We are pleased that our Leader has engendered interest, thank Prof
Lippi and his colleagues for their letter, and are grateful to the Journal
for the opportunity to reply. We fully agree with their ideas: using
normative data from non-athletic population may well result in over-
investigation and unnecessary worries for athletes. This is why we believe
that serum concentrations of the enzymes in quest...
We are pleased that our Leader has engendered interest, thank Prof
Lippi and his colleagues for their letter, and are grateful to the Journal
for the opportunity to reply. We fully agree with their ideas: using
normative data from non-athletic population may well result in over-
investigation and unnecessary worries for athletes. This is why we believe
that serum concentrations of the enzymes in question should be only part
of the picture, and accurate clinical history and examination should still
rule: a purely mechanistic approach would not serve our patients well.
Also, data should be generated for oher sports: for example, athletes
involved in contact sports and high level martial arts seem to have higher
levels of CK than endurance athletes[1], as have athletes on anabolic
steroids, as pointed out in our Leader. In the absence of a clinical picture of frank pathololgy, we would not
subject these athletes to tests. Furthermore, to further diminish
unnecessary invasive investigations, if CK and LDH levels are elevated, we
suggest a rest from athletic activities for two weeks before testing again
CK and LDH levels[2]. If still elevated, then further, more invasive,
investigations may be necessary
Paola Brancaccio, Francesco Mario Limongelli, Nicola Maffulli
Seconda Università di Napoli
Department of Experimental Medicine
Centre of Excellence of Cardiovascular Disease
Napoli, Italy (PB, FML)
Department of Trauma and Orthopaedic Surgery
Keele University School of
Medicine
Thornburrow Drive
Hartshill, Stoke on Trent
ST4 7QB Staffs
ENGLAND (NM)
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.
We read with great interest the article published in BJSM by
Dickinson et al (February 2006) (1) on challenge methods for screening
elite winter athletes for exercise induced asthma (EIA). We are in
agreement with the commentary by Professor Rundell that this is a solid
and clear paper reaffirming the efficacy of eucapnic voluntary
hyperventilation (EVH) in diagnosing EIA. However, we believe that...
We read with great interest the article published in BJSM by
Dickinson et al (February 2006) (1) on challenge methods for screening
elite winter athletes for exercise induced asthma (EIA). We are in
agreement with the commentary by Professor Rundell that this is a solid
and clear paper reaffirming the efficacy of eucapnic voluntary
hyperventilation (EVH) in diagnosing EIA. However, we believe that the
negative findings observed by the authors in regards to the laboratory
based exercise challenge may in fact be due to a number of procedural
limitations of the method selected. Anderson and Holzer (2) assert that
EIA is primarily determined via the level of ventilation achieved and
sustained during exercise, which reflects the intensity of exercise and
the water content of the inspired air; thus explaining recommendations for
the 2006 Turin Winter Olympic Games (3) “that the exercise test should be
performed breathing dry air for 8 minutes with the intensity of exercise
close to maximal for the last 4 minutes.” Indeed, in our laboratory, when
we conduct exercise challenge tests on elite athletes with physician-
diagnosed EIA we typically exercise them to volitional exhaustion (4).
Therefore the use of 90% of maximum heart rate for elite endurance
athletes by Dickerson et al (1) does not seem to be an adequate intensity
to allow them to ventilate at sufficiently high rates in order to elicit
airway drying and hence evoke symptoms of EIA. Perhaps reporting the
ventilation rates for each challenge would allow a better comparison of
the different testing procedures.
In addition, Evans et al. (5) recently demonstrated that dryness of
the test conditions rather than a cold temperature is essential to the EIB
response. It is generally accepted that inhaling cold-dry air at high
ventilation rates initiates EIA (4, 5). Rundell and coworkers (6) have
shown that out of 23 subjects who tested positive for EIA in cold-dry air,
18 (78%) subjects tested negative in ambient conditions (21oC and 50%
relative humidity). This suggests that the exercise protocol performed in
ambient conditions in the Dickinson et al. (1) study may have been less
sensitive to identifying changes in airway hyperresponsiveness following
exercise due to inadequate environmental stress.
Sincerely,
Martin R. Lindley, Ph.D.
Timothy D. Mickleborough, PhD. FACSM.
Indiana University.
References
1. Dickinson JW, Whyte GP, McConnell AK, Harries MG. Screening elite
winter athletes for exercise induced asthma: a comparison of three
challenge methods. Br J Sports Med 2006; 40: 179-183.
2. Anderson SD, Holzer K. Exercise-induced asthma: is it the right
diagnosis in elite athletes? J Allergy Clin Immunol 2000; 106: 419-428.
3. International Olympic Committee. Beta2 adrenoceptor agonists and
the Olympic Games in Turin. 2005.
http://multimedia.olympic.org/pdf/en_report_981.pdf (accessed 12 February
2006).
4. Mickleborough TD, Murray RL, Ionescu AA, Lindley MR. Fish oil
supplementation reduces severity of exercise-induced bronchoconstriction
in elite athletes. Am J Respir Crit Care Med 2003;168: 1181-1189.
