It was a pleasure to read Paul McRory championing the cause of comparative animal and human physiology, and of his equine example.(1) To the latter he might have added that, because the horse is entirely a nasal breather, attempts were made, from 1800 BC in Egypt to 17th century Europe, to increase its ventilation by slitting the nostrils, paralleling the (equally futile) attempts of modern runners with nas...
It was a pleasure to read Paul McRory championing the cause of comparative animal and human physiology, and of his equine example.(1) To the latter he might have added that, because the horse is entirely a nasal breather, attempts were made, from 1800 BC in Egypt to 17th century Europe, to increase its ventilation by slitting the nostrils, paralleling the (equally futile) attempts of modern runners with nasal strip dilators.
More seriously, alongside its ventilatory-locomotor coupling due to the threefold effects of the visceral piston, the cervical pendulum and scapular-thoracic-compression which he mentioned, is the fact that the horse effectively blood dopes during its race warm-up. Autonomic splenic contraction releases enough erythrocytes to increase the haematocrit from a resting mean of around 40% to an extraordinary racing level of 60% or higher. The horse also undergoes a longer term training hypervolaemia comparable to human endurance athletes. All this gives it a VO2max of the order of 180? 200ml.kg.min, and a mile time of 1min 35s, so perhaps the horse is not particularly 'physiologically limited'? Mind you, this hardly compares with the VO2max of ~300ml.kg.min, and 58mph top speed, of the North American Pronghorn Antelope. However, the horse's particular pulmonary hypertension and highly elevated left atrial pressure are believed to cause stress failure of pulmonary capillaries, giving the syndrome of equine exercise-induced pulmonary haemorrhage,(2) although the exact pathogenesis has not been elucidated. Finally, regarding the horse and its rider, in some equine events, the rider may be nearer the human maxima for heart rate and blood lactate than the horse is to its maxima, i.e. the rider may be working harder than the horse.
Competing interests
None declared
References
1 McCrory P. Horses for courses. Br J Sports Med 2005; 39:581.
2 West JB, Matthieu-Costello O. Stress failure of pulmonary capillaries
as a mechanism for exercise-induced pulmonary hypertension in the horse.
Equine Vet J 1994; 26: 441-7.
We thank Mitchell and Hayen for their criticisms of our consensus
definition of cricket injuries. We agree that our “injury” definition is
based on maintenance of high level function (i.e., ability to continue
playing at elite level) rather than physical tissue damage. We accept that
this introduces a certain bias into the definition, namely that some
players may be able to continue to play with a cert...
We thank Mitchell and Hayen for their criticisms of our consensus
definition of cricket injuries. We agree that our “injury” definition is
based on maintenance of high level function (i.e., ability to continue
playing at elite level) rather than physical tissue damage. We accept that
this introduces a certain bias into the definition, namely that some
players may be able to continue to play with a certain level of physical
injury whereas others may need to stop playing with apparently the same
physical damage.
An alternate definition based on “physical tissue damage” rather than
function would introduce a more problematic bias. The incidence of
physical tissue damage in elite cricketers is extremely high.[1] Of
course, not every physical symptom is investigated, nor is it even
necessarily reported to the team injury surveillance recorder. The
variation in what might be reported as a cricket injury with a “tissue
damage” definition would be enormous and we believe would be far greater
than the variations in ability to function under our proposed definition.
A further benefit of our injury definition is that an “injury” can be
more easily verified by an independent surveillance coordinator: that is,
for each match in question, was the player physically able to play or not?
(And, therefore, if he was physically unable to play, we have defined him
as being injured). If physical tissue damage was present at the time of a
match but it was forgotten or ignored, then it would be much more
difficult to recover this information at a later date.
