We read the recent publication by Nathan, Davies & Swaine (2018) with great interest due to a mutual interest in the subject of Generalised Joint Hypermobility (GJH) and its influence on injuries within elite sport. The authors of this paper should be commended for undertaking a study with such good participant numbers over a range of sports. We believe that the findings of this study suggesting that GJH may be protective of joint ligament damage may be a very important initial paper leading to valuable further exploration within specific sports and specific joints. However despite this good work we would like to take the opportunity to raise a concern over one of their conclusions and how this may confuse readers of the article.
In the discussion section of this paper Nathan et al. (2018) suggest that the findings of this study may suggest that “regular stretching may increase flexibility, and this could subsequently reduce rates of injury in those that are less flexible.” We believe that this statement may lead to misunderstanding as the terms “flexibility” and “joint hypermobility” are two completely different entities.
GJH is a hereditary physiological entity whereby most synovial joints move beyond their normal limits (Pacey et al., 2010) and may, or may not be symptomatic. This entity is commonly classified by the use of the Beighton Scale, as in the Nathan et al. (2018) paper, whereby adult participants are deemed positive i...
We read the recent publication by Nathan, Davies & Swaine (2018) with great interest due to a mutual interest in the subject of Generalised Joint Hypermobility (GJH) and its influence on injuries within elite sport. The authors of this paper should be commended for undertaking a study with such good participant numbers over a range of sports. We believe that the findings of this study suggesting that GJH may be protective of joint ligament damage may be a very important initial paper leading to valuable further exploration within specific sports and specific joints. However despite this good work we would like to take the opportunity to raise a concern over one of their conclusions and how this may confuse readers of the article.
In the discussion section of this paper Nathan et al. (2018) suggest that the findings of this study may suggest that “regular stretching may increase flexibility, and this could subsequently reduce rates of injury in those that are less flexible.” We believe that this statement may lead to misunderstanding as the terms “flexibility” and “joint hypermobility” are two completely different entities.
GJH is a hereditary physiological entity whereby most synovial joints move beyond their normal limits (Pacey et al., 2010) and may, or may not be symptomatic. This entity is commonly classified by the use of the Beighton Scale, as in the Nathan et al. (2018) paper, whereby adult participants are deemed positive if they score five or more out of nine on the scale (Juul-Kristensen et al., 2017). The term flexibility however would commonly be recognised as the length of the muscle crossing the joint. It is suggested that within the paper the term “flexible joint” is overused, and the correct terminology should be “lax joint” as this would more closely match the fact that the authors are looking to further understand the influence of joint hypermobility.
We would suggest concluding that greater flexibility would decrease injury risk means the authors are misleading readers. It would be hypothesised that the decreased risk of injury within the ankle for example, may come from the ability of the athlete to enter ranges of inversion without stressing the passive ligamentous structures of the ankle which is thought to be in part due to the abnormal ratio of mobile type III collagen in hypermobile participants (Child, 1986). Flexibility of the muscles around the ankle joint is unlikely to provide a protective effect in this position. It is also worth noting that the terminology in the paper suggests that rates of joint sprains are lower in hypermobile participants highlights the fact that the authors were looking at ligamentous injury, and not muscular pathologies. It is unlikely that a stretching protocol would be able to influence the mobility of the passive ligamentous structures to such a degree that they would subsequently be classed as hypermobile, and therefore potentially at decreased risk of injury.
We would again like to highlight that this piece of work by Nathan et al. (2018) is a very important piece in the early stages are trying to better understand the influence of GJH upon injury risk. It is hoped that greater utilisation of the Lower Limb Assessment Score in sports where lower limb pathologies are most common may be able to assist in addressing the impact on practice suggestions from the authors.
References
Child, A.H. (1986). Joint hypermobility syndrome: Inherited disorder of collagen synthesis. The Journal of Rheumatology, 13(2), 239-243.
Juul-Kristensen, B., Schmedling, K., Rombaut, L., Lund, H. & Engelbert, R.H.H. (2017). Measurement properties of clinical assessment methods for classifying generalized joint hypermobility- A systematic review. American Journal of Medical Genetics Part C (Seminars in Medical Genetics), 175C, 116-147.
Nathan, J.A., Davies, K. & Swaine, I. (2018). Hypermobility and sports injury. BMJ Open Sport & Exercise Medicine, 4.
Pacey, V., Nicholson, L.L., Adams, R.D., Munn, J. & Munns, C.F. (2010). Generalized Joint Hypermobility and Risk of Lower Limb Joint Injury During Sport: A Systematic Review with Meta-Analysis. The American Journal of Sports Medicine, 38(7), 1487-1497.
We read with great interest the systematic review by Joschtel et al.1 on the effects exercise training on physical and psychological health in children with pediatric respiratory diseases such as asthma, bronchiectasis, bronchopulmonary dysplasia and cystic fibrosis (CF). Undoubtedly, the authors should be commended for their effort that they have put into this systematic review on an important research topic. However, we would like to take the opportunity to express some methodological concerns related to the CF studies included in this review.
Joschtel et al.1 included studies on children, adolescents and young adults aged between 4 and 21 years and excluded those with a study population mean age of 21 years. These contradictory criteria have led to a false inclusion of one study 2 that included patients aged 12-40 years (although with a mean (SD) age of 19.5 (6.4) and 19.4 (5.3) for the intervention and control groups, respectively). Other studies 3 4, in which the mean age of the participants is <21 years were not considered for this review. Specifically, 3 out of 4 groups from the Kriemler et al. study 3 would qualify to be included in this review. Joschtel et al.1 did not publish a review protocol and therefore pre-specified inclusion and exclusion criteria cannot be verified.
Joschtel et al.1 have conducted a meta-analysis on peak oxygen uptake (VO2peak), despite substantial heterogeneity of study characteristics (i.e., study...
We read with great interest the systematic review by Joschtel et al.1 on the effects exercise training on physical and psychological health in children with pediatric respiratory diseases such as asthma, bronchiectasis, bronchopulmonary dysplasia and cystic fibrosis (CF). Undoubtedly, the authors should be commended for their effort that they have put into this systematic review on an important research topic. However, we would like to take the opportunity to express some methodological concerns related to the CF studies included in this review.
Joschtel et al.1 included studies on children, adolescents and young adults aged between 4 and 21 years and excluded those with a study population mean age of 21 years. These contradictory criteria have led to a false inclusion of one study 2 that included patients aged 12-40 years (although with a mean (SD) age of 19.5 (6.4) and 19.4 (5.3) for the intervention and control groups, respectively). Other studies 3 4, in which the mean age of the participants is <21 years were not considered for this review. Specifically, 3 out of 4 groups from the Kriemler et al. study 3 would qualify to be included in this review. Joschtel et al.1 did not publish a review protocol and therefore pre-specified inclusion and exclusion criteria cannot be verified.
Joschtel et al.1 have conducted a meta-analysis on peak oxygen uptake (VO2peak), despite substantial heterogeneity of study characteristics (i.e., study durations ranged from <3 weeks up to 3 years; comparison of supervised versus non-supervised studies using different training modalities in different settings etc). Excluding the Hebestreit et al.2 study, which does not meet the age inclusion criterion of 4 to 21 years, the effects on VO2peak became smaller [standardized mean difference (SMD) 0.77 mL.kg-1.min-1 95% CI 0.25 to 1.29 versus 0.70 mL.kg-1.min-1 95% CI 0.12 to 1.29]. Further, it could be argued that the in-hospital trial by Selvadurai et al.5, in which children were treated for an acute infectious pulmonary exacerbation, is not comparable with the other studies in a meta-analysis, where children were treated as outpatients and those in unstable clinical condition were excluded. If this study is also excluded, the effects on VO2peak are no longer existent (SMD 0.77 mL.kg-1.min-1 95% CI 0.25 to 1.29 versus SMD 0.54 mL.kg-1.min-1 95% CI -0.04 to 1.12).
The authors1 also did a meta-analysis on health-related quality of life (HRQoL) in patients with asthma and CF and concluded that their analysis shows “a large significant effect size for HRQoL (SMD 1.36, 95% CI 0.42 to 2.30)” and that “exercise training significantly improves HRQoL in children with asthma and CF”. It is important to note that the meta-analysis for CF was based on two small-sized studies (n=22 and n=20) from the same research group 6 7, of which one study showed a statistically significant result in favor of exercise training. The authors of the original publications assessed HRQoL with the validated Cystic Fibrosis Questionnaire (CFQ-R) - the younger children ( 11 years) were interviewed and children >12 years completed the questionnaire themselves. In both original studies, no statistically significant effects were reported for HRQoL after exercise training.6 7 The authors of the two studies reported pre- and post median (min, max) values for the exercise and control groups, respectively. We could not reproduce the HRQoL data in the forest plot (Figure 4) by Joschtel et al.1 following Cochrane handbook instructions (as the authors report using for their analysis) for the conversion of median (ranges) into mean (standard deviation) values.
Finally, systematic reviews aim to provide patients and healthcare professionals with the best available evidence on a specific topic and are used to guide healthcare decisions. However, conclusions drawn from systematic reviews (and meta-analysis) that are based on questionable methodology and non-reproducible data are unlikely to be helpful for either patients or healthcare professionals.
References
1. Joschtel B, Gomersall SR, Tweedy S, et al. Effects of exercise training on physical and psychosocial health in children with chronic respiratory disease: a systematic review and meta-analysis. BMJ Open Sport Exerc Med 2018;4(1):e000409.
2. Hebestreit H, Kieser S, Junge S, et al. Long-term effects of a partially supervised conditioning programme in cystic fibrosis. Eur Respir J 2010;35:578-83.
3. Kriemler S, Kieser S, Junge S, et al. Effect of supervised training on FEV1 in cystic fibrosis: A randomised controlled trial. J Cyst Fibros 2013;12:714-20.
4. Del Corral T, Cebria IIMA, Lopez-de-Uralde-Villanueva I, et al. Effectiveness of a Home-Based Active Video Game Programme in Young Cystic Fibrosis Patients. Respiration 2018;95:87-97.
5. Selvadurai HC, Blimkie CJ, Meyers N, et al. Randomized controlled study of in-hospital exercise training programs in children with cystic fibrosis. Pediatr Pulmonol 2002;33:194-200.
6. Santana Sosa E, Groeneveld IF, Gonzalez-Saiz L, et al. Intrahospital weight and aerobic training in children with cystic fibrosis: a randomized controlled trial. Med Sci Sports Exerc 2012;44:2-11.
7. Santana-Sosa E, Gonzalez-Saiz L, Groeneveld IF, et al. Benefits of combining inspiratory muscle with 'whole muscle' training in children with cystic fibrosis: a randomised controlled trial. Br J Sports Med 2014;48:1513-7.
We read with great interest the recently published article by Tibana and de Sousa (1) titled “Are extreme conditioning programmes effective and safe? A narrative review of high intensity functional training methods research paradigms and findings.” We appreciate the opportunity to write this letter and hope to clarify some of the authors’ conclusions. Although the authors provide several examples of what they refer to as “extreme conditioning programs” we will focus mainly on the statements and evidence related to High Intensity Functional Training (HIFT), more commonly known as CrossFitTM training, as the authors’ review focuses primarily on this particular training program. We feel the authors have taken a biased position in describing this type of training and that their position is based on inaccurate and highly speculative interpretations of a fraction of the existing literature.
Research examining the acute and long-term responses to HIFT, as well as the incidence of injury, is quite limited. The observed responses predominantly describe changes from baseline and in the case of long-term adaptations, generally show a positive outcome. Further, the few studies that make comparisons to other exercise forms only show select differences. More importantly, by the authors’ own admission, research examining the risk of injury do not suggest HIFT/CrossFitTM to be different from other forms of recreational exercise. Yet, the authors descri...
We read with great interest the recently published article by Tibana and de Sousa (1) titled “Are extreme conditioning programmes effective and safe? A narrative review of high intensity functional training methods research paradigms and findings.” We appreciate the opportunity to write this letter and hope to clarify some of the authors’ conclusions. Although the authors provide several examples of what they refer to as “extreme conditioning programs” we will focus mainly on the statements and evidence related to High Intensity Functional Training (HIFT), more commonly known as CrossFitTM training, as the authors’ review focuses primarily on this particular training program. We feel the authors have taken a biased position in describing this type of training and that their position is based on inaccurate and highly speculative interpretations of a fraction of the existing literature.
Research examining the acute and long-term responses to HIFT, as well as the incidence of injury, is quite limited. The observed responses predominantly describe changes from baseline and in the case of long-term adaptations, generally show a positive outcome. Further, the few studies that make comparisons to other exercise forms only show select differences. More importantly, by the authors’ own admission, research examining the risk of injury do not suggest HIFT/CrossFitTM to be different from other forms of recreational exercise. Yet, the authors describe this risk as “alarming” and “becoming more prevalent.” We certainly agree that additional research is needed on this popular form of exercise, but at this time, and based on the available evidence, any definitive conclusions are premature at best.
From their terminology to generalized conclusions, it is clear that Tibana and de Sousa (1) have taken a position on HIFT/CrossFitTM that fits the definition of “extreme”. However, the Merriam-Webster dictionary describes extreme as something “existing in a very high degree,” or “exceeding the ordinary, usual, or expected” or even “relating to, or being an activity or a form of a sport (such as skiing) that involves an unusually high degree of physical risk” (2). Yet, the scientific literature around HIFT/CrossFitTM does not support this notion or the use of “extreme” as an accurate descriptor. More importantly, the authors seem to have misrepresented some of the data. For example, alternating sets of push-ups and pull-ups on each minute for 48 minutes and totaling 400 push-ups and 200 pull-ups is equivalent to completing approximately ~16 push-ups and ~8 pull-ups per minute. Although this might appear to be a difficult task to some, it is not made clear by Tibana and de Sousa (or the original authors) how these tasks were performed (e.g., push-up starting position; assisted, butterfly, or kipping pull-ups) which would impact the severity of the exercise (3, 4). More importantly, the authors failed to mention that the individual played ice hockey on the following night and participated in another high-intensity workout the day after before seeing a medical professional. The authors also described additional protocols (e.g., 105 push-ups in 6 minutes [or 17 push-ups per minute]; 3 sets of chin-ups to failure over a 20-minute period) as being “extreme” when they were generally in line with the recommended prescription for endurance exercise (5). Another example of misrepresentation occurred with their description of the ‘Sissy Test’. This workout consists of 240 total repetitions evenly split between kettlebell swings and burpees, not 672 total repetitions. Likewise, the competition workout that included “unaccustomed exercise” (i.e., 60 GHD’s) is simply a version of the sit-up exercise performed with greater range of motion. In short, if we are to accurately describe HIFT and assess its merits and limitations, it is important to maintain perspective, describe protocols in detail, and avoid exaggerations.
Feito et al. (6) provided a working definition for HIFT: “a training style [or program] that incorporates a variety of functional movements, performed at high-intensity [relative to an individual’s ability], and designed to improve parameters of general physical fitness (e.g., cardiovascular endurance, strength, body composition, flexibility, etc.) and performance (e.g., agility, speed, power, strength, etc.).” Unlike “Extreme Conditioning Programs,” which would suggest that training is “abnormal” or “inherently dangerous,” this definition provides an objective description of workout modality and intensity, as well as its targeted outcomes. We acknowledge that this particular definition may not have been available at the time of the authors’ manuscript submission, but it is not drastically different than the definition provided by CrossFitTM itself: “constantly varied, high-intensity, functional movement” (7). Further, the term “HIFT” was first introduced in 2014, when Heinrich and colleagues (8) compared high-versus moderate-intensity training programs and has been used in more than a dozen other studies since. Tibani and de Sousa use ‘HIFT’ within their title, but the term is otherwise absent throughout their manuscript. We believe this omission, along with their exclusion of other works, represents a considerable amount of bias and limits the ability of the authors (and readers) to form accurate, objective conclusions on the impact of HIFT. Moreover, several studies have provided insight to the cardiovascular responses of HIFT training (9-11) and suggest these programs fit within the current exercise prescription recommendations provided by the American College of Sports Medicine (12).
Regarding injuries related to HIFT, the authors acknowledge that the incidence of injury (approximately 2 – 4 injuries per 1000 hours) is similar to that of weightlifting and other recreational activities and lower than several contact sports. Though limited by the cross-sectional nature and small sample sizes, these rates are consistent with what others have reported (13-19). As such, we agree with the authors that additional studies are needed to elaborate on the potential risk of this training modality, particularly among different population subgroups (i.e. youth, older adults, etc.). However, we do diverge from the authors’ presentation of this information throughout the manuscript. The authors introduce three areas of concern that are related to participant’s safety: “(1) use of fast movements with a high number of repetitions and insufficient rest intervals; (2) participants with a weak motor repertoire to perform complex movements and (3) a possible lack of educated, certified and experienced ECPs professionals, especially in the integration of all training methods.” Unfortunately, the authors do not provide evidence to validate these concerns.
Tibana and de Sousa cite a pair of studies that indicate a greater occurrence of overuse injuries (20) and a higher prevalence of shoulder injuries (14) following HIFT, but neither of these studies report the programming characteristics (i.e., training volume, relative intensity loads, or exercise frequency) employed by their participants. To make generalizable conclusions such as these, these authors (14, 20), as well as Tibani and de Sousa, must assume that higher training volumes, high training intensities, and complex movements are consistently employed across training. If we are to assume that HIFT/CrossFitTM is being appropriately employed, then this cannot be the case. By definition (6, 7), HIFT is constantly varied and scalable (i.e., intensity is relative to the individual), and would suggest that participants do not regularly employ any specific volume, intensity or modality with sufficient regularity to evoke overuse injuries. Nevertheless, without an accurate programming record, it is impossible to conclude that HIFT/CrossFitTM participants are regularly exposed to inappropriate complex movements that lead to injury. Likewise, it is not suitable to assume HIFT participants possess a “weak motor repertoire to perform complex movements” or that coaches lack education, certification, or experience. Although not provided by the authors, evidence refuting these claims have been provided by Tafuri et al. (21) and Waryasz et al (22), respectively.
Another important topic related to injury discussed by the authors is that of exertional rhabdomyolysis (ER). Regardless of the activity, developing ER is an extreme case that is detrimental to physical performance improvements and may lead to death. Nevertheless, the authors provide a very narrow view of how ER can develop and their conclusion that it is “becoming increasingly more prevalent” in HIFT is unsupported. The evidence provided within the manuscript consists of nine case studies that detail the occurrence of ER in 15 individuals. When put into perspective, the incidence of ER in relation to HIFT is quite small. Compared to the number of CrossFitTM affiliates existing worldwide (approximately 13,000), this would equate to 0.12% of participants if each location had a single member develop ER. Compared to the number of participants in the 2018 Open competition (N = 429,157 competitors), it would equate to less than 0.004%. A closer look at the literature related to ER demonstrates a similar number of case studies that support the development of ER in other activities (23-25), such as stationary cycling (26-28), ultimate frisbee (29) and even hiking (30).
In the most current and comprehensive study of HIFT related injuries, Feito et al. (19) demonstrated the overall low incidence of injuries associated with HIFT programs. According to that study, which included over 3,000 participants over a 4-year period, only 0.6% of participants reported the occurrence of ER (19). Even though the study by Feito and colleagues (19) is also limited in its ability to depict incidence of ER, it certainly provides a more appropriate measure of prevalence than any case study alone. Moreover, Knafl and colleagues (31) reported an increased number of ER cases being admitted to an emergency room in Brisbane, Australia and alluded to high-intensity workouts (e.g., CrossFitTM training) as a potential cause. However, this may have been merely speculation by the authors, as the underlying causes were divided into seven specific categories: 1) gym, 2) marathon/running, 3) manual labor, 4) military/police training, 5) team sports, 6) walking/heat, and 7) other (31). Therefore, we certainly agree that additional studies are warranted to accurately portray the incidence of ER, but we cannot yet conclude that HIFT presents any greater danger than other exercise forms.
In regards to the physiological responses to HIFT, Tibana and de Sousa refer to a number of studies documenting a larger inflammatory response compared to traditional exercise protocols. They summarize and interpret the literature as follows: “These results indicate that ECPs elicited a higher metabolic, cardiovascular, hormonal and inflammation response. Therefore, strength and conditioning professionals need to be aware of the level of stress imposed on individuals when performing metabolic workouts of ECPs… it is recommended that the incorporation of lower intensity sessions (e.g., through the rating of perceived exertion or HR) and/or resting days would help to minimize this exacerbated physiological response.” Although the authors partly summarize the more pronounced physiological responses, the recommendation to reduce intensity is not warranted, nor is the subjective description of the response as “exacerbated.” It is well documented that neuroendocrine and inflammatory responses play a critical role in exercise-induced signals for health-related benefits, including cardiovascular and metabolic adaptations (32, 33). It is further documented that these responses are directly correlated to the intensity of the exercise bout, and the degree of adaptations to exercise are, accordingly, primarily linked to the intensity of the exercise stimulus (34, 35). Therefore, we express the concern that the recommendation put forth by Tibana and de Sousa to reduce exercise intensity is tantamount to recommending a suboptimal exercise stimulus that would produce smaller magnitude health benefits compared to HIFT. Indeed, the authors failed to mention a very important recent study demonstrating that HIFT reduces fat mass, increases insulin sensitivity, increases fat oxidation, reduces blood concentrations of the pro-inflammatory cytokine resistin and increases levels of the anti-inflammatory cytokine adiponectin in people with type 2 diabetes (36).
With respect to the chronic adaptations associated with HIFT, Tibana and de Sousa reach the conclusion that the “scientific literature showed few or no chronic effects on body composition and improvements in physical fitness and psychological parameters; however further studies are important.” For two reasons, we fail to understand how the authors reached this particular conclusion. First, the evidence provided by the authors seems to contradict their conclusions. Namely, the majority (i.e., 6 out of 11 studies) of these studies demonstrate positive effects of HIFT interventions on both body composition and fitness outcomes. Second, the authors fail to include two recent (but available prior to the date of publication) investigations that further demonstrate these positive effects (37, 38). Thus, we would like to offer an alternative interpretation of the authors’ presented evidence with respect to the chronic adaptations to HIFT. We would argue that not only does the majority of the evidence support the efficacy of HIFT for multiple domains associated with health and fitness, it also demonstrates efficacy across multiple population subgroups (e.g., teens, cancer survivors, people with Type 2 Diabetes, etc.). Further, the considerable heterogeneity across these studies with respect to intervention dosing (e.g., included interventions ranged from five weeks to six months in duration) suggests the likelihood of a dose-response relationship between HIFT and its desired outcomes. Current evidence suggests that at least 15 HIFT sessions, over a 3 – 5-week period, are needed to elicit changes in fitness outcomes, but the minimum effective dose specific to body composition changes is not well established and could potentially be significantly higher than it is for fitness-related outcomes.
Overall, we commend Tibana and de Sousa’s for their work and their attempt to review the current available literature related to HIFT. However, based on our interpretation of the evidence presented herein, we urge caution on the part of the BMJ readership in regards to its presentation and applying the recommendations put forth in their article.
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37. Crawford DA, Drake NB, Carper MJ, DeBlauw J, Heinrich KM. Are Changes in Physical Work Capacity Induced by High-Intensity Functional Training Related to Changes in Associated Physiologic Measures? Sports (Basel). 2018;6(2).
38. Feito Y, Hoffstetter W, Serafini P, Mangine G. Changes in body composition, bone metabolism, strength, and skill-specific performance resulting from 16-weeks of HIFT. PLoS One. 2018;13(6):e0198324.
Thank you to the authors for emphasizing this topic. Physical inactivity remains the big problem and major pandemic in the world. Besides Sweden, many developing and developed countries have this serious problems. Researchers may suggest that physical inactivity cost lead to bigger healthcare cost and economic burden in the future. Physical inactivity is contributed to about 6-10% of ischaemic heart disease, stroke, diabetes, breast and colon cancer(1). Global physical inactivity cost is estimated $67.5 billions in total which consist direct cost around $53.8 billions and indirect cost around $13.7 billions (2). As for Europe and North America, it remains higher cost than in Asia. In China, the total cost of physical inactivity is estimated total about $6.7 billions (3). As for Korea, cost as much as 83.6 million was contributed to physical inactivity(4). While in North America and Europe, it remains high each $28.9 billions and $15.5 billions in total cost (2).
It is much appreciated that the research filling the gap of data especially in Sweden. Other countries especially developing countries, should have the same idea about calculating the economic cost of physical inactivity. The current data in developing countries are inadequate, both direct and indirect cost which are very important. So that, the government can realize the important and dangerous effects of physical inactivity. Implementation should be underlined more on promotive and preventive action rath...
Thank you to the authors for emphasizing this topic. Physical inactivity remains the big problem and major pandemic in the world. Besides Sweden, many developing and developed countries have this serious problems. Researchers may suggest that physical inactivity cost lead to bigger healthcare cost and economic burden in the future. Physical inactivity is contributed to about 6-10% of ischaemic heart disease, stroke, diabetes, breast and colon cancer(1). Global physical inactivity cost is estimated $67.5 billions in total which consist direct cost around $53.8 billions and indirect cost around $13.7 billions (2). As for Europe and North America, it remains higher cost than in Asia. In China, the total cost of physical inactivity is estimated total about $6.7 billions (3). As for Korea, cost as much as 83.6 million was contributed to physical inactivity(4). While in North America and Europe, it remains high each $28.9 billions and $15.5 billions in total cost (2).
It is much appreciated that the research filling the gap of data especially in Sweden. Other countries especially developing countries, should have the same idea about calculating the economic cost of physical inactivity. The current data in developing countries are inadequate, both direct and indirect cost which are very important. So that, the government can realize the important and dangerous effects of physical inactivity. Implementation should be underlined more on promotive and preventive action rather than curative one. It can be emphasized in cost-effectiveness programme that can intervene the factors of physical inactivity. Another thing, the data are not updated yet. The current global and regional data in 2013 and need to be regularly updated (2).
Reference:
(1) Lee, I. M., Shiroma, E. J., Lobelo, F., Puska, P., Blair, S. N., & Katzmarzyk, P. T. (2012). Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy. Lancet, 380(9838), 219-229. doi:10.1016/s0140-6736(12)61031-9
(2) Ding, D., Lawson, K. D., Kolbe-Alexander, T. L., Finkelstein, E. A., Katzmarzyk, P. T., van Mechelen, W., & Pratt, M. (2016). The economic burden of physical inactivity: a global analysis of major non-communicable diseases. Lancet, 388(10051), 1311-1324. doi:10.1016/s0140-6736(16)30383-x
(3) Zhang, J., & Chaaban, J. (2013). The economic cost of physical inactivity in China. Prev Med, 56(1), 75-78. doi:10.1016/j.ypmed.2012.11.010
(4) Min, J. Y., & Min, K. B. (2016). Excess Medical Care Costs Associated with Physical Inactivity among Korean Adults: Retrospective Cohort Study. Int J Environ Res Public Health, 13(1). doi:10.3390/ijerph13010136
We read with interest the article by Parrish et al, “Normal platelet function in platelet concentrates requires non-platelet cells: a comparative in vitro evaluation of leucocyte-rich (type 1a) and leucocyte-poor (type 3b) platelet concentrates.”(1)
Parrish et al define PRP as a preparation with a platelet concentration of at least 5x over baseline, yet the LP-PRP they prepared (Arthrex Autologous Conditioned Plasma) was significantly lower at 2x over baseline, while the LR-PRP (Mitek Sports Medicine PEAK PRP) was significantly higher at 8x over baseline. We might reasonably expect that the ratio of growth factors between their LR-PRP and their LP-PRP to be approximately 8x/2x or 4:1, and this was indeed the case as seen in their Figure 4.
Subsequently, the authors grew tenocytes (tendon cells) exposed to serum derived from LR-PRP and LP-PRP preparations. Given that their LR-PRP was approximately 4 times richer in growth factors than their LP-PRP, we might reasonably expect that the 2.5% solution of serum derived from their LR-PRP have approximately the same effect as the 10% solution of serum derived from their LP-PRP. However, their 10% LP-PRP solution actually resulted in higher growth of tenocytes (2656 light units) than their 2.5% LR-PRP solution (1001 light units), as seen in their Table 5, but not discussed by the authors. The fact that their 10% LR-PRP-derived serum caused tenocytes to grow to confluence while their 10% LP-PRP-derived serum did...
We read with interest the article by Parrish et al, “Normal platelet function in platelet concentrates requires non-platelet cells: a comparative in vitro evaluation of leucocyte-rich (type 1a) and leucocyte-poor (type 3b) platelet concentrates.”(1)
Parrish et al define PRP as a preparation with a platelet concentration of at least 5x over baseline, yet the LP-PRP they prepared (Arthrex Autologous Conditioned Plasma) was significantly lower at 2x over baseline, while the LR-PRP (Mitek Sports Medicine PEAK PRP) was significantly higher at 8x over baseline. We might reasonably expect that the ratio of growth factors between their LR-PRP and their LP-PRP to be approximately 8x/2x or 4:1, and this was indeed the case as seen in their Figure 4.
Subsequently, the authors grew tenocytes (tendon cells) exposed to serum derived from LR-PRP and LP-PRP preparations. Given that their LR-PRP was approximately 4 times richer in growth factors than their LP-PRP, we might reasonably expect that the 2.5% solution of serum derived from their LR-PRP have approximately the same effect as the 10% solution of serum derived from their LP-PRP. However, their 10% LP-PRP solution actually resulted in higher growth of tenocytes (2656 light units) than their 2.5% LR-PRP solution (1001 light units), as seen in their Table 5, but not discussed by the authors. The fact that their 10% LR-PRP-derived serum caused tenocytes to grow to confluence while their 10% LP-PRP-derived serum did not is irrelevant given that the latter was obtained from 4-fold fewer platelets.
One of the purported new findings of the study was that LP-PRP was “deficient” in terms of coagulation, clot retraction and platelet growth factor release. This statement was based on an average 20% lower release of growth factors relative to whole blood following activation with CaCl2, as seen in their Figure 5. In addition, the authors stated “Exogenous thrombin addition rescues coagulation and clot retraction deficits and improves platelet growth factor release in LP-PRP.” These statements are not supported by their research because coagulation and clot retraction assays were not conducted in this study, and use of the word “rescues” is misleading.
Platelet concentrations vary broadly (150-450K/µL) in normal individuals (2) with normal coagulation and clot retraction function. Whether an average 20% lower immediate release of growth and coagulation factors induced by CaCl2 would translate into an actual in-vitro or in-vivo coagulation or clot retraction deficit is not clear and was not assessed by this study. Furthermore, platelet growth factor release is temporal and multiphasic in nature and there is a known differential between preparation methods (3-5). Hence, whatever differences were seen at 80 minutes, the time point when serum was collected from the preparations, may not have been present at later time points.
Another purported new finding, reflected by the title of the article, was that non-platelet cellular components in platelet concentrates are important for proper platelet function, including thrombin generation and clot retraction. Again, this was not supported by their research because platelet function, thrombin generation and clot retraction studies were not done and the statement appears to hinge on growth factors released within 80 minutes of the preparations.
In conclusion, the presented findings must be considered as artifacts of the specific materials, methods and time points selected. If an implicit goal of the article was to demonstrate the superiority of LR-PRP over LP-PRP, then the platelet concentrations should have been similar and platelet rich plasma used instead of serum. Nevertheless, correcting for platelet concentration LP-PRP serum appears to have been at least twice as effective at inducing tenocyte proliferation. Furthermore, even if LR-PRP and LP-PRP were produced with similar levels of growth factors, LR-PRP has pro-inflammatory and catabolic factors attributable to leucocytes, a fact not acknowledged by the authors. (6,7)
Acknowledgement: We would like to thank the Napa Medical Research Foundation, a 501(c)3 non-profit foundation, for their encouragment and support.
References
1 Parrish, W. R. et al. Normal platelet function in platelet concentrates requires non-platelet cells: a comparative in vitro evaluation of leucocyte-rich (type 1a) and leucocyte-poor (type 3b) platelet concentrates. BMJ Open Sport Exerc Med 2, e000071, doi:10.1136/bmjsem-2015-000071 (2016).
2 Brown, L. M. et al. A normal platelet count may not be enough: the impact of admission platelet count on mortality and transfusion in severely injured trauma patients. J Trauma 71, S337-342, doi:10.1097/TA.0b013e318227f67c (2011).
3 Schar, M. O., Diaz-Romero, J., Kohl, S., Zumstein, M. A. & Nesic, D. Platelet-rich concentrates differentially release growth factors and induce cell migration in vitro. Clin Orthop Relat Res 473, 1635-1643, doi:10.1007/s11999-015-4192-2 (2015).
4 McCarrel, T. & Fortier, L. Temporal growth factor release from platelet-rich plasma, trehalose lyophilized platelets, and bone marrow aspirate and their effect on tendon and ligament gene expression. J Orthop Res 27, 1033-1042, doi:10.1002/jor.20853 (2009).
5 David, M. D. E. et al. Do the Fibrin Architecture and Leukocyte Content Influence the Growth Factor Release of Platelet Concentrates? An Evidence-based Answer Comparing a Pure Platelet-Rich Plasma (P-PRP) Gel and a Leukocyte- and Platelet-Rich Fibrin (L-PRF). Current Pharmaceutical Biotechnology 13, 1145-1152, doi:http://dx.doi.org/10.2174/138920112800624382 (2012).
6 Sundman, E. A., Cole, B. J. & Fortier, L. A. Growth factor and catabolic cytokine concentrations are influenced by the cellular composition of platelet-rich plasma. Am J Sports Med 39, 2135-2140, doi:10.1177/0363546511417792 (2011).
7 Anitua, E., Zalduendo, M., Troya, M., Padilla, S. & Orive, G. Leukocyte inclusion within a platelet rich plasma-derived fibrin scaffold stimulates a more pro-inflammatory environment and alters fibrin properties. PLoS One 10, e0121713, doi:10.1371/journal.pone.0121713 (2015).
I have read Dr Robergs’ article 1 with much enthusiasm, from the first to the last paragraph. He criticized my occasional piece article suggesting a probable Kuhnian paradigm shift in Exercise Sciences2. I was expecting comments and critiques to my provocative essay since its publication, approximately five years ago. Perhaps, as Philosophy of Science is complex and purely reflexive, just a few exercise scientists have devoted enough time to study it. I now have the opportunity to continue debating and applying some Philosophy in the Exercise Sciences perspective.
Reading Dr Robergs’ 1 article drove me back to the Philosophy of Science to reexamine some crucial academic works essential to a better understanding of how science operates. Since my first critical essay as a beginner student in science, about “The objective knowledge” of Karl Popper 3 during lectures on the Philosophy of Science by Emeritus Professor Michel Paty at the University of São Paulo, my thinking has evolved through different views of science, from Francis Bacon to Karl Popper, from Thomas Kuhn to Paul Feyerabend. Thus, the biased commentary promoted by Dr Robergs towards the falsification method did not surprise me because Karl Popper was one of the first philosophers I read as a beginner in science. Neither was Dr Robergs’ 1 claim in favor of the falsification criteria in Exercise Sciences entirely new 4. As a philosophy-oriented scientist I learned that we may benefit from a wider view of scie...
I have read Dr Robergs’ article 1 with much enthusiasm, from the first to the last paragraph. He criticized my occasional piece article suggesting a probable Kuhnian paradigm shift in Exercise Sciences2. I was expecting comments and critiques to my provocative essay since its publication, approximately five years ago. Perhaps, as Philosophy of Science is complex and purely reflexive, just a few exercise scientists have devoted enough time to study it. I now have the opportunity to continue debating and applying some Philosophy in the Exercise Sciences perspective.
Reading Dr Robergs’ 1 article drove me back to the Philosophy of Science to reexamine some crucial academic works essential to a better understanding of how science operates. Since my first critical essay as a beginner student in science, about “The objective knowledge” of Karl Popper 3 during lectures on the Philosophy of Science by Emeritus Professor Michel Paty at the University of São Paulo, my thinking has evolved through different views of science, from Francis Bacon to Karl Popper, from Thomas Kuhn to Paul Feyerabend. Thus, the biased commentary promoted by Dr Robergs towards the falsification method did not surprise me because Karl Popper was one of the first philosophers I read as a beginner in science. Neither was Dr Robergs’ 1 claim in favor of the falsification criteria in Exercise Sciences entirely new 4. As a philosophy-oriented scientist I learned that we may benefit from a wider view of science as there is no infallible mode to understand science whatsoever. The falsification method assumptions may have implications on how we conceive the scientific development in Exercise Sciences, nevertheless omitted by Dr Robergs.
It is beyond of this rebuttal to present all pros and cons relative to different views of science, thus beginners in Exercise Sciences are encouraged to read different views of science in full, in order to assume a more critical positioning in scientific debates. This would be of value to understand the points I highlight ahead about the weakness of Dr Robergs’ article.
Problems of the Falsification Principle
To criticize my earlier Kuhnian Paradigm Shift in Exercise Science essay 2 Dr Robergs classified Karl Popper as the most contemporary philosopher of science, the owner of “the single valid approach to scientific method in Exercise Sciences” 1. According to Dr Robergs, “Popper had a simplistic view of the delineation between science and pseudoscience, any non-critical application of science, that not based on efforts at falsification, was pseudoscientific”. Curiously, Dr Robergs did not warn readers about the important limitations of the falsification criteria.
Popper believed that the more falsifiable the hypothesis of a theory, the better the theory 5. However, the number of potential falsifiers for a given hypothesis is always infinite so that there is no measure to ensure asymmetric comparison between theories. In fact, some have argued that because falsification is never completely conclusive, the asymmetry of falsification principle proposed by Popper is actually impossible 5 6 7. For example, assuming the perspective I suggested for Exercise Sciences in 2012 2 that a “the growing acceptance of a centrally-regulated effort theory has replaced the dichotomized central vs peripheral fatigue theory”, exercise scientists guided by the falsification principle should know, a priori, all possible falsifiers between these two theories in order to choose the finest one. Because a given hypothesis of a theory can be false only if we take the theory as a whole in our test, the falsification of a theory is not a straightforward schema and, therefore, the application of falsification principle (in strict terms) in Exercise Sciences to test the Central Governor Model (CGM) is consequently impracticable.
Moreover, the need to know all conditions met by the theory before testing a hypothesis, forces scientists to oversimplify the theory since the knowledge of all conditions would be obviously possible only in simple conjectures. This controversy of falsification would drive the theory to a likely separation of its important components in order to create hypothesis possibly falsifiable. As a result, the application of the falsification method to test the CGM theory would lead, at least momentously, to an oversimplification of the exercise tolerance phenomenon. Remember, the CGM was formulated as a complex, non-linear, neurophysiological-psychological model of exercise performance 8-10. As stated by Duhem (apud Ladyman, 2002 5) using Physics as an example, “physical science is a system that must be taken as a whole; it is an organism in which one part cannot be made to function except when the parts that are most remote from it are called into play, some more so than others, but all to some degree”. Accordingly, Micklewright 11 stated that “the CGM cannot be adequately tested by observing its components in isolation”.
There are other two limitations of the falsification principle that readers must be aware. First, some statements cannot be experimentally falsifiable 5. A simple and embarrassing example is the following statement: “time and space are infinite”. Logically, the falsification of such a statement is experimentally impossible. Therefore, a theory asserting the existence of a phenomenon cannot be automatically classified as pseudoscience if someone fails to apply the falsification method over it. Another limitation is that the failure to find a phenomenon under some circumstances or to formulate refutable hypothesis in experimental setups may be a simple consequence of the lack of instruments to make crucial measurements 5. An exemplification of the need for instruments capable of measuring a given phenomenon was recently provided in Physics, as parts of the Gravitational Waves theory were only confirmed as a result of the investment into expensive technology. Accordingly, confirmation of the Heliocentric theory initially proposed by Copernicus was confirmed later, after the invention of the telescope 5. Regarding the CGM, some statements may not be momentously falsified due to the lack of means to falsify the theory. A technology capable of providing online feedback and feedforward measures integrated in the central nervous system, in a real-time exercise is a crucial limitation in attempts to refute the CGM.
Finally, some hypothesis may not be falsified simply because they can be part of a science that is seemingly unfalsifiable 5. For example, an unfalsifiable statement includes the Uncertainty Principle, which asserts that the more precise the determination of the position of a particle, the less precise the estimation of its momentum, and vice versa. This principle is apparently unfalsifiable, as results that do not match a given estimation cannot work to refute the theory. In fact, the falsification principle is unable to deal with probabilistic statements, being an inconvenient mismatch between logic and observation in the falsification perspective 5. Although one may argue that the CGM theory does not fit to probabilistic statements, the knowledge of such a limitation is important to highlight that falsification principle is far for being a universal principle for Philosophy of Science. In fact, incredible progress observed in Epidemiology and Pharmacy sciences (among others) cannot be explained by falsification.
We Benefit More by Using Different Philosophies of Science
I acknowledge that the Critical Rationalism embedded in the falsification method of Karl Popper could lead to a more critical and rational use of the scientific method in Exercise Sciences, as this may guide scientists to crucial questions and important investigations in some circumstances. Nonetheless, the falsification principle must be applied with balance, just as we should do with positive induction process. Otherwise, Popperian philosophy will be incompatible with the actual practice in science.
Different from Dr Robergs’ conclusion, Katch (1986) 12 seemed to have referred to Karl Popper just to highlight the importance of inductive inferences derived from exclusion research. In my opinion, Katch (1986) did not affirm that “Karl Popper was the philosopher who has contributed most to the understanding of the ideal tenants of the scientific method”. For example, when Dr Katch referred to experiments by Dr Brooks challenging the anaerobic threshold concept (page 594) 12, he suggested the use of “disproofability” as a vein to provide answers to important questions, instead of a method to decide between rival theories. Katch 12 wrote that “A new dimension to Wasserman hypothesis has been added that has made the hypothesis all the richer”. In my opinion, he indicated that refutation provided by Dr Brooks was of value to improve hypotheses of the theory, rather than refute the theory as a whole. Therefore, although recognizing that falsification principles may be of value to strengthen a given theory in some circumstances, we should be aware that they are only a critical approach to apply the scientific method occasionally. As argued above, this has nothing to do with a straightforward way to set a theory as acceptable/valid, once the choice between rival theories may involve a more complex dilemma. Accordingly, the best scenario of falsification method in Exercise Sciences is to guide scientists when using the scientific method in critical enquiries. Therefore, the acceptance or rejection of the CGM theory based exclusively on the falsification criteria is not practicable.
It is important to point out that Popperian scientists make their initial judgments about a hypothesis based on accepted knowledge derived from prior theories and experimentations. Hence, Popperian scientists must accept past experiences in order to formulate falsifiable hypothesis, thus falling back in induction. Actually, a scientist can believe in empirical consequences of a given theory only if he believes in the truth of the background assumptions. Popperian scientists should consciously admit the use of induction process in their observations when proposing balanced experimentation, because it is impossible to leave induction processes out from scientific scenarios. This is crucial for scientists intending to avoid novel assumptions when formulating a hypothesis and its experimentation, otherwise a purely naïve Popperian approach may lead them to reject a theory and its predictions before having a better theory for replacement. This is what happens if we take Dr Robergs’ suggestion integrally (despite arguing that CGM theory is a pseudoscience, he offered no alternative explanation for the phenomenon).
An important aspect that beginners in science should consider is that some have argued that the change of meaning of terms and logic is sometimes reasonable and more convenient than rejecting a particular theory 5. The Atomic theory provides a simple example of a change of meaning of a term, as this theory first defined the atom as the least indivisible particle, however when scientists found that atom was divisible they redefined the meaning of atom in order not to abandon the theory. In this example, the use of naïve falsification principles may have led scientists to abandon the Atomic theory, thus blocking an incredible scientific progress in Biology, Chemistry and other sciences. Therefore, rather than abandoning the CGM theory, perhaps is time to redefine the meaning of some terms to refine the theory, as recently suggested elsewhere 13 14. The final word about the acceptability of this theory belongs to the scientific community.
The Kuhnian Paradigm Shift in Exercise Sciences
I agree with Dr Roberg, “Kuhn did not write his text with the intention of presenting a model for how the scientific method, or science itself, should work”, accordingly neither I defended such a principle in my previous article 2. I am not sure about the implicit message left by him suggesting my Kuhnian approach as inadequate 1. As argued in my paper, there has occurred a change on how the Exercise Sciences community has focused on the limits of exercise tolerance 2. My suggestion of Paradigm Shift in Exercise Sciences was based on aspects that, together, may indicate a change of focus of the Exercise Sciences community and growing acceptance of a new theory.
Besides the omission of the work of Karl Popper, the most fundamental concern of Dr Robergs was the use of citations number in my essay (the argument that Exercise Physiology is not a discipline is irrelevant to this debate), since he conceived I used the number of citations by itself, to infer acceptance of a topic/theory. He correctly argued that “Journal citations or topical preference cannot be interpreted as evidence of acceptance or agreement” 1. Curiously, Dr Robergs omitted the fact that I used two other aspects together, to indicate a growing acceptance of a centrally-regulated effort model. Thus, he misunderstood that I used the number of citations to indicate “focus”, rather than “agreement or acceptance”. As I wrote in my previous article 2, “number of citations about a specific theme could indicate the focus of a particular scientific community along time”. Furthermore, in addition to number of citations I used the number of views on specific websites as an indication to where the Exercise Sciences community has its focus.
Besides the number of citations (1), I pointed out that the increased debate on issues challenged by the CGM (2) and the inclination of the scientific community to incorporate a new interpretation (3) could indicate, together, a growing acceptance. I argued that traditional important journals of Exercise Sciences had published specific contents about fatigue mechanisms, highlighting central mechanisms that could be involved in the exercise regulation. Furthermore, important researchers involved with mechanisms of the traditional central vs peripheral fatigue dilemma had started to recognize the importance of integrative explanations for the limits of exercise tolerance. I further assumed that “Perhaps, the most relevant is that scientists from different fields have highlighted mechanisms included in the CGM to understand the limits of exercise”. Therefore, different from what Dr Robergs suggested 1, I used three different aspects to indicate where the Exercise Sciences community has focused on, probably suggesting an intellectual trajectory towards the acceptance of a different theory.
According to a Kuhnian view of Science, the degree of confirmation given by experimentation is not objective, therefore no demarcation criteria can determine logically which theory is most justified by the evidence 6 15. The scientific community as a whole regards the theory as justified 5. I wrote on page 2 of my paper 2 that “the impossibility of performing neutral comparisons with standardized rules to determine the truth of a theory, labelled by Kuhn as “incommensurability of theories”, collective judgement is an important criterion to decide between rival theories in the Kuhnian process”. Thus, criteria 1, 2 and 3 together may suggest that the Exercise Sciences community has changed the focus toward a growing acceptance of a new, integrative theory.
Updating the Kuhnan view in Exercise Sciences
I agree that there is a flaw in my previous occasional piece, once I presented the number of citations of only two theoretical articles proposing the CGM theory. However, its proponents orchestrated this theory within five theoretical papers in an approach comparable to the elegant approach of Archibald V. Hill and colleagues almost hundred years earlier 16 17. First, proponents of the CGM theory presented sequential arguments rebutting the current paradigm 18, thereafter they suggested a novel model of integrative central neural regulation 8-10, 19. Thus, instead of using two of these five theoretical reviews arbitrarily determined, all five prepositional studies should have been used. Encouraged by this debate, I present now an updated number of citations of these works (Figure 1). It is important to warn readers that the number of citations by itself does not indicate too much, as others have presented relevant theoretical reviews with a high number of citations, but without changing the focus of the scientific community. Examples include the conservation of the traditional anaerobic threshold concept 20 as originally proposed by Wasserman and colleagues 21 22, even after evidences has accumulated against this traditional paradigm 23, as well as the lactate-derived acidosis dilemma promoted by Dr Robergs 24. Hence, rather than the number of citation by itself, other marks should be used together to strengthen the argument in favor a paradigm shift as proposed in 2012 2.
An important result predicted by the Kuhnian Scientific Revolution is the incorporation of new terms by scientific community to characterize the new paradigm 5. In this regard, new terms have emerged since the original proposition of the CGM theory. Thus, perhaps it is time to use new terms to verify how the Exercise Sciences community has incorporated the CGM. For example, “pacing strategy” and “decision-making” may reflect the original ideas promoted by the CGM theory, as both constructs has been related to a centrally-orchestrated neuro-psychological regulation 25 26. Although other terms could be also included to reflect the original CGM theory, it is beyond the aim of this article to present an updated list of new terms. Just as examples, I present the citation report having “central governor and exercise”, “pacing strategy and exercise” and “decision-making and exercise” as truncated keywords, therefore showing an increasing number of articles working with central, neuro-psychological regulation concepts (Figure 2). Thus, when compared to data presented in my first Kuhnian essay 2, it is possible to note that concepts derived from the CGM theory have been used, increasingly.
Furthermore, as originally suggested in 2012 2, there was an increased debate on issues challenged by the CGM (item 2 of the Kuhnian paper). Currently, important journals have still devoted relevant volumes to discuss concepts connected to this new paradigm 27 28. It is important to make clear that the present article is limited to discuss the probable Kuhnian Scientific Revolution in Exercise Sciences having the CGM as an example, thus it is beyond of this rebuttal to discuss other integrative interpretations to the exercise tolerance phenomenon 29 30, that appeared after the Kuhnian Scientific Revolution triggered by the CGM 8-10 19. Actually, the appearance of other ways to interpret the phenomenon may be indicative of a Kuhnian Scientific Revolution.
Additional Concerns of Dr Robergs
In his review 1 Dr Robergs included as an additional concern that proponents of CGM theory advocated the presence and function of a new brain location, which they referred to as the “teleoanticipatory central nervous system”. Then, he claimed that CGM proponents “provided no empirical evidence of this centre”. After several readings of the original theoretical CGM papers, I have never found such a reference, since my understanding of the CGM theory was that the integrative regulation involves multiple physiological systems under the control of brain regulatory mechanisms, in a dynamic and continuous interaction 13 19. The presence of a “new” brain location was never my understanding, as I always considered a central governor as the central nervous system as a whole. Therefore, despite of its helplessness utility, the name “Central Governor” seemed to be no more than a semantic choice.
Regarding the peer review process mentioned by Dr Robergs, from my perspective as an independent author, I have seen theoretical articles in favor 14 as well as against 31 this theory being published by this journal. Discussion about an “open, double-visible” review process in scholarly journals is fruitful and demanded, but it is beyond the aim of this review.
CONCLUSIONS
Thomas Kuhn predicted that scientists attached to the old paradigm would resist the acceptance of a novel paradigm. The skepticism of Dr Robergs to accept the CGM theory seems to belong to a different category, that based on naïve falsification principle. This category apparently matches with Thomas Kuhn’s view of science, that of “The scientist who pauses to examine every anomaly he notes will seldom get significant work done” 5 6. Therefore, rather than focusing the scientific debate on a biased-single view of science, the Exercise Sciences may benefit more from different views of science.
REFERENCE
1. Robergs RA. Lessons from Popper for science, paradigm shifts, scientific revolutions and exercise physiology. BMJ Open Sport Exerc Med 2017;3(1):e000226. doi: 10.1136/bmjsem-2017-000226 [published Online First: 2017/08/16]
2. Pires FO, de Oliveira Pires F. Thomas Kuhn's 'Structure of Scientific Revolutions' applied to exercise science paradigm shifts: example including the Central Governor Model. Br J Sports Med 2013;47(11):721-2. doi: 10.1136/bjsports-2012-091333
3. Popper KR. Objective Knowledge. Oxford: Claredon Press 1972.
4. Noakes TD. Is it time to retire the A.V. Hill Model?: A rebuttal to the article by Professor Roy Shephard. Sports Med 2011;41(4):263-77. doi: 10.2165/11583950-000000000-00000
5. Ladyman J. Understanding Philosophy of Science. London: Taylor & Francis 2002.
6. Kuhn T. The Structure of Scientific Revolutions. Chicago: University of Chicago Press 1962.
7. Feyerabend PK. Against Method: Outline of an Anarchistic Theory of Knowledge. Minneapolis: University of Minnesota Press 1970.
8. Lambert EV, St Clair Gibson A, Noakes TD. Complex systems model of fatigue: integrative homoeostatic control of peripheral physiological systems during exercise in humans. Br J Sports Med 2005;39(1):52-62. doi: 10.1136/bjsm.2003.011247
9. Noakes TD, St Clair Gibson A, Lambert EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans. Br J Sports Med 2004;38(4):511-4. doi: 10.1136/bjsm.2003.009860
10. Noakes TD, St Clair Gibson A, Lambert EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions. Br J Sports Med 2005;39(2):120-4. doi: 10.1136/bjsm.2003.010330
11. Micklewright D, Parry D. The central governor model cannot be adequately tested by observing its components in isolation. Sports Med 2010;40(1):91-2; author reply 92-4. doi: 10.2165/11531360-000000000-00000
12. Katch V. "The burden of disproof...". Med Sci Sports Exerc 1986;18(5):593-5.
13. St Clair Gibson A, Swart J, Tucker R. The interaction of psychological and physiological homeostatic drives and role of general control principles in the regulation of physiological systems, exercise and the fatigue process - The Integrative Governor theory. Eur J Sport Sci 2017:1-12. doi: 10.1080/17461391.2017.1321688 [published Online First: 2017/05/06]
14. Venhorst A, Micklewright D, Noakes TD. Towards a three-dimensional framework of centrally regulated and goal-directed exercise behaviour: a narrative review. Br J Sports Med 2017 doi: 10.1136/bjsports-2016-096907 [published Online First: 2017/08/23]
15. Kuhn T. The Essential Tension. Chicago: University of Chicago Press 1977.
16. Hill AV, Lupton H. Muscular Exercise, Lactic Acid and the Supply and Utilization of Oxygen. The Quartely Journal of Medicine 1923;16:36. doi: 10.1093/qjmed/os-16.62.135
17. Hill AV, Long CN, Lupton H. The effect of fatigue on the relation between work and speed, in contraction of human arm muscles. J Physiol 1924;58(4-5):334-7.
18. Noakes TD, St Clair Gibson A. Logical limitations to the "catastrophe" models of fatigue during exercise in humans. Br J Sports Med 2004;38(5):648-9. doi: 10.1136/bjsm.2003.009761
19. St Clair Gibson A, Noakes TD. Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans. Br J Sports Med 2004;38(6):797-806. doi: 10.1136/bjsm.2003.009852
20. Meyer T, Lucía A, Earnest CP, et al. A conceptual framework for performance diagnosis and training prescription from submaximal gas exchange parameters--theory and application. Int J Sports Med 2005;26 Suppl 1:S38-48. doi: 10.1055/s-2004-830514
21. WASSERMAN K, MCILROY MB. DETECTING THE THRESHOLD OF ANAEROBIC METABOLISM IN CARDIAC PATIENTS DURING EXERCISE. Am J Cardiol 1964;14:844-52.
22. Wasserman K, Whipp BJ, Koyl SN, et al. Anaerobic threshold and respiratory gas exchange during exercise. J Appl Physiol 1973;35(2):236-43.
23. Brooks GA. Anaerobic threshold: review of the concept and directions for future research. Med Sci Sports Exerc 1985;17(1):22-34.
24. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol 2004;287(3):R502-16. doi: 10.1152/ajpregu.00114.2004
25. Renfree A, Martin L, Micklewright D, et al. Application of decision-making theory to the regulation of muscular work rate during self-paced competitive endurance activity. Sports Med 2014;44(2):147-58. doi: 10.1007/s40279-013-0107-0
26. Smits BL, Pepping GJ, Hettinga FJ. Pacing and decision making in sport and exercise: the roles of perception and action in the regulation of exercise intensity. Sports Med 2014;44(6):763-75. doi: 10.1007/s40279-014-0163-0
27. Meeusen R, Pires FO, Pinheiro FA, et al. Commentaries on Viewpoint: A role for the prefrontal cortex in exercise tolerance and termination. J Appl Physiol (1985) 2016;120(4):467-9. doi: 10.1152/japplphysiol.00967.2015
28. Hettinga FJ, Renfree A, Pageaux B, et al. Editorial: Regulation of Endurance Performance: New Frontiers. Front Physiol 2017;8:727. doi: 10.3389/fphys.2017.00727 [published Online First: 2017/09/21]
29. Marcora S. Perception of effort during exercise is independent of afferent feedback from skeletal muscles, heart, and lungs. J Appl Physiol (1985) 2009;106(6):2060-2. doi: 10.1152/japplphysiol.90378.2008 [published Online First: 2008/05/15]
30. Amann M. Central and peripheral fatigue: interaction during cycling exercise in humans. Med Sci Sports Exerc 2011;43(11):2039-45. doi: 10.1249/MSS.0b013e31821f59ab
31. Weir JP, Beck TW, Cramer JT, et al. Is fatigue all in your head? A critical review of the central governor model. Br J Sports Med 2006;40(7):573-86; discussion 86. doi: 10.1136/bjsm.2005.023028
I was surprised the authors did not take into consideration heel-to-toe height variances in SRSs, which can be significant (10+ mm). While this may have less effect on one's ability to land "softly" when running uphill, the opposite holds true on downward slopes; depending on the degree of slope, the heel is more likely to contact ground before or concurrent to the forefoot. At least, this has been my experience.
Secondly, while it may be true that a directive to "run softly" will effect the gait and form of a runner upon hearing the instructions, and may even hold sway for a few minutes, the truth is that we all tend to revert to habits after a time, and doubly so when fatigue sets in.
To the editor,
The postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of...
To the editor,
The postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of increase in pulmonary vascular pressure in IPE occurrence. They, furthermore, proposed several possible explanations for IPE and SIPE: 1) transient impairment of left ventricular (LV) systolic function, 2) reduced diastolic LV compliance. They suggested that redistribution from the periphery into the thorax combined with a less compliant LV would lead to a higher LV end-diastolic pressure and pulmonary artery pressure and pulmonary artery wedge pressure in SIPE-susceptible individuals. The authors proposed that, with augmented preload attributable to immersion in cold water, a greater LV wall stiffness in SIPE-susceptible individuals could be the cause of higher LV filling pressure during exercise in cold water.
We recently investigated the relationship between altered cardiac function and the development interstitial pulmonary edema in SCUBA divers. Fifteen healthy males performed a 30-min SCUBA dive in open sea. Echocardiography and lung ultrasound were performed before and immediately after immersion. We observed an increased preload and a right-left heart imbalance. Immediately following the dive the diameter of the inferior vena cava increased by 47 ± 5.2%, systolic pulmonary artery pressure increased by 105 ± 8.6%, left atrial volume increased by 18.0 ± 3.3% and left ventricle end-diastolic volume increased by 10.1 ± 2.4% suggesting both right and left ventricular filling pressures were elevated. Doppler studies showed an increased mitral E peak (+2.5 ± 0.3%) and E/A ratio (+22.5 ± 3.4%) with a decreased mitral A peak (-16.4 ± 2.7%), E peak deceleration time decreased (-14.5 ± 2.4%) consistent with rapid early left ventricular filling but there was no change in left ventricular stroke volume. There was an increase in right/left ventricle diameter ratio (+33.6 ± 4.8%) suggesting a relative increase in right heart output compared to the left.
We suggest the changes probably reflect rapid early LV filling driven by the higher pulmonary artery pressures secondary to increased work done by the right ventricle.3 It is unlikely our subjects had reduced left ventricular compliance due to an abnormality interstitial collagen or changes in intracellular titin (in the absence of known heart disease or hypertension). It is, however, plausible that the subjects reached the left ventricular/pericardial elastic limit towards the end of diastole, required higher end-diastolic pressures to achieve greater end-diastolic volumes in the presence of thick walled ventricle or developed abnormal intracellular calcium homeostasis during effort.4
Energy needs to be either added to the fluid or converted (say from kinetic energy) to create a higher pressure. A higher left ventricle end-diastolic pressure cannot be directly caused by diastolic dysfunction as the latter is not a form of energy. We think that the changes in left ventricle (LV) filling patterns are the result of an increased pulmonary venous pressure causing a rapid early diastolic filling due to the higher initial atrio-ventricular pressure gradient. The reduced A-wave velocity is a consequence of the higher end-diastolic pressure as the LV is already well filled. The “blood shift” induced by immersion will, sequentially, increases the right ventricular filling pressure, increasing right ventricle end-diastolic volume triggering the Frank-Starling mechanism, RV contraction and sequentially increasing pulmonary artery pressure, capillary pressure and, finally, LV filling pressure.3 At the same time, dilatation of the right heart might hamper filling of the left ventricle (ventricular interdependence) because of the limited distensibility of the pericardium and, so, may inhibit LV stroke volume.
We observed that increased preload and a right-left heart imbalance were correlated with the accumulation of extravascular lung water (EVLW). We showed that it was the changes in right ventricular physiology rather than changes in left ventricular indices that correlated with the development of interstitial pulmonary edema. The severity of interstitial pulmonary edema, was significantly correlated with measures of increased cardiac preload, right ventricular area change (a surrogate of right ventricle ejection fraction) and pulmonary artery pressure, but not left ventricle ejection fraction (LVEF) or left ventricle stroke volume (LVSV). Furthermore, the lung comet score correlated significantly with IVC diameter, systolic pulmonary artery pressure, right/left ventricle diameter ratio and E-wave deceleration time.
We have previously suggested acute pulmonary edema resulted from a mismatch or imbalance between the right and left ventricular stroke volume (SV)5. Although the pathophysiology of pulmonary (alveolar) edema (APE) is generally described in terms of a failing left ventricle, in reality, for APE to occur, there must be a mismatch between the right and left ventricular SV as fluid is lost from the circulation into the airspaces. The augmentation of right ventricular contractility increases stroke volume (and pulmonary pressures) relative to left ventricular SV which could then cause an increase in capillary hydrostatic pressure leading to transudation of fluid into the lung interstitium.5 A failure to increase LV stroke volume (relative to the RV stroke volume) due to a higher peripheral vascular resistance brought about by conditions such as systemic hypertension or cold water may increase the likelihood of occurrence of SIPE and IPE. The extravasation of fluid into the lung interstitium due to the RV/LV stroke volume mismatch is further exacerbated by higher heart rates explains interstitial pulmonary edema during exercise in divers.6
We provide a greater understanding to the pathophysiological mechanisms proposed by Moon and colleagues.1, 2 The altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema. Our findings may have implications for the pathogenesis of immersion pulmonary edema and could help reduce the deaths in swimming induced pulmonary edema.
We would be pleased to answer any request for further information.
Yours respectfully,
Olivier Castagna, M.D., Ph.D.
1. Moon RE, Martina SD, Peacher DF and Kraus WE. Deaths in triathletes: immersion pulmonary oedema as a possible cause. BMJ Open Sport Exerc Med. 2016;2:e000146.
2. Moon RE, Martina SD, Peacher DF, Potter JF, Wester TE, Cherry AD, Natoli MJ, Otteni CE, Kernagis DN, White WD and Freiberger JJ. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation. 2016;133:988-96.
3. MacIver DH, Adeniran I, MacIver IR, Revell A and Zhang H. Physiological mechanisms of pulmonary hypertension. Am Heart J. 2016;180:1-11.
4. Adeniran I, MacIver DH, Hancox JC and Zhang H. Abnormal calcium homeostasis in heart failure with preserved ejection fraction is related to both reduced contractile function and incomplete relaxation: An electromechanically detailed biophysical modelling study. Frontiers Physiology. 2015;6:1-14.
5. MacIver DH and Clark AL. The vital role of the right ventricle in the pathogenesis of acute pulmonary edema. The American journal of cardiology. 2015;115:992-1000.
6. Castagna O, Gempp E, Poyet R, Schmid B, Desruelle AV, Crunel V, Maurin A, Choppard R and MacIver DH. Cardiovascular Mechanisms of Extravascular Lung Water Accumulation in Divers. Am J Cardiol. 2017;119:929-932.
To the Editor,
We read the recent publication by Nathan, Davies & Swaine (2018) with great interest due to a mutual interest in the subject of Generalised Joint Hypermobility (GJH) and its influence on injuries within elite sport. The authors of this paper should be commended for undertaking a study with such good participant numbers over a range of sports. We believe that the findings of this study suggesting that GJH may be protective of joint ligament damage may be a very important initial paper leading to valuable further exploration within specific sports and specific joints. However despite this good work we would like to take the opportunity to raise a concern over one of their conclusions and how this may confuse readers of the article.
In the discussion section of this paper Nathan et al. (2018) suggest that the findings of this study may suggest that “regular stretching may increase flexibility, and this could subsequently reduce rates of injury in those that are less flexible.” We believe that this statement may lead to misunderstanding as the terms “flexibility” and “joint hypermobility” are two completely different entities.
GJH is a hereditary physiological entity whereby most synovial joints move beyond their normal limits (Pacey et al., 2010) and may, or may not be symptomatic. This entity is commonly classified by the use of the Beighton Scale, as in the Nathan et al. (2018) paper, whereby adult participants are deemed positive i...
Show MoreTo the Editor,
We read with great interest the systematic review by Joschtel et al.1 on the effects exercise training on physical and psychological health in children with pediatric respiratory diseases such as asthma, bronchiectasis, bronchopulmonary dysplasia and cystic fibrosis (CF). Undoubtedly, the authors should be commended for their effort that they have put into this systematic review on an important research topic. However, we would like to take the opportunity to express some methodological concerns related to the CF studies included in this review.
Joschtel et al.1 included studies on children, adolescents and young adults aged between 4 and 21 years and excluded those with a study population mean age of 21 years. These contradictory criteria have led to a false inclusion of one study 2 that included patients aged 12-40 years (although with a mean (SD) age of 19.5 (6.4) and 19.4 (5.3) for the intervention and control groups, respectively). Other studies 3 4, in which the mean age of the participants is <21 years were not considered for this review. Specifically, 3 out of 4 groups from the Kriemler et al. study 3 would qualify to be included in this review. Joschtel et al.1 did not publish a review protocol and therefore pre-specified inclusion and exclusion criteria cannot be verified.
Joschtel et al.1 have conducted a meta-analysis on peak oxygen uptake (VO2peak), despite substantial heterogeneity of study characteristics (i.e., study...
Show MoreDear Editor in Chief:
We read with great interest the recently published article by Tibana and de Sousa (1) titled “Are extreme conditioning programmes effective and safe? A narrative review of high intensity functional training methods research paradigms and findings.” We appreciate the opportunity to write this letter and hope to clarify some of the authors’ conclusions. Although the authors provide several examples of what they refer to as “extreme conditioning programs” we will focus mainly on the statements and evidence related to High Intensity Functional Training (HIFT), more commonly known as CrossFitTM training, as the authors’ review focuses primarily on this particular training program. We feel the authors have taken a biased position in describing this type of training and that their position is based on inaccurate and highly speculative interpretations of a fraction of the existing literature.
Research examining the acute and long-term responses to HIFT, as well as the incidence of injury, is quite limited. The observed responses predominantly describe changes from baseline and in the case of long-term adaptations, generally show a positive outcome. Further, the few studies that make comparisons to other exercise forms only show select differences. More importantly, by the authors’ own admission, research examining the risk of injury do not suggest HIFT/CrossFitTM to be different from other forms of recreational exercise. Yet, the authors descri...
Show MoreThank you to the authors for emphasizing this topic. Physical inactivity remains the big problem and major pandemic in the world. Besides Sweden, many developing and developed countries have this serious problems. Researchers may suggest that physical inactivity cost lead to bigger healthcare cost and economic burden in the future. Physical inactivity is contributed to about 6-10% of ischaemic heart disease, stroke, diabetes, breast and colon cancer(1). Global physical inactivity cost is estimated $67.5 billions in total which consist direct cost around $53.8 billions and indirect cost around $13.7 billions (2). As for Europe and North America, it remains higher cost than in Asia. In China, the total cost of physical inactivity is estimated total about $6.7 billions (3). As for Korea, cost as much as 83.6 million was contributed to physical inactivity(4). While in North America and Europe, it remains high each $28.9 billions and $15.5 billions in total cost (2).
It is much appreciated that the research filling the gap of data especially in Sweden. Other countries especially developing countries, should have the same idea about calculating the economic cost of physical inactivity. The current data in developing countries are inadequate, both direct and indirect cost which are very important. So that, the government can realize the important and dangerous effects of physical inactivity. Implementation should be underlined more on promotive and preventive action rath...
Show MoreWe read with interest the article by Parrish et al, “Normal platelet function in platelet concentrates requires non-platelet cells: a comparative in vitro evaluation of leucocyte-rich (type 1a) and leucocyte-poor (type 3b) platelet concentrates.”(1)
Parrish et al define PRP as a preparation with a platelet concentration of at least 5x over baseline, yet the LP-PRP they prepared (Arthrex Autologous Conditioned Plasma) was significantly lower at 2x over baseline, while the LR-PRP (Mitek Sports Medicine PEAK PRP) was significantly higher at 8x over baseline. We might reasonably expect that the ratio of growth factors between their LR-PRP and their LP-PRP to be approximately 8x/2x or 4:1, and this was indeed the case as seen in their Figure 4.
Subsequently, the authors grew tenocytes (tendon cells) exposed to serum derived from LR-PRP and LP-PRP preparations. Given that their LR-PRP was approximately 4 times richer in growth factors than their LP-PRP, we might reasonably expect that the 2.5% solution of serum derived from their LR-PRP have approximately the same effect as the 10% solution of serum derived from their LP-PRP. However, their 10% LP-PRP solution actually resulted in higher growth of tenocytes (2656 light units) than their 2.5% LR-PRP solution (1001 light units), as seen in their Table 5, but not discussed by the authors. The fact that their 10% LR-PRP-derived serum caused tenocytes to grow to confluence while their 10% LP-PRP-derived serum did...
Show MoreI have read Dr Robergs’ article 1 with much enthusiasm, from the first to the last paragraph. He criticized my occasional piece article suggesting a probable Kuhnian paradigm shift in Exercise Sciences2. I was expecting comments and critiques to my provocative essay since its publication, approximately five years ago. Perhaps, as Philosophy of Science is complex and purely reflexive, just a few exercise scientists have devoted enough time to study it. I now have the opportunity to continue debating and applying some Philosophy in the Exercise Sciences perspective.
Show MoreReading Dr Robergs’ 1 article drove me back to the Philosophy of Science to reexamine some crucial academic works essential to a better understanding of how science operates. Since my first critical essay as a beginner student in science, about “The objective knowledge” of Karl Popper 3 during lectures on the Philosophy of Science by Emeritus Professor Michel Paty at the University of São Paulo, my thinking has evolved through different views of science, from Francis Bacon to Karl Popper, from Thomas Kuhn to Paul Feyerabend. Thus, the biased commentary promoted by Dr Robergs towards the falsification method did not surprise me because Karl Popper was one of the first philosophers I read as a beginner in science. Neither was Dr Robergs’ 1 claim in favor of the falsification criteria in Exercise Sciences entirely new 4. As a philosophy-oriented scientist I learned that we may benefit from a wider view of scie...
I was surprised the authors did not take into consideration heel-to-toe height variances in SRSs, which can be significant (10+ mm). While this may have less effect on one's ability to land "softly" when running uphill, the opposite holds true on downward slopes; depending on the degree of slope, the heel is more likely to contact ground before or concurrent to the forefoot. At least, this has been my experience.
Secondly, while it may be true that a directive to "run softly" will effect the gait and form of a runner upon hearing the instructions, and may even hold sway for a few minutes, the truth is that we all tend to revert to habits after a time, and doubly so when fatigue sets in.
PM
To the editor,
Show MoreThe postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of...