated through data from three different sports (Australian football, cricket and rugby league)(187)”. The reference 187 is one of the two editorials(1) for which we asked the retraction. So on one side the Editor in Chief insists that it is just an illustrative (flawed) model, but on the other side the same Editor in Chief, co-author (with one of the proponents of the model) of the IOC consensus wrote and published that it...
Show MoreDear Drs. McGuine, Hetzel, and Kliethermes,
Thank you for your thorough response to my initial comment.
I am wondering if you could help me understand the new AE-level as-treated analysis you have done in response to Point 2. This accounts for all non-compliant AEs among all athletes, correct? If I understood you correctly, there were somewhat more than the 711 non-compliant AEs reported in the paper and which you reported in your response to Point 4, correct?
What would be very helpful to see is a.) the number of AEs and b.) the number of SRCs that occurred during those AEs for each of the following groups when considering any non-compliant AE, not just ones from athletes who suffered an SRC while non-compliant or were non-compliant >50% of the time:
Assigned HG/Did Not Wear:
Assigned HG/Did Wear:
Assigned No HG/Did Not Wear:
Assigned No HG/Did Wear:
Thank you again for your thorough response.
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