We also accept that there is an argument that perhaps we should not
have included “injuries” or “illnesses” that clearly occurred outside
cricket. However, there are quite a few injuries or medical conditions
that may fall into a grey area in terms of mechanism. Was the pain
associated with a lumbar disc degeneration caused by bowling or lifting
objects around the house? Was a player’s dehydration due to a gastric
virus or heat stress on the field? By including all injuries or medical
conditions which incapacitate a player (irrespective of cause) we again
use function as the yardstick and avoid any confusion over causation. The
majority of conditions which prevent the playing of cricket will still
appear to have been caused by cricket.[2]
Our published article is the first international consensus definition
of injury in a particular sport. We therefore did not have any previously
successful models in sport on which to base our statement. The success of
our definitions can be judged by whether or not future published studies
comply with our proposed definitions and whether or not the results of
studies from different authors appear to be directly comparable, which is
the ultimate goal. Future consensus definitions (for different sports or
cricket at amateur levels) may be similar to ours or alternatively based
on either “physical tissue damage” or on presentation to medical staff. It
will be interesting to see which of these definitional approaches is best
able to achieve compatibility between different studies.
References
(1) Ranson CA, Kerslake RW, Burnett AF et al. Magnetic resonance
imaging of the lumbar spine in asymptomatic professional fast bowlers in
cricket. J Bone Joint Surg Br; 2005;87(8):1111-6.
(2) Orchard J, James T, Alcott E et al. Injuries in Australian
cricket at first class level 1995/1996 to 2000/2001. Br J Sports Med;
2002;36(4):270-4.
While Orchard and colleagues[1,2] should be congratulated for their
attempt at developing an international consensus on the definition of a
cricket-related injury, a broader look at the literature on definitions of
injury might have provided a more robust definition of a cricket injury.
Orchard et al.[1, 2] define a cricket injury (or significant injury)
as “any injury or other medical conditio...
While Orchard and colleagues[1,2] should be congratulated for their
attempt at developing an international consensus on the definition of a
cricket-related injury, a broader look at the literature on definitions of
injury might have provided a more robust definition of a cricket injury.
Orchard et al.[1, 2] define a cricket injury (or significant injury)
as “any injury or other medical condition that either (a) prevents a
player from being fully available for selection for a major match or (b)
during a major match, causes a player to be unable to bat, bowl, or keep
wicket when required by either the rules or the team’s captain.” While
the definition proposed seems easy to implement in practice, it does not
actually define what would be considered to be a cricket-related injury in
terms of physical tissue damage, which is the basis of generally accepted
definitions of injury, nor does it define what is a medical condition.
The confusion may stem from the theoretical versus the operational
definitions of an injury. For example, one of the most common theoretical
injury definitions defines an injury as being “...caused by acute exposure
to physical agents such as mechanical energy, heat, electricity,
chemicals, and ionizing radiation interacting with the body in amounts or
at rates that exceed the threshold of human tolerance. In some cases (for
example, drowning and frostbite), injuries result from the sudden lack of
essential agents such as oxygen or heat”.[3] However, to operationalise
this definition of an injury, many injury professionals rely on the
International Classification of Disease, 10th revision (ICD-10) injury and
poisoning chapter XIX (S00-T98)[4] or the earlier ICD-9 external cause
codes (800-999)[5] to define what constitutes an injury.
What is lacking for the Orchard et al injury definition for
cricketers is how an injury would be specifically defined theoretically
(i.e. in terms of physical tissue damage), and then how such a definition
would be operationalised (i.e. how will physical tissue damage be
consistently identified and recorded). Although latent effects of
physical tissue damage, such as musculoskeletal injuries, are excluded
from the general theoretical injury definition above, as these conditions
do not immediately exceed the threshold of human tissue tolerance (but
rather often result from low energy exposures that can accumulate over
time until tolerance is exceeded)[6], it is likely that Orchard et al
would wish to include these injuries in an operational definition of a
cricket-related injury as musculoskeletal injuries represent a large
proportion of reported cricket-related injuries.[7,8] In addition, using
Orchard et al’s injury definition, other medical conditions (for example,
an illness such as influenza) would also be included, even those these are
not injuries. Indeed, it is unclear whether something like stress would
be included under their definition. Finally, it is also unclear whether
an injury sustained outside the sporting arena, for example from a motor
vehicle crash, that prevented the player from being ‘fully available for
selection’ would be included in the Orchard et al definition of injury.