5. Evans TM, Rundell KW, Beck KC, Levine AM, Baumann JM. Cold air
inhalation does not affect the severity of EIB after exercise or eucapnic
voluntary hyperventilation. Med Sci Sports Exerc 2005; 37:544-549.
6. Rundell KW, Wilber RL, Szmedra L, Jenkinson DM, Mayers LB, Im J.
Exercise-induced asthma screening of elite athletes: field versus
laboratory exercise challenge. Med Sci Sports Exerc 2000; 32: 309-316.
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.
Having trained for, competed in, and served as ringside physician for
numerous full-contact martial arts competitions, I took great interest in
reading Dr. G.H. Bledsoe’s letter “Mixed martial arts not all bad.”[1] I
appreciated his feedback regarding my article[2] and applaud his drive to
research combat sports with utmost objectivity. Acknowledging the dangers
of participation both from the perspe...
Having trained for, competed in, and served as ringside physician for
numerous full-contact martial arts competitions, I took great interest in
reading Dr. G.H. Bledsoe’s letter “Mixed martial arts not all bad.”[1] I
appreciated his feedback regarding my article[2] and applaud his drive to
research combat sports with utmost objectivity. Acknowledging the dangers
of participation both from the perspective of a researcher and former
fighter, I would like to address some of Dr. Bledsoe’s insights regarding
mixed martial arts (MMA).
Dr. Bledsoe commented, “Sanctioning [of MMA] brought about many rule
changes that mandated weight classes, time limits for rounds and matches,
and eliminated many of the most dangerous techniques including stomps,
head butts, and groin attacks.”[1] Unsanctioned until 2000, the United
States-based MMA organisation (USMMAO) used in my study had already
mandated rounds in 1995, weight classes in 1997, and “protective” MMA
gloves shortly thereafter. Since its inception in 1997, the Japan-based
MMA organisation (JMMAO) used in my study mirrored the same rules and
regulations of the sanctioned USMMAO events. In addition, no matches in my
study were stopped as the direct result of head butts (when legal) and 2
of the 642 matches (0.3%) were stopped due to stomps to the head. At the
time this letter was released, head stomps remained a legal technique in
the JMMAO despite sanctioning.
Dr. Bledsoe noted that MMA was sanctioned in September 2001. Although
this referred to the first MMA event in Las Vegas approved by the Nevada
State Athletic Commission, the New Jersey State Athletic Control Board was
actually the first to sanction the sport in Atlantic City one year prior.
I compared match stoppages due to head impact in the USMMAO during
1993-1997 (MMA gloves not mandatory) to those during 1998-2003 (MMA gloves
mandatory). Twenty-four of 120 matches (20.0%) were stopped due to head
impact from 1993-1997, while 98 of 287 matches (34.1%) were stopped due to
head impact from 1998-2003 (chi square analysis, p=0.01). Hence, mandatory
wear of MMA gloves and subsequent sanctioning of USMMAO events were not
associated with a reduction in match stoppages due to head impact.
Sanctioned or not, the sport will remain inherently risky so long as the
primary intent of the MMA encounter is to inflict trauma on one’s
opponent.
Dr. Bledsoe stated, “The fact that MMA has no ‘standing eight count’
enabling a concussed participant time to recover and continue fighting is
a tremendous step toward diminishing traumatic brain injury.”[1] The
validity of this statement should be assessed via neuropsychological
testing, neuroimaging, and/or neural biomarkers.[3,4] Since concussion
(e.g., transient loss of consciousness following a blow to the head) does
not reliably correspond to injury severity,[5] the MMA competitor that is
removed from a match following concussion may receive no advantage in
neuronal preservation over the boxer who continues fighting following a
standing eight count. Independent of rules, blunt head trauma sustained
among those who train and compete in MMA merits further research.
I look forward to reading the article by Dr. Bledsoe and
colleagues,[6] as their work will serve to further elucidate those medical
issues most salient to this burgeoning sport. I appreciate your objective
consideration of the combat sports and, through our continued efforts, we
will hopefully prevent undue morbidity and mortality.
Sincerely,
George J. Buse MD, CSCS
Department of Aerospace / Preventive Medicine, Cannon USAF Clinics,
Cannon Air Force Base, New Mexico
References
1. Bledsoe GH. Mixed martial arts not all bad. Br J Sports Med, 9 Feb
2006, http://bjsm.bmjjournals.com/cgi/eletters/40/2/169 (accessed 15 Feb
06).
2. Buse GJ. No holds barred sport fighting: a 10 year review of mixed
martial arts competition. Br J Sports Med 2006;40:169-72.
3. Erlanger DM, Kutner KC, Barth JT, et al. Neuropsychology of sports
-related head injury: dementia pugilistica to post concussion syndrome.
Clin Neuropsychol 1999;13:193-209.
4. Chen DQ, Zhu LL. Dynamic change of serum protein S100b and its
clinical significance in patients with traumatic brain injury. Chin J
Traumatol 2005;8:245-8.
5. McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement
statement of the 2nd International Conference on Concussion in Sport,
Prague 2004. Br J Sports Med 2005;39:196-204.
6. Bledsoe GH, Hsu EB, Grabowski JG, Brill JD, Li G. Incidence of
injury in professional mixed martial arts competitions. The Journal of
Sports Science and Medicine (in press).
Disclaimer: The views expressed herein are not to be construed as reflecting the policies of the United States Air Force or Department of Defense.
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.
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).
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
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.
Montain et al.(1) use a simplified version of the Nguyen-Kurtz
equation to predict a new plasma sodium concentration. This equation
accounts for the three principle determinants of change in plasma sodium
concentration, namely the mass balances of water, sodium and potassium.
However, the y-intercept in the original Edelman equation, appearing here
as 23.9 mEq/liter, is assumed in the simplified Ng...
Montain et al.(1) use a simplified version of the Nguyen-Kurtz
equation to predict a new plasma sodium concentration. This equation
accounts for the three principle determinants of change in plasma sodium
concentration, namely the mass balances of water, sodium and potassium.
However, the y-intercept in the original Edelman equation, appearing here
as 23.9 mEq/liter, is assumed in the simplified Nguyen-Kurtz equation to
remain constant. Nguyen and Kurtz(2) showed that the y-intercept is the
sum of four terms, and identified situations, in particular SIADH and
hyperglycemia, for which one or more of these terms has changed in turn
causing the y-intercept to change(2). In the simplified equation that
Montain et al. use, the first 23.9 (in parentheses, added to [Na+]p1)
represents the y-intercept for the initial conditions, or y1; and the
second 23.9 (subtracted at the end of the line) represents the y-intercept
for the final conditions, or y2 (4).
One of the four terms comprising the y-intercept is the sum of
exchangeable but osmotically inactive sodium and potassium divided by TBW,
or (Nai + Ki) /TBW. Osmotic inactivation of sodium has been hypothesized
to explain the subset of very low plasma sodium concentrations
occasionally observed in Syndrome of Inappropriate Antidiuretic Hormone
SIADH (cited in 2). Conversely, osmotic activation of sodium stores can
account for the recovery of very low plasma sodium concentrations to
values higher than can be explained by excretion of water and retention of
sodium (2). Mass balance studies of athletes hospitalized with severe
Exercise-Associated Hyponatremia (EAHN) suggest osmotic inactivation of
exchangeable sodium, and hence SIADH, as integral to the etiology of
severe EAHN (3). Mass balance studies of the same athletes during their
recovery are also consistent with osmotic activation of exchangeable
sodium stores (3).
Thus, while mass balance of TBW, Nae and Ke are the main determinants
of change in [Na+]p it is important to be mindful of other determinants,
accounted for by the y-intercept term, which may become significant during
exercise.
References
1 Montain SJ, Cheuvront SN, Sawka MN. Exercise associated
hyponatraemia: quantitative analysis to understand the aetiology. Brit J
Sport Med 2006;40:98-106
2 Nguyen MK, Kurtz I. Are the total exchangeable sodium, total
exchangeable potassium and total body water the only determinants of the
plasma water sodium concentration? Nephrol Dial Transplant 2003;18:1266-
71.
3 Noakes TD, Sharwood K, Speedy D, et al. Three independent
biological mechanisms cause exercise-associated hyponatremia: Evidence
from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U
S A 2005.
4 Weschler LB. Exercise-associated hyponatraemia: a mathematical
review. Sports Med 2005;35(10):899-922.
Dear Editor,
We are pleased that our Leader has engendered interest, thank Prof Lippi and his colleagues for their letter, and are grateful to the Journal for the opportunity to reply. We fully agree with their ideas: using normative data from non-athletic population may well result in over- investigation and unnecessary worries for athletes. This is why we believe that serum concentrations of the enzymes in quest...
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...
Dear Editor,
We read with great interest the article published in BJSM by Dickinson et al (February 2006) (1) on challenge methods for screening elite winter athletes for exercise induced asthma (EIA). We are in agreement with the commentary by Professor Rundell that this is a solid and clear paper reaffirming the efficacy of eucapnic voluntary hyperventilation (EVH) in diagnosing EIA. However, we believe that...
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 Editor,
Having trained for, competed in, and served as ringside physician for numerous full-contact martial arts competitions, I took great interest in reading Dr. G.H. Bledsoe’s letter “Mixed martial arts not all bad.”[1] I appreciated his feedback regarding my article[2] and applaud his drive to research combat sports with utmost objectivity. Acknowledging the dangers of participation both from the perspe...
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...
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...
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
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...
Dear Editor,
Montain et al.(1) use a simplified version of the Nguyen-Kurtz equation to predict a new plasma sodium concentration. This equation accounts for the three principle determinants of change in plasma sodium concentration, namely the mass balances of water, sodium and potassium. However, the y-intercept in the original Edelman equation, appearing here as 23.9 mEq/liter, is assumed in the simplified Ng...
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