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Recent eLetters

Displaying 1-10 letters out of 271 published

  1. Response to "Is tendinopathy research at a crossroads?"

    I fully agree with comments made by Masci regarding treatment for tendinopathy. I also practice at the coalface, treating tendon pain from elite to recreational athletes. The reality I face when prescribing exercise protocols is both a lack of evidence base as to the optimum program, and the harsh reality that most non-elite athletes will not strictly comply with complex home exercise programs, particularly where there is no rapid improvement in symptoms- people have busy and complex lives and it is not possible to simplify a complex life into a single tendon. I frequently opt for platelet rich plasma injections, as do many of my sports medicine colleagues. Anecdotally these work well, which, despite failing the evidence base test, passes the word of mouth test, and word of mouth is the source of many of my referrals. This is perhaps the major difference between research and the real world. If we adhere strictly to the evidence base, we should stop treating tendons altogether, and leave our patients in pain, as even the most widely used treatment programs have questionable evidence behind them. My approach is largely common sense based. Patients who are prepared to reduce loading on a painful tendon and work on a graded and comprehensive exercise program are offered that. Those who state outright that they will not do an exercise program, but wish to try PRP injections (because their friend/ relative/ sports colleague had great benefit) are not turned away, but given the treatment. I perform injections under ultrasound control, and treat gluteal and rotator cuff tendons as well as Achilles, patellar, and elbow tendons. Anecdotally most get better, and although this is not science, I am happy to inhabit the large grey area of tendinopathy treatment. I am also happy to follow the research, and change my approach as are knowledge evolves.

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  2. Dichotomy in translation raises the need for careful definition in use

    Clarification on the definition of use of the term 'intensity' as raised by Steele certainly serves to highlight the continuing variation - and confusion - around use of this term. Due to the ambiguity as to whether intensity is a measured load or is synonymous with perceived level of exertion, Steele recommended abandonment of intensity as a descriptive word.

    However it is my belief that the very dichotomy raised by Steele emphasises the need to quantify and define the term through the development and adoption of reliable and objective outcome measures, and ones that capture the dichotomy: i.e. the psychological (perceived level of exertion) and physiological (load) components of intensity.

    Translation and definition of terms are fundamentally important in the communication of science: in fact the imperative of research papers reporting the details of the research methods employed depends in turn on the definition and language used to communicate the methods.

    While I acknowledge that there are inherent problems in translation of the term intensity, I further believe there are issues surrounding the choice of definition being either 'load', or 'perception of exertion'.

    For example, an individual's maximum 'load', or 1RM, is not constant: rather, it represents a hypothetical 'best'. It fails to recognise differing circumstances, including human factors, and instead assumes a mechanistic uniformity in ability for 1 RM. However, there are a number of factors which may affect the ability of a individual to achieve a 1RM, including stressors; injury or muscle tightness; pre-fatigue from other lifts; DOMS (delayed onset muscle soreness); or even calorific deficit or inadequate nutrition. In such instances the measured load of 1RM would be altered (albeit transiently), but the (reported) intensity of the session would be higher despite lower loading.

    'Load' also does not capture other factors which affect the 'load' such as 'time'; if the lift is slowed down then there is more effort exerted without altering the load. Other ways of increasing the intensity of a lift without altering the load include reduced rest periods, more repetitions and 'concentration' sets whereby the person is restricted to main area of the workload (such as in squats the bottom half of range of movement).

    Similarly there are challenges in advocating intensity as being synonymous with perceived level of exertion, which requires the objective ability of the participant to distinguish with accuracy the effort required in a given exercise session. This presents two problems: often the complete novice participant has low experience in determining what their effort is on a continuum, when compared to (say) that of the experienced lifter/athlete. Further to this, there is the issue that, both the novice and advanced lifter are inclined to responder bias in such circumstances. Although for the advanced lifter their experience while provide a more accurate quantification of perceived level of exertion (perhaps due to more instances for comparison), in both cases the accuracy is contingent on the responder (and their associated prior agendas/preconceptions).

    It is my recommendation that intensity is not a term that becomes neglected or ceases to be used. The term must instead be defined in terms of reliable measures with which to underpin the definition in the respective study. These outcome measures should reflect the dual nature, and therefore, ambiguity in translation: they should include both physiological and psychological concepts, and measures. This would include and capture the level of exertion used while providing a more scientific foundation for replication.

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  3. Economical with the evidence!

    Although good to see researchers putting forward hypotheses for improving rehabilitation protocols I do believe there needs to be a balance of promoting their own work published in another journal (Scandinavian Journal of Medicine & Science in Sports) with incomplete presentation in an editorial article of another. In the original paper there were no differences between groups at 1, 6, and 12 months. There was no mention of this in the editorial paper. At 12 months, the Foot Function Index was lower in the stretch group. So if all our patients were just interested in how they functioned at 3 months post commencement of treatment it may be more relevant. There could be a variety of reasons for a transient difference at 3 months including chance, the sensitivity of the instrument, sample size etc. There may have been no difference at 4 months and it was a transient 'blip in the data. Perhaps an explanation of reported improvements at 3 months but not at 1,6 & 12, should have been hypothesised in relation to the high-load' model. Self-interest promotion of one's own model will be considered more seriously by others if the authors objectively present the data. Too often we are told of the next great step in treatment based on limited science and then have to readjust it and confuse our patients yet again.

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  4. Stand up for better research - avoiding cherry picking when reporting results

    With great interest we read Sj?gren et al.'s contribution that analyzed changes in telomere length in association to the time spent exercising and the time spent sitting in a 6-month randomized controlled trial in 49 older sedentary and overweight men and women. Sj?gren et al. concluded that reduced sitting time was significantly associated with telomere lengthening. These findings are of great potential interest, as highlighted in the accompanying press release. However, several questions remained for us after carefully reading this contribution: 1. In Figure 1 the associations for change in exercise time and change in telomere lengths for control and intervention group are given. When looking only at those participants with no or positive changes in exercise time, there seems to be a zero or even slightly positive association between change in exercise time and change in telomere length. With regard to the main hypothesis as laid down by the authors, we wonder why participants with reduced exercise time over the course of the study show highest values of lengthening. These are participants who exercised up to 500 minutes per week less at the end of the study than they did at baseline. It would be interesting to see an ANCOVA analysis of both groups combined including baseline telomere length values and baseline exercise time values. This would account for differences in baseline values of each subject and additionally for a possible curvilinear relationship between the change in exercise time and the change in telomere length. 2. Sj?gren et al. stated that they did not find significant associations between changes in steps per day and changes in telomere lengths. It would be helpful to see some descriptive statistics and the test results for that statement. Thus, the reader may get a more comprehensive picture of the study result; e. g., non-significance may just be due to small sample size. 3. The main result of the study is provided in figure 2: associations of change in sitting time and change in telomere length by group. Interestingly Sj?gren et al. only refer to the (significant) result in the intervention group which compiles data from 12 individuals. There is almost no association to be seen in the control group. This raises additional questions: How would the authors explain the differential results for the control and the intervention group? Was change in sitting time related to changes in steps per day or to changes in exercise time? 4. To gain a more comprehensive picture of the associations of interest, additional information as outlined above would be helpful. Furthermore, the role of confounders should be more thoroughly discussed, and results from the entire trial included in the discussion. Generally, it should be avoided to focus only on the subgroup with significant test results (Dwan et al. 2008).

    Getting the information to the points above would shine more light on the association between time spent for sitting, exercising and telomere lengths.

    Reference: Dwan K, Altman DG, Arnaiz JA, Bloom J, Chan AW, Cronin E, Decullier E, Easterbrook PJ, Von Elm E, Gamble C, Ghersi D, Ioannidis JP, Simes J, Williamson PR. (2008). Systematic review of the empirical evidence of study publication bias and outcome reporting bias. PloS one, 3(8), e3081.

    Conflict of Interest:

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  5. Thoracic outlet and pectoralis minor syndromes in sports

    The article by Dr. Twaij and associates nicely covers the range of thoracic outlet syndromes (TOS) seen in athletes. However, several important points have been overlooked. The chief diagnostic tool for neurogenic TOS is physical examination that includes four provocative maneuvers: Upper limb tension test (ULTT}, elevated arm stress test (EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the authors that pulse deficits by the Adson maneuver are too unreliable to use.

    The most important objective test is measurement of latency and amplitute of the medial antebrachial sensory cutaneous nerve (MAC) on EMG. 2 (Machanic2008) For neurogenic TOS, the only imaging study of value is the plain X-ray of the chest to reveal cervical or anomalous first ribs. MRI is helpful for recognizing associated or differential diagnoses, such as cervical spine or shoulder disease, but MRA to reveal arterial stenosis is not helpful in diagnosing neurogenic TOS because it is relying on a vascular sign to diagnose a neurologic condition. There are too many false negatives and positives.

    The underlying pathology in NTOS, is scarred muscle, not muscle hypertrophy. This comes from the healing of torn muscle fibers from neck trauma, which can be from a single acute accident or repetitive stress injury. 3 (Sanders 1990).

    The second observation in the article is failure to mention another group of closely related diagnoses in athletes that have similar symptoms, but lie below the clavicle in the subpectoral area--namely neurogenic pectoralis minor syndrome (NPMS), as well as arterial pectoralis minor syndrome (APMS) and venous pectoralis minor syndrome (VPMS). It is important to recognize the subpectoral conditions, as when they are present they can be treated by minimal risk surgical procedures, performed as outpatients and have recovery times of only one or two weeks.

    NPMS is a condition seen in athletes who use their arms above shoulder level to throw or pull, such as swimming, baseball, volleyball, gymnastics, and weight lifting. The pectoralis minor muscle (PMM) attaches to the coracoid process of the scapula. As such, repetitive actions of the shoulder that pull back the scapula stress the PMM. In time, the PMM scars, tightens, and can put pressure on any of the three structures in the axillary neurovascular bundle, but most often on the cords and branches of the brachial plexus.

    Symptoms of NPMS are the same as NTOS, pain, numbness, tingling, and weakness in the upper extremity, pain over the trapezius, and a lesser degree of neck pain and occipital headache. It is quite common for NPMS to accompany NTOS.

    Physical examination may reveal the same positive findings as NTOS, but in addition, there are two findings specific for NPMS: Tenderness over the PMM, just below the clavicle, and tenderness in the axilla. These two findings are not from NTOS, but indicate NPMS.

    A very helpful diagnostic test is a PMM muscle block with local anesthetic. After this is performed, the physical examination is repeated and the tenderness in those areas should temporarily disappear or be greatly reduced; provocative maneuvers show improvement. 4 (Sanders 2010)

    Arterial PMS is a condition seen almost exclusively in athletes who use there arms for vigorous overhead throwing. Baseball pitchers and volleyball players are the ones most often affected but it also can occur in mechanics and laborers who work with their arms above their heads. The pathology is either in the axillary artery or one of its branches, most often the posterior circumflex humeral artery(PCHA). This artery traverses the quadralateral space and wraps around the humeral head increasing resistance within the artery and causing aneurysm formation at the axillary-PGHA junction. These aneurysms tend to thrombose. When thrombus breaks off, it enters the axillary artery and embolizes distally.

    Arterial PMS elicits the same symptoms as Arterial TOS: Coldness, palor, arm claudication, and ischemic fingers. Diagnosis is by arteriograms revealing arterial occlusion by emboli in the forearm or hand. It also reveals a normal subclavian artery and may or may not reveal a normal axillary artery. Other mechanisms of APMS are compression of the axillary artery between the PMM and head of the humerus. This can result in axillary artery stenosis or even occlusion. 5 (Atema 2012 )

    Finally, venous PMS is rarely seen and caused by PMM compression of the axillary vein. It is the result of repetitive overhead activities with the upper extremities. Its symptoms are similar to venous TOS, intermittent swelling and cyanosis of the upper extremity. To date, all reported cases have been axillary vein obstruction without thrombosis.6 (Sanders 2007)

    Treatment for neurogenic PMS initially is physical therapy which is mainly stretching exercises of the PMM. If this fails, surgical treatment is minimum risk, outpatient pectoralis minor tenotomy (PMT) with a short recovery time. Treatment for venous TOS is also PMT.

    Arterial PMS is a surgical problem. Physical therapy is not an option. If the problem is stenosis of the axillary artery, PMT may be all that is required. If the axillary artery is aneurysmal or too badly scarred, repair by patch or replacement graft is required.7 (Duwayri 2011)

    Above all, the most important point is to recognize whether the pathology lies above the clavicle in the thoracic outlet area, or below the clavicle in the pectoralis minor area.

    References

    1. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100 operations for pectoralis minor syndrome alone or accompanied by neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.

    2. Machanic BI, Sanders RJ. Medial antebrachial cutaneous nerve measurements to diagnose neurogenic thoracic outlet syndrome. Ann Vasc Surg 2008; 22:248-254.

    3. Sanders RJ, Jackson CGR, Banchero N, Pearce WH: Scalene muscle abnormalities in traumatic thoracic outlet syndrome. Am J Surg. 1990; 159:231-6.

    4. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100 operations for pectoralis minor syndrome alone or accompanied by neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.

    5. Atema JJ, Unlu C, Reekers JA, Idu MM. Posterior circumflex humeral artery (PCHA) injury with distal embolizaion in professional volleyball players: Discussion of three cases. Eur J Vasc endovascular Surg 2012;44:195-198.

    6. Sanders RJ, Rao NM. Pectoralis minor obstruction of the axillary vein: Report of six patients. J Vasc Surg 2007; 45:1206-1211.

    7. Duwayri YM, Emery VB, Driskill MR, Earley JA, Wright RW, Paletta GAJr, Thompson RS. Position compression of the axillary artery causing upper extremity thrombosis and embolism in the elite overhead throwing athlete. J Vasc Surg 2011;53:1329-1340.

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  6. Role of intermittent hypoxic expression of Hypoxia Inducible Factors and NFKB in endurance exercise

    We have read the respective article and we agreed with all great findings. Nevertheless, we wish to emphasize the need to address the role of some molecular and physiological markers that may elaborate and possibly support the findings of the study. Intermittent hypoxia exposure can enhance the generation of red blood cells, which may consequentially increase hemoglobin concentration and hematocrit depending on the model of IHE exposure and its effect on serum hypoxia inducible factors (HIF-1 alpha, HIF-2alpha and HIF-3 alpha), erythropointin (EPO) levels and some signaling pathways (such as those mediated by the nuclear factor-kappa light chain B: NF-kB for stress and inflammation examinations) [1]. Hypoxia-inducible factors (HIF-1 alpha, HIF-2alpha and HIF-3alpha) are transcriptional regulatory factors that orchestrate cellular responses to hypoxia and regulates oxygen homeostasis[2]. However hypoxic induction of HIF-1alpha and HIF-2alpha leads to the transcriptional activation of HIF- 3alpha expression as a target gene, which in turn is involved in the reverse negative regulation of other HIFs activities [3]. Less intramuscular hypoxic shifts of metabolic parameters (lactate and pyruvate concentration, lactate/pyruvate and NAD/NADH ratios) after IHT [4] are accompanied by marked decrease of HIF-3alpha expression and increase in the resistance to physical exercise (with up to 70% increase endurance and 25% oxygen pressure in muscle). This indicates the importance of establishing the changes in HIFs system included in this study. Successive normobaric hypoxia-reoxygenation cycles in intermittent hypoxia exposure is associated with generation of cytosolic reactive oxygen species (ROS) which aid in transduction of cellular signals by stabilizing the HIF alpha subunits and promoting its translocation to nucleus and subsequent dimeruization with its alpha subunit to form complexes that binds to hypoxia response element (HRE) to express certain genes (e.g EPO, VEGF, NOS/HO-1 etc) that mediate cellular oxygen adaptation mechanism that will in the long run reflect on exercise performance and endurance[5]. Erythropoiesis is a classic physiologic response to hypoxia that is mediated by the HIFs through inducing cell-type specific gene expression changes that result in increased erythropoietin (EPO) production in kidney, liver and facilitates erythroid progenitor maturation and proliferation. HIF-2 is the main transcription factor that regulates EPO synthesis in the kidney and liver and plays a critical role in the regulation of intestinal iron uptake [6]. Although the heart rate during graded swim test was found to be the same before and after IHE, cardiac responses to hypoxia are quite dependent on carotid body function, which is deeply affected by its oxygen sensing capability. Tissue specificity of HIF-1 homolog (HIF-2alpha) may play an important role in the stable heart rate observed because irrespective of the wide expression of HIF-1 in many cells, including the carotid body glomus cells, hypoxia elicits different responses in different cell types [7]. Additionally, endurance training and intermittent hypoxia are effective preventive strategies against stress induced cardiac and mitochondrial dysfunction. There is need to support the findings of normal heart rate with further studies on signaling pathways, consequent metabolic and redox remodeling associated with a cardioprotective phenotype. This could be achieved by analyzing the myocardial heat shock proteins, cyclooxygenase-2 activity, endoplasmic reticulum stress proteins, nitric oxide production, myocardial antioxidant capacity, sarcolemmal and mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels [8]. In order to obtain a viable result, the inclusion and exclusion criteria must address previous exposure ti intermittent hypobaric hypoxia as it has been reported to decreases myocardial infarction size, reduces the number of ventricular arrhythmias, and improves the recovery of cardiac contractile function against acute ischemia-reperfusion (I/R) injury [9]. The crucial role of mitochondria in cellular energetics, metabolism and intracellular signaling processes regulating cell death and survival [10] has made it important to assess the role of mitochondria in the 4.8% and 1.6% performance declines observed in middle-distance (MD) and long-distance (LD) subjects as reported by the study.

    References: [1]. Zhang, C. Y., Zhang, J. X., L?, X. T., & Li, B. Y. (2009). Effects of intermittent hypoxic exposure on the parameter of erythrocyte and serum hypoxia inducible factor-1 alpha and erythropoietin levels. Xi bao yu fen zi mian yi xue za zhi= Chinese journal of cellular and molecular immunology, 25(10), 932. [2]. Semenza, G. (2009). Regulation of oxygen homeostasis by hypoxia- inducible factor 1. Physiology, 24:97-106. [3]. Hara, S., Hamada, J., Kobayashi, C., Kondo, Y., Imura, N. (2001). Expression and characterization of hypoxia-inducible factor (HIF)-3? in human kidney: suppression of HIF-mediated gene expression by HIF-3?. Biochemical and Biophysical Research Communications, 287:808-813. [4]. Semenza, G.L. (2001). HIF-1 O2 and the 3 PHDs: how animal cells signal hypoxia to the nucleus. Cell 107, 1-3. [5]. Mankovskaya, I., Drevitskaya, T., Dosenko, V., Gavenauskas, B., Moiseenko E. (2006). Expression of transcriptional factor HIF subunits in rat tissues under acute and intermittent hypoxia. Hypoxia Medical Journal, 35:1-2. [6]. Haase, V. H. (2013). Regulation of erythropoiesis by hypoxia- inducible factors. Blood reviews, 27(1), 41-53. [7]. Lahiri, S., Di Giulio, C., & Roy, A. (2002). Lessons from chronic intermittent and sustained hypoxia at high altitudes. Respiratory physiology & neurobiology, 130(3), 223-233. [8]. Kavazis, A.N. (2009). Exercise preconditioning of themyocardium. Sports Med, 11:923-35 [9]. Ostadal, B. and Kolar, F. (2007). Cardiac adaptation to chronic high- altitude hypoxia: beneficial and adverse effects. Respir Physiol Neurobiol. 2(3):224-36. [10]. Ascensao A, Magalhaes J, Soares JM, et al. Moderate endurance training prevents doxorubicin-induced in vivo mitochondriopathy and reduces the development of cardiac apoptosis. Am J Physiol Heart Circ Physiol 2005;2:H722-31.

    Conflict of Interest:

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  7. Angiogenesis towards Adipogenesis: Role of vascular endothelial growth factor

    We have read the respective article and we agreed with all great findings. But just need to emphasized on some thing very important and crucial. We are working with adipocytes and adipose tissue is capable of expanding many-fold during adulthood, therefore requiring the formation of new vasculature to supply growing and proliferating adipocytes. The expansion of the vasculature in adipose tissue occurs through angiogenesis, where new blood vessels develop from those pre-existing within the tissue (Corvera et al., 2013). Previous studies indicated that adipogenesis may be regulated by factors that drive angiogenesis. Fundamental aspects of angiogenesis, including basement membrane breakdown, vasculogenesis, angiogenic remodeling, vessel stabilization, and vascular permeability. Critical angiogenic factors include vascular endothelial growth factor (VEGF), VEGF receptors, angiopoietins (Ang), ephrins, matrix metalloproteinases, and the plasminogen enzymatic system. Vascular endothelial growth factor is the most critical factor because it initiates the formation of immature vessels and disruption of a single VEGF allele leads to embryonic lethality in mice. Expression of VEGF is influenced by hypoxia, insulin, growth factors, and several cytokines (Hausman et al., 2004). The VEGF has been reported to be modulated by leptin and hCG (Islami et al., 2003) and more recently the expression of angiogenic regulators, VGEF and leptin has been reported to be regulated by the EGF/PI3K/STAT3 pathway (Cascio et al., 2009). These vital findings reflects a regulation of secondary diseases related to obesity to be the result of complex molecular events and adipose tissue vasculature as a source of new targets for metabolic disease therapies. This gene is located on chromosome 11q13 (7 exons). VEGFB has been reported to have a role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation must be transported through the vascular endothelium to be metabolized by tissue cells. Bioinformatic analysis showed that VEGFB was tightly coexpressed with nuclear-encoded mitochondrial genes across a large variety of physiologic conditions in mice, pointing to a role for VEGFB in metabolism. VEGF specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb-/- mice showed less uptake and accumulation of lipids in muscle, heart, and brown adipose tissue, and instead shunted lipids to white adipose tissue. The co-expression of VEGFB and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated (Hagberg et al., 2012). In our study, we are also looking in to identify the mutation(s) in the VEGF-B gene in Malayisan Obese attributes towards CHD risk. We hypothesized, if there is a mutation in VGEF-B, then the obese subject will be predicted to have hypertension and if there will be no mutation then signs of metabolic syndrome and diabetes type II will be predicted in obese attribute in future. Most important the role of VEGF as major autocrine mediator of FGF-2-induced angiogenesis and proliferation (Naim et al 2005) should be considered by respective researchers in future.

    References:

    Cascio S, Ferla R, D'Andrea A, Gerbino A, Bazan V, Surmacz E, Russo A. Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells. J Cell Physiol. 2009 Oct;221(1):189-94. doi: 10.1002/jcp.21843.

    Corvera S, Gealekman O. Adipose tissue angiogenesis: Impact on obesity and type-2 diabetes. Biochim Biophys Acta. 2013 Jun 12. doi:pii: S0925-4439(13)00211-1. 10.1016/j.bbadis.2013.06.003.

    Hagberg CE, Mehlem A, Falkevall A, Muhl L, Fam BC, Orts?ter H, Scotney P, Nyqvist D, Sam?n E, Lu L, Stone-Elander S, Proietto J, Andrikopoulos S, Sj?holm A, Nash A, Eriksson U. Targeting VEGF-B as a novel treatment for insulin resistance and type 2 diabetes. Nature. 2012 Oct 18;490(7420)

    Islami D, Bischof P, Chardonnens D. Modulation of placental vascular endothelial growth factor by leptin and hCG. Mol Hum Reprod. 2003 Jul;9(7):395-8.

    Naim R, Chang RC, Sadick H, Bayerl C, Bran G, Hormann K. Effect of vascular endothelial growth factor on fibroblasts from external auditory canal cholesteatoma. Arch Med Res. 2005 Sep-Oct;36(5):518-23. PubMed PMID: 16099332.

    Conflict of Interest:

    Nil

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  8. Fundamentally important information

    Having taught medical students about the benefits of PA for the past 20 years and lived through WHO's 2002 World health day on PA, I had the belief that PA was now integrated and implemented in everyday practice. This nice little piece of research reminds us how difficult it is to change "routine" and how uncomfortable some of us feel when encouraging people to change their behaviour. Back to the drawing board...

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  9. Endurane Running and nutrition

    The article suggests that using fat as an energy source is how to fuel endurance events.

    Why is it that top marathons runners and the SKY/GB team don't do this but have a good balance of mainly carbohydrate and protein?

    Because using fat requires 3% more oxygen for the same amount of energy. Thus energy release is slower and it is why top athletes train specifically to perform glycogen depleted. If you understand the physiology it is so wrong. Why do cyclists consume carbohydrate during long stages

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  10. Can evolution explain the jumper's knee paradox?

    Dear Editor

    I read the excellent study by Halland et al with great interest (1). This study adds further support to the link between higher jumping performance and the development of patellar tendinopathy, as the authors note in the discussion (2). The reasons for this link are unclear but it is worth considering evolutionary theory in any explanation. The 'pleiotropy' theory for the evolution of ageing proposes that there are genetically determined 'trade-offs' between benefits to younger organisms and their viability at older ages (3, 4). In this way the advantage conferred by better jumping performance at a young age may be part of the same genetic package that results in the disadvantage of an increased susceptibility to tendinopathy at an older age.

    1. Helland C, Bojsen-Moller J, Raastad T, Seynnes OR, Moltubakk MM, Jakobsen V, et al. Mechanical properties of the patellar tendon in elite volleyball players with and without patellar tendinopathy. British journal of sports medicine. 2013. Epub 2013/07/09. 2. Visnes H, Aandahl HA, Bahr R. Jumper's knee paradox--jumping ability is a risk factor for developing jumper's knee: a 5-year prospective study. British journal of sports medicine. 2013;47(8):503-7. Epub 2012/10/13. 3. Kirkwood TB. Evolution of ageing. Mechanisms of ageing and development. 2002;123(7):737-45. Epub 2002/03/01. 4. Partridge L, Gems D. Mechanisms of ageing: public or private? Nature reviews Genetics. 2002;3(3):165-75. Epub 2002/04/25.

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