Poorly defined operational definitions of injury are not new to the
sports area.[9] We would encourage Orchard and colleagues to consider the
development and publication of a more specific theoretical definition
together with an operational definition of cricket-related injury in order
to ensure standardisation of a case definition and to contribute towards
obtaining high sensitivity and specificity for identification of injuries
to cricketers. Otherwise the incidence of cricket-related injury is sure
to vary due to different interpretations of what is an injury, making
international comparisons difficult.
Furthermore, the currently proposed cricket injury definition appears
to be intended for elite cricketers and whether or not this definition
could be consistently applied to other levels of the competition (eg.
community level) would be of interest.
References
1. Orchard, J., Newman, D., Stretch, R., Frost, W., Mansingh, A., and
Leipus, A., Methods for injury surveillance in international cricket.
British Journal of Sports Medicine, 2005. 39(4): p. e22-e29.
2. Orchard, J., Newman, D., Stretch, R., Frost, W., Mansingh, A., and
Leipus, A., Methods for injury surveillance in international cricket.
Journal of Science & Medicine in Sport, 2005. 8(1): p. 1-14.
3. Baker, S., O'Neil, B., Ginsburg, M., and Guohua, L., The Injury
Fact Book. 1992, New York: Oxford University Press.
4. World Health Organisation, ICD-10 International Classification of
Diseases, 10th revision. 1992, Geneva: WHO.
5. World Health Organisation, ICD-9 International Classification of
Diseases, 9th revision. 1977, Geneva: WHO.
6. Kumar, S., Theories of musculoskeletal injury causation.
Ergonomics, 2001. 44(1): p. 17-47.
7. Leary, T. and White, J., Acute injury incidence in professional
country club cricket players (1985-1995). British Journal of Sports
Medicine, 2000. 34: p. 145-147.
8. Orchard, J., James, T., Alcott, E., Carter, S., and Farhart, P.,
Injuries in Australian cricket at first class level 1995/1996 to
2000/2001. British Journal of Sports Medicine, 2002(270-275).
9. Finch, C.F., An overview of some definitional issues for sports
injury surveillance. Sports Medicine, 1997. 24(3): p. 157-63.
Much of the controversy about the cooling methods
used in hyperthermia arises because of a failure to
consider the underlying physiology. There are two
distinct mechanisms for the development of
hyperthermia, SLOW and FAST, and each requires a
different method of cooling.
The SLOW hyperthermia involves exposure to heat with
only mild physical activity. In this situation the
hyperthermia develo...
Much of the controversy about the cooling methods
used in hyperthermia arises because of a failure to
consider the underlying physiology. There are two
distinct mechanisms for the development of
hyperthermia, SLOW and FAST, and each requires a
different method of cooling.
The SLOW hyperthermia involves exposure to heat with
only mild physical activity. In this situation the
hyperthermia develops purely because of an
inadequacy of the heat loss mechanisms. The body is
then in a situation where skin vasodilatation is maximal
and there is very little heat being generated by the body.
In this case cold on the skin will cause a reduction in
the vasodilatation, a reduction in heat loss with a
possible stimulus to increased heat production and the
core temperature will continue to rise and cause
disaster. This mechanism is found in the elderly, those
with heart disease, and, classically, among the
pilgrims to Mecca. The safest cooling method for this
group is bathing with warm/tepid water and fanning.
The FAST hyperthermia involves vigorous exercise in
hot conditions with the complication that in some cases
the conditions may not be excessively hot but the
casualty has been wearing too much body insulation.
This is the type found in sport and also, classically, in
situations such as military personnel running across
mudflats wearing wetsuits. In this mechanism the
main problem is the excess generation of heat from the
skeletal muscles, and survival will depend mainly on
curbing this excess heat production. These muscles
are subcutaneous and any vasoconstrictor stimulus
from cold on the skin will be overridden by the
excessive subcutaneous heat generation. For FAST
hyperthermia therefore ice or very cold water will not be
harmful but will be beneficial because it will penetrate
to the muscles and will reduce their heat generation by
direct cooling. Failure to stop the continuing heat
generation will be disastrous.
As in any medical situation deciding treatment on a
single measurement diagnosis (in this case
temperature) can be disastrous cf anaemia or
hypothermia, and a history should be taken before
treatment is decided. Safety is more important than
rate of cooling.
It is with interest we read the comments by Rompe, regarding our
systematic review and we take this opportunity to respond.
1. Rompe found it ‘annoying’ that our systematic review showed no
benefit in the use of extracorporeal shock wave therapy (ESWT) for lateral
epicondylalgia (LE) and did not include recent evidence. The census date
of our comprehensive database searches was clearly stated...
It is with interest we read the comments by Rompe, regarding our
systematic review and we take this opportunity to respond.
1. Rompe found it ‘annoying’ that our systematic review showed no
benefit in the use of extracorporeal shock wave therapy (ESWT) for lateral
epicondylalgia (LE) and did not include recent evidence. The census date
of our comprehensive database searches was clearly stated in our review[1] (p412, ‘Selection’ column 1, paragraph 1), which was prior to the
studies Rompe mentions.
2. Rompe questions the methodology we used in performing a meta-
analysis on LE. We followed the methodology recommended by the Cochrane
Collaboration[3] and believe this to be appropriate.
3. Rompe considers inter-study heterogeneity to bias the assessment
of ESWT. Heterogeneity is a serious issue when considering the
implications of RCTs. The influence of heterogeneity on outcomes of RCTs
has been studied in LE. Smidt et al.[4] assessed heterogeneity between
three studies on LE and found this did not significantly affect the
outcomes of the studies, nor the conclusions drawn. In our review, the
two studies on ESWT[2,5] found similar results, despite the inter-study
heterogeneity. There is no clear evidence that implicates population
heterogeneity as a significant determinant of outcomes for RCTs in LE.
4. Rompe justifies his standing on heterogeneity based on
recommendations of the Cochrane Back Review Group. This is not a credible
basis. Treatment and patient selection for back studies cannot be
compared to those for LE studies. It is well accepted that the cause of
most low back pain cannot be diagnosed and 80% of presentations are
therefore classified as ‘non-specific’. There is substantial
heterogeneity within the back pain patient population.[8,9] This same
patient heterogeneity does not exist in patients with LE. LE is easily
recognisable through clinical examination, there are well documented
inclusion / exclusion criteria that are consistent across most studies and
apart from length of duration and previous treatments, there is little
difference between patient populations of LE. Moreover, the two pooled
papers that looked at ESWT in our review[2,5] showed no significant
difference on statistical tests for heterogeneity. The combined results
supported the conclusions of the individual studies. Therefore we were
justified in stating that, at the time our systematic review was
completed, the heterogeneity between these two studies did not
significantly influence their outcome or our conclusions.
5. Rompe performs a selective qualitative review on ESWT. His search
was limited to English-only papers within MEDLINE and the FDA Databases.
The Cochrane Reviewer’s Handbook[3] clearly states that a search strategy
restricted by language leads to bias, as English language papers are more
likely to report results in favour of the intervention, which may result
in an overestimate of effectiveness.[10-13]
It is noteworthy that Rompe did not include Speed et al.[2] in his
review because it failed to meet his rating criteria. We found the paper
by Speed rated sufficiently well (73%) to be included in our review. The
PEDro database (http://www.pedro.fhs.usyd.edu.au/index.html) has rated the
Speed et al paper at 80%, which supports the inclusion of this paper in
our systematic review.
6. Rompe alleges serious debate amongst participating centres in the
Haake et al.[5] RCT. We are not aware of this debate, as it was not
reported within the paper.
7. Since our published review, we have conducted an updated
systematic review on ESWT using the same methodology. We identified three
papers[6,7,14] that met our inclusion criteria and rated them using the
same criteria in our original systematic review. The results were: (i)
Chung B and Wiley J[14] which rated 11/15 (73%); (ii) Rompe J et al.[6]
which rated 13/15 (87%) and (iii) Pettrone F and McCall B[7] which rated
13/15 (87%).
Two of these studies[6,7] reported results in favour of the ESWT
intervention and one[14] found no significant effect over that of a
placebo. We were able to pool data from 4 studies[2,5-7] for Pain
Visual Analogue Scale under strain at three months and calculated a pooled
standardised mean difference of 0.29 and 95%CI: -0.03 to 0.62. For this
outