We read with interest the Review Article "Rotator cuff tendinopathy: A review", by Lewis, doi:10.1136/bjsm.2008.052175.
This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.
We read with interest the Review Article "Rotator cuff tendinopathy: A review", by Lewis, doi:10.1136/bjsm.2008.052175.
This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.
We investigated supraspinatus tendon samples obtained from patients undergoing arthroscopic repair of a rotator cuff tear to examine the distribution of tendinopathic changes associated with this condition. At arthroscopy, a full thickness supraspinatus tendon biopsy was harvested
close to the tear edge. We found more frequent tendon changes on the articular side of the rotator cuff[4]. We found more cartilage-like changes in patients affected by rotator cuff tears, but not in our control group. Recent biomechanical data suggest that the stress-shielded and
transversely-compressed side of the enthesis has a distinct tendency to develop cartilage-like or atrophic changes in response to the lack of tensile load [2,7,9,10]. Over a long period, this process may develop into a primary degenerative lesion in that area of the tendon. This may explain why the tendinopathy is not always clearly activity related, and can be strongly correlated with age. In this manner, it could almost be considered an ‘‘underuse’’ injury rather than an overuse injury as a result of stress-shielding [7,9,10]. The formation of cartilage-like changes
in the enthesis in many ways can be considered a physiological adaptation to the compressive loads [12-14]. It may not allow the tendon to maintain its ability to withstand high tensile loads in that region of the tendon.
As the stress-shielding may have led to tensile weakening over time, an injury may occur more easily in this region. In this manner, insertional tendinopathy could be considered an overuse injury, but predisposed by pre
-existing weakening of the tendon [12-14].
In another study 3 to evaluate the histopathological features of macroscopic intact tendon portion of patients with rotator cuff tears, we demonstrated that the supraspinatus tendons of patients undergoing
arthroscopic repair for a rupture show profound histopathologic changes, while the tendons of aged persons with no known tendon abnormalities have, as a group, little histological evidence of pathological changes. Moreover, tendon changes are not only localized at the site of rupture, but also in the macroscopic intact tendon portion.
Several centres are undertaking studies on tendinopathy [11,16,17] and the individual studies are unlikely to be large enough to result in adequate power for reliable evaluation. Therefore, combining the data from those
studies with a similar study design will be essential. Consistent high-quality pathology data are thus remarkably important for the success of the studies. Two scoring systems can be used for classification of the histopathological findings of tendinopathy: the Movin score [15] and its validated modifications [4,6,12] and the Bonar score [1]. We performed a study to answer the question whether these two scores of abnormal tendon
tissue were comparable [8]. In our hands, Movin and Bonar scores assess the same characteristics of tendon pathology.
In an frequency-matched case-control study we determined the plasma glucose levels in non diabetic patients with rotator cuff tear [5]. We found that normal, but in the high range of normal, increasing plasma glucose levels may be a risk factor for rotator cuff tear.
Lastly, although it is likely that the histopathology of tendinopathy is similar, of not the same, regardless of its location, this has only been shown in a formal fashion in the Achilles and patellar tendons [12]: we were slightly surprised of the fact that a number of papers dealing with
pathology of other tendons (i.e., patellar tendon, Achilles Tendon, and extensor carpi radialis brevis tendon (tennis elbow) are quoted referring to rotator cuff tendinopathy (references n°23,24,25,26,81,94,96,97,98,147,148).
Nicola Maffulli
Umile Giuseppe Longo
Vincenzo Denaro
References
1. Cook, J.; Feller, J.; Bonar, S.; and Khan, K. Abnormal tenocyte morphology is more prevalent than collagen disruption in asymptomatic athletes' patellar tendons. J Orthop Res 2004;22:334-338.
2. Gardner, K.; Arnoczky, S. P.; Caballero, O.; and Lavagnino, M. The effect of stress-deprivation and cyclic loading on the TIMP/MMP ratio in tendon cells: An in vitro experimental study. Disabil Rehabil 2008:1-7.
3. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Rabitti, C.; Morini, S.; Maffulli, N.; and Denaro, V. Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med 2008;36:533-8.
4. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Rabitti, C.; Morini, S.; Maffulli, N.; Forriol, F.; and Denaro, V. Light microscopic histology of supraspinatus tendon ruptures. Knee Surg Sports Traumatol Arthrosc
2007;15:1390-4.
5. Longo, U. G.; Franceschi, F.; Ruzzini, L.; Spiezia, F.; Maffulli, N.; and Denaro, V. Higher fasting plasma glucose levels within the normoglycemic range and rotator cuff tears. Br J Sports Med 2008;
6. Maffulli, N.; Barrass, V.; and Ewen, S. W. Light microscopic histology of achilles tendon ruptures. A comparison with unruptured tendons. Am J Sports Med 2000;28:857-63.
7. Maffulli, N.; Khan, K. M.; and Puddu, G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy 1998;14:840-3.
8. Maffulli, N.; Longo, U. G.; Franceschi, F.; Rabitti, C.; and Denaro, V. Movin and Bonar scores assess the same characteristics of tendon histology. Clin Orthop Relat Res 2008;466:1605-11.
9. Maffulli, N.; Reaper, J.; Ewen, S. W.; Waterston, S. W.; and Barrass, V. Chondral metaplasia in calcific insertional tendinopathy of the Achilles tendon. Clin J Sport Med 2006;16:329-34.
10. Maffulli, N.; Sharma, P.; and Luscombe, K. L. Achilles tendinopathy: aetiology and management. J R Soc Med 2004;97:472-6.
11. Maffulli, N.; Testa, V.; Capasso, G.; Bifulco, G.; and Binfield, P. M.
Results of percutaneous longitudinal tenotomy for Achilles tendinopathy in middle- and long-distance runners. Am J Sports Med 1997;25:835-40.
12. Maffulli, N.; Testa, V.; Capasso, G.; Ewen, S. W.; Sullo, A.; Benazzo, F.; and King, J. B. Similar histopathological picture in males with Achilles and patellar tendinopathy. Med Sci Sports Exerc 2004;36:1470-5.
13. Maffulli, N.; Waterston, S. W.; and Ewen, S. W. Ruptured Achilles tendons show increased lectin stainability. Med Sci Sports Exerc 2002;34:1057-64.
14. Maffulli, N.; Wong, J.; and Almekinders, L. C. Types and epidemiology of tendinopathy. Clin Sports Med 2003;22:675-92.
15. Movin, T.; Gad, A.; Reinholt, F.; and Rolf, C. Tendon pathology in long-standing achillodynia. Biopsy findings in 40 patients. Acta Orthop
Scand 1997;68:170-5.
16. Murrell, G. A. Oxygen free radicals and tendon healing. J Shoulder Elbow Surg 2007;16:S208-14.
17. Murrell, G. A. Using nitric oxide to treat tendinopathy. Br J Sports Med 2007;41:227-31.
I have Type 2 diabetes. I'm 53 years old. My blood sugar level was 22
mml/L and I was obese. Now I have reached the ideal weight within 3 months
following a strict diabetes diet together with a 30 or 45 minute exercise
daily and Glucophage 850 twice a day.
Now I am off medication but still on dieting and exercise.
My fasting blood Sugar level is stable at around 5.6 - 5.8 every morning
and stays so after 3 hours of meals. T...
I have Type 2 diabetes. I'm 53 years old. My blood sugar level was 22
mml/L and I was obese. Now I have reached the ideal weight within 3 months
following a strict diabetes diet together with a 30 or 45 minute exercise
daily and Glucophage 850 twice a day.
Now I am off medication but still on dieting and exercise.
My fasting blood Sugar level is stable at around 5.6 - 5.8 every morning
and stays so after 3 hours of meals. The 2-hour level is usually higher,
but it does not go higher than 9.0 mml/L, and it always comes down to 5.6
- 5.8 after 3 hours or sometimes 4.
I mentioned all that so that I can say that a 45 minute exercise
daily (treadmill) with some aerobics, is much more effective in reducing
the blood sugar level than a
30 minute one. I hope this will help others. But it could also be an
individual case.
We are pleased that Dr. Shephard agrees with our views. In contrast
to his retrospective assertions, dispassionate analysis of what he has
written in the past shows that his conversion to our drinking guidelines
has occurred only with the publication of his most recent letter.
Professor Shephard continues to be dismissive of most of the work of
our Cape Town research unit [1, 2]. To our knowledge we have lar...
We are pleased that Dr. Shephard agrees with our views. In contrast
to his retrospective assertions, dispassionate analysis of what he has
written in the past shows that his conversion to our drinking guidelines
has occurred only with the publication of his most recent letter.
Professor Shephard continues to be dismissive of most of the work of
our Cape Town research unit [1, 2]. To our knowledge we have largely
single-handedly led the battle against overdrinking [3-6] beginning with
our 1985 paper [7]; we are not aware that Professor Shephard ever
contributed to that campaign although we obviously welcome his belated
support. To state that this is a “relatively new insight for
investigators in Cape Town” is perhaps the most remarkable distortion to
be published in the British Journal of Sports Medicine in the past 40
years that the senior author has been reading this journal. It brings to
mind the famous statement to the effect that truth goes through three
distinct phases. First other scientists say that what you claim is
completely wrong. Next they acknowledge that your claim is indeed true
but they continue to dismiss it as “completely irrelevant”. Finally they
claim your truth as their own declaring that “we always said it anyway”.
About six years ago Professor Shephard concluded that the drinking
guidelines in Lore of Running [8] were completely wrong, perhaps
dangerous. Now apparently he was the first to propose those identical
guidelines “26 years ago”.
Our analysis of what appears in Professor Shephard’s book is not
“totally incorrect”. His book is cited only once in our paper (table 1)
[9]. The book does not provide a set of drinking guideline for athletes.
Instead at different parts of the text, there are references that
Professor Shephard now claims can be cobbled together to produce a set of
drinking guidelines. For example his assertions 1 and 3 in his letter
(pp. 42 and 72 respectively in [10]) are not drinking guidelines.
Assertion 2 is also not written as part of a drinking guideline. Rather
it appears as part of a review of previous work of fluid intake and
runners. For example on page 43 of his book Shephard writes: “…Kavanagh
and Shephard (1977a) followed middle-aged men over a 4- to 5-hr run; their
group sustained a fluid intake of up to 630 ml.hr-1, the largest volumes
again being ingested by those who were provided with pure water” [10].
Nowhere in his text does Professor Shephard define optimum rates of fluid
intake during exercise, what we would consider a core component of
responsible drinking guidelines. Of course providing specific drinking
guidelines involves personal accountability and not everyone is prepared
to accept that responsibility.
A more complete examination of the book reveals further examples of
advice that is so vague that it is of little value. For example on page 42
Professor Shephard writes: “the water balance of a distance runner or team
sportsman can be improved if he is preloaded with up to 500ml of fluid 15-30min before exercise commences. Further small quantities of fluid should
be taken at regular intervals as exercise proceeds” [10].
Finally in contrast to Professor Shephard’s certainty that his book
does not contain advice which would encourage athletes to “drink beyond
thirst”, page 309 contains the following specific advice: “During exercise
or heat exposure, thirst is not a sufficient indicator of fluids needs
(Adolph, 1947)”. Thus Professor Shephard’s book like most of the other
material that we reviewed, does indeed promote overdrinking.
In summary, one of the points of our article was to show how
textbooks can perpetuate old and often out-of-date advice. Professor
Shephard’s response extends that argument by showing that some authors are
unaware of exactly what is in their own textbooks and how dated and
incorrect that advice might be.
References
1. Shephard RJ. Do the Numbers Add Up? Clin J Sport Med. 13(3):192,
May 2003.
2. Shephard RJ. Hard evidence for a Central Governor is still
lacking! J Appl Physiol, in press 2008.
3. Noakes TD. Drinking guidelines for exercise: What evidence is
there that athletes should drink “as much as tolerable”, to “replace the
weight lost during exercise” or “ad libitum”? J Sports Sci 2007;25(7):781-
796.
4. Noakes TD, Sharwood K, Speedy D, et al. Three independent
biological mechanisms cause exercise-associated hyponatraemia: evidence
from 2,135 weighed competitive athletic performances. Proc Nat Acad Sci
USA 2005;102(51):18550-18555.
5. Hew T, Almond C, Ayus C, et al. Consensus Statement of the 1st
International Exercise-Associated Hyponatraemia Consensus Development
Conference, Cape town, South Africa 2005. Clin J Sport Med 2005;15:208-
213.
6. Noakes TD, Martin DE. IMMDA advisory statement on guidelines for
fluid replacement during marathon running. New Studies in Athletics
2002;17(1):15-24.
7. Noakes TD, Goodwin N, Rayner BL, Branken T, Taylor RK. Water
intoxication: a possible complication during endurance exercise. Med Sci
Sports Exerc. 1985 Jun;17(3):370-5.
8. Noakes TD. Lore of running. 4th ed. Champaign, Il: Human Kinetics,
2003.
9. Beltrami FG, Hew-Butler T, Noakes TD. Drinking policies and
exercise-associated hyponatremia: is anyone still promoting overdrinking?
Br J Sports Med 2008; 42:496-501.
10. Shephard RJ. Physiology and Biochemistry of Exercise. New York:
Prager Publications, 1982.
Yes, the pendulum has swung but it happened last year.
Readers might be interested in reading 'The Myth of Core Stability' by E.
Lederman found at:
http://www.ppaonline.co.uk/download/myth_of_core_stability.doc
This is a forward-looking study in which modern day footballs were
employed to assess the possible impact on the brain by heading. Old style
heavy footballs, however, may well have been associated with brain damage
as pointed out by Dr Breimer.
That the brains of woodpeckers would be full of plaques and signs of
neuronal damage is a tall story. One case of cereb...
This is a forward-looking study in which modern day footballs were
employed to assess the possible impact on the brain by heading. Old style
heavy footballs, however, may well have been associated with brain damage
as pointed out by Dr Breimer.
That the brains of woodpeckers would be full of plaques and signs of
neuronal damage is a tall story. One case of cerebral amyloid angiopathy
(a very common and unspecific ageing sign) has been reported in an aged
great spotted woodpecker (Nakayama H, et al., Neurobiol Aging. 1999 Jan-Feb;20(1):53-6). In contrast, the woodpecker is very well adapted by
evolution to repeated head blows by different anatomical structures that
protect the brain (see May PR, et al., Lancet. 1976 Feb 28;1(7957):454-5;
and Schwab IR, Br. J. Ophthalmol. 2002;86;843 for examples).
It could be argued that this study has been performed with the wrong
type of ball, one unlikely to reflect the type of brain stress inflicted
on old footballers, because the old style ball absorbed dampness from the
grass and became increasingly heavy and stiff, even if it had not been
raining; on a rainy day the weight had increased a lot by the end of the
match. Such balls needed power to kick, yet,...
It could be argued that this study has been performed with the wrong
type of ball, one unlikely to reflect the type of brain stress inflicted
on old footballers, because the old style ball absorbed dampness from the
grass and became increasingly heavy and stiff, even if it had not been
raining; on a rainy day the weight had increased a lot by the end of the
match. Such balls needed power to kick, yet, as a corollary, they flew
like cannonballs and were hard for goalies to stop, so many goals were
scored towards the end of the match, often from distance shots. Heading
them was something else.
I seem to remember that the brains of woodpeckers are full of plaques
and signs of neuronal damage. Albeit that woodpeckers need not solve
differential equations or even remember their latin names, notwithstanding
they may be suitable models to study for serum biomarkers of repetitive
brain trauma. Given that one would be studying the natural behaviour of
woodpeckers ethics approval should be straightforward while repeating the
study with a thoroughly doused old-style football might present a
challenge.
There is one recent textbook which explains the problem and promotes
'sensible' drinking policies.
Grant S, Lloyd E. Training and Performance in difficult
environments.
Crowood Press 2006.
ISBN-10 1 86126 881 5 & ISBN-13 978 1 86126 881 5
This was published in Dec 2006 and is planned to be readable for
competitive
and social athletes, coaches, physios and doctors both sports medicine
orientated and general. It covers physiology and science at practical
levels,
and covers the drinking controversy in considerable detail.
Beltrami and colleagues are correct to castigate the continued over-ingestion of fluids by marathon runners [1]. This may be a relatively new
insight for investigators in Cape Town, where reports of over-hydration
first surfaced. However, if the authors of the present report [1] will
reread my textbook (wrongly described as published in 1974!), they will
discover that it contains advice on fluid intake for distance runner...
Beltrami and colleagues are correct to castigate the continued over-ingestion of fluids by marathon runners [1]. This may be a relatively new
insight for investigators in Cape Town, where reports of over-hydration
first surfaced. However, if the authors of the present report [1] will
reread my textbook (wrongly described as published in 1974!), they will
discover that it contains advice on fluid intake for distance runners,
advice which in my view requires little modification in 2008 [2]. The
topic is discussed in chapters 2 and 3 of the cited text [2]. Among the
recommendations that were made some 26 years ago are:
recognizing that a cumulative weight loss of up to 2 kg is compatible
with euhydration over the course of a marathon run,
allowing ad-libitum, thirst-guided drinking of up to 600 ml/h of
water or other fluids during the course of such an event, and
weighing of runners immediately before and after a race offers the
best simple check on hydration status.
The interpretation of Beltrami and colleagues (p. 498) that advice in
my text is either absent or falls within the range ‘from “drink to match
sweat rates” to “drink beyond thirst” ‘ is unfortunately totally
incorrect.
References
1. Beltrami FG, Hew-Butler T, Noakes TD. Drinking policies and
exercise-associated hyponatremia: is anyone still promoting overdrinking?
Br J Sports Med 2008; 42:496-501.
2.Shephard RJ. Physiology and Biochemistry of Exercise. New York: Prager
Publications.
I appreciate the randomised-controlled trial comparing eccentric
training with or without an additional night splint in mid-portion
Achilles tendinopathy. [1] This trial could not demonstrate an additional
benefit of a night splint besides eccentric training in terms of pain
reduction, VISA score, patient satisfaction or neovessels score.
Despite the differences of a night splint and a daily Achilles wrap
these...
I appreciate the randomised-controlled trial comparing eccentric
training with or without an additional night splint in mid-portion
Achilles tendinopathy. [1] This trial could not demonstrate an additional
benefit of a night splint besides eccentric training in terms of pain
reduction, VISA score, patient satisfaction or neovessels score.
Despite the differences of a night splint and a daily Achilles wrap
these results may be interpreted in line with our RCT comparing eccentric
training with or without a pneumatic Achilles wrap (AirHeel) over 12
weeks. [2] While eccentric training could reduce pain, improve FAOS scores
and improve Achilles tendon microcirculation, the combined group was not
significantly better in terms of pain reduction (37% reduction in the
combination group vs. 34% pain reduction in the eccentric training only
group). This is somehow supported by another AirHeel randomized trial by
Petersen, where the combination of eccentric training and AirHeel was not
superior to each measure alone in terms of pain, AOFAS ankle score, and SF
-36 score. [3]
Interestingly, de Jonge and coworkers did not found any predictive value
of baseline score of neovessels and the one year outcome in terms of the
VISA score. To date, in line with several previous reports [4,5] , nobody
could establish a close relationship between the power Doppler result of
the amount of neovessels and the clinical response. This is intriguing at
least in my personal view. Given the fact that we should follow and
address patients’ symptoms first, the VISA score or other validated scores
are to be appreciated as the gold, the primary end points of future
tendinopathy trials.
At this time it is at least questionable, given not only de Jonge’s
observation, that the neovessel score at all has any clinical correlate.
References
[1] de Jonge S, de Vos RJ, van Schie HT, Verhaar JA, Weir A, Tol JL.
One-year follow-up of a randomized controlled trial on added splinting to
eccentric exercises in chronic midportion Achilles tendinopathy. Br J
Sports Med 2008 Oct 6.
[2] Knobloch K, Schreibmueller L, Longo UG, Vogt PM. Eccentric
exercises for the management of tendinopathy of the main body of the
Achilles tendon with or without he AirHeel brace. A randomized controlled
trial. A: Effects on pain and microcirculation. Disabil Rehabil 2008;5:1-
7.
[3] Chronic Achilles tendinopathy: a prospective randomized study
comparing the therapeutic effect of eccentric training, the AirHeel brace,
and a combination of both. Am J Sports Med 2007;35(10):1659-67.
[4] Knobloch K. The use of a neovascularisation score to predict
clinical severity in Achilles tendinopathy. Am J Sports Med
2008;36(2):395.
[5] de Vos RJ, Weir A, Cobben LP, Tol JP. The value of power Doppler
ultrasonography in Achilles tendinopathy: a prospective study. Am J Sports
Med 2007;35(10):1696-701.
I would like to thank Dr. Arno Müller for his thoughtful
response to my recent editorial, and for raising several important points
that I did not tackle in my brief consideration of the mass ECG screening
of athletes.
Firstly, mass ECG screening is required by law in Italy
[1], and is recommended by the European Society of Cardiology [2], but is
not recommended by either the American Heart Assoc...
I would like to thank Dr. Arno Müller for his thoughtful
response to my recent editorial, and for raising several important points
that I did not tackle in my brief consideration of the mass ECG screening
of athletes.
Firstly, mass ECG screening is required by law in Italy
[1], and is recommended by the European Society of Cardiology [2], but is
not recommended by either the American Heart Association or the American
College of Cardiology [3]. Nevertheless, Dr. Müller is correct in
underlining that there is no rigid transatlantic divide on this issue.
Some groups in Europe accept that screening is inappropriate, and some
supporters of mass screening can undoubtedly be found in North America.
Secondly, a family history of sudden premature death
undoubtedly gives some indication of an increased risk of sudden death in
a young athlete. But unfortunately, a family history of premature death
is by no means universal in patients with hypertrophic cardiomyopathy. Is
genetic technology helpful in identifying a sub-group of vulnerable
individuals, thus allowing cost-effective detailed investigation with a
low burden of false positive test results? Certainly, a variety of
genetic mutations have been associated with hypertrophic cardiomyopathy,
including abnormalities that affect cardiac troponins T and I, the beta-
myosin heavy chain, alpha tropomyosin, alpha-actin and myosin-binding
protein C [4-10]. At only one of several possible sites of mutation, the
chromosomal locus 14ql, as many as 36 possible abnormalities of the β-MHC gene have been implicated [5]; some of these mutations are associated
with a dramatic shortening of life span, but with others,
the life span is virtually normal. The phenotypic penetrance of the
abnormal genotype is often low, and sometimes there is an interaction with
environmental factors; if myocardial hypertrophy develops at all, it may
not be seen until middle age. Further, about a half of the cases of
hypertrophic cardiomyopathy apparently have no genetic basis [5]. The
rarity and heterogeneity of the relevant genetic abnormalities, and the
variability of their penetrance are important obstacles. Genetic screening
is also tedious, time-consuming and expensive. Thus, at present this
approach cannot be recommended as a method of triage prior to more
detailed electrocardiographic and echocardiographic screening.
Does a sinister fear of legal action cause some physicians
to oppose universal ECG screening? One would certainly hope not. In
general, if there is fear of a malpractice suit in North America, it acts
in the opposite sense to what Dr. Müller suggests. There is a regrettable
tendency to perform tests that are unnecessary or have little diagnostic
value, because the physician fears criticism for not undertaking a
thorough enough screening protocol. B.J. Maron argues that a
successful action for malpractice in relation to pre-participation
screening would require evidence of negligence, including deviation from
accepted medical practice, and a failure to use established diagnostic
criteria that would have disclosed the risk of sudden death during
exercise [11]. At least in North America, neither of these conditions is
satisfied if a physician has advised against ECG screening.
Does an athlete have the right to insist on ECG
screening? Given that little useful information is likely to result, this
should not be permitted if the costs of testing are to be met from the
public purse. However, if the competitor or the parents are prepared to
assume this expense, there can be little objection, provided that the
fallibility of the test has been explained clearly to them. The only
potential harm to the athlete is a false positive test result, and thus an
unnecessary subsequent restriction of physical activity.
A related question is whether athletes want to know about
possible contraindications to participation in their chosen sport. In
general, both the individual and society accept that we are unlikely to
achieve zero risk in competitive sports. For activities such as mountain
climbing and snow-boarding, risk is an inherent part of the experience for
the participant. Equally, in traditional sports such as North American
football, most team members recognize and accept the current risks of
major trauma and fatalities, and few would wish to abandon competition
because they cannot be assured of a 100 per cent safety record.
References
1. Corrado D, Basso C, Pavei A, et al. Trends in sudden
cardiovascular death in young competitive athletes after implementation of
a preparticipation screening program. JAMA 2006;296:1593–601.
2. Corrado D, Pelliccia A, Bjornstad HH, et al. Cardiovascular pre-
participation screening of young competitive athletes for prevention of
sudden death: Proposal for a common European protocol. Consensus Statement
of the Study Group of Sport Cardiology of the Working Group of Cardiac
Rehabilitation and Exercise Physiology and the Working Group of Myocardial
and Pericardial Diseases of the European Society of Cardiology. Eur Heart
J 2005;26:516–24.
3. Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and
considerations related to preparticipation screening for cardiovascular
abnormalities in competitive athletes: 2007 update: A scientific statement
from the American Heart Association Council on Nutrition, Physical
Activity, and Metabolism: Endorsed by the American College of Cardiology
Foundation. Circulation 2007;115:1643–55.
4. Geisterfer-Lowrance AAT, Kass S,Tanigawa G et al. A molecular
basis for familial hypertrophic cardiomyopathy: a β-myosin heavy
chain gene mutation. Cell 1990; 62: 999-1006.
5. Marian AJ, Roberts R. Recent advances in the molecular genetics of
hypertrophic cardiomyopathy. Circulation 1995; 92:1336-47.
6. Schwarz K, Carrier L, Guicheney P et al. Molecular basis of
familial cardiomyopathies, Circulation 1995; 91: 532-540.
7. Spirito P, Seidman CE, McKenna WJ et al. The management of
hypertrophic cardiomyopathy. N Engl J med 1997; 336: 775-785.
8. Thierfelder L, Watkins H, MacRae C et al. α-tropomyosin and
cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a
disease of the sarcomere. Cell 1994; 77: 701-712.
9. Watkins H, Conner D, Thierfelder L et al. Mutations in the cardiac
myosin binding protein-C gene on chromosome 11 cause familial hypertrophic
cardiomyopathy. Nature Genetics 1995; 11: 434-437.
10. Daw EW, Chen SN, Czernuszewicz G. et al. Genome-wide mapping of
modifier chromosomal loci for human hypertrophic cardiomyopathy. Human Mol
Genet 2007; 16:2463-71, 2007.
11. Maron BJ. Considerations for preparticipation cardiovascular
screening in young competitive athletes. In: Endurance in Sport, 2nd ed.
Editors: R.J. Shephard, P-O Åstrand. Oxford, UK: Blackwell Scientific,
2000; pp. 667-681.
Dear Sir,
We read with interest the Review Article "Rotator cuff tendinopathy: A review", by Lewis, doi:10.1136/bjsm.2008.052175.
This manuscript may have been submitted before the publication of our investigations. Nevertheless, we would like to call your attention to the fact that we have performed several studies on the aetiology, histopathology and management of rotator cuff tendinopathy.
We investig...
I have Type 2 diabetes. I'm 53 years old. My blood sugar level was 22 mml/L and I was obese. Now I have reached the ideal weight within 3 months following a strict diabetes diet together with a 30 or 45 minute exercise daily and Glucophage 850 twice a day. Now I am off medication but still on dieting and exercise. My fasting blood Sugar level is stable at around 5.6 - 5.8 every morning and stays so after 3 hours of meals. T...
We are pleased that Dr. Shephard agrees with our views. In contrast to his retrospective assertions, dispassionate analysis of what he has written in the past shows that his conversion to our drinking guidelines has occurred only with the publication of his most recent letter.
Professor Shephard continues to be dismissive of most of the work of our Cape Town research unit [1, 2]. To our knowledge we have lar...
Yes, the pendulum has swung but it happened last year. Readers might be interested in reading 'The Myth of Core Stability' by E. Lederman found at: http://www.ppaonline.co.uk/download/myth_of_core_stability.doc
Reply: Right type of ball used in study
This is a forward-looking study in which modern day footballs were employed to assess the possible impact on the brain by heading. Old style heavy footballs, however, may well have been associated with brain damage as pointed out by Dr Breimer.
That the brains of woodpeckers would be full of plaques and signs of neuronal damage is a tall story. One case of cereb...
Dear Editor
It could be argued that this study has been performed with the wrong type of ball, one unlikely to reflect the type of brain stress inflicted on old footballers, because the old style ball absorbed dampness from the grass and became increasingly heavy and stiff, even if it had not been raining; on a rainy day the weight had increased a lot by the end of the match. Such balls needed power to kick, yet,...
Dear Sir
There is one recent textbook which explains the problem and promotes 'sensible' drinking policies.
Grant S, Lloyd E. Training and Performance in difficult environments. Crowood Press 2006.
ISBN-10 1 86126 881 5 & ISBN-13 978 1 86126 881 5
This was published in Dec 2006 and is planned to be readable for competitive and social athletes, coaches, physios and doctors b...
Beltrami and colleagues are correct to castigate the continued over-ingestion of fluids by marathon runners [1]. This may be a relatively new insight for investigators in Cape Town, where reports of over-hydration first surfaced. However, if the authors of the present report [1] will reread my textbook (wrongly described as published in 1974!), they will discover that it contains advice on fluid intake for distance runner...
I appreciate the randomised-controlled trial comparing eccentric training with or without an additional night splint in mid-portion Achilles tendinopathy. [1] This trial could not demonstrate an additional benefit of a night splint besides eccentric training in terms of pain reduction, VISA score, patient satisfaction or neovessels score.
Despite the differences of a night splint and a daily Achilles wrap these...
Dear Editor
I would like to thank Dr. Arno Müller for his thoughtful response to my recent editorial, and for raising several important points that I did not tackle in my brief consideration of the mass ECG screening of athletes.
Firstly, mass ECG screening is required by law in Italy [1], and is recommended by the European Society of Cardiology [2], but is not recommended by either the American Heart Assoc...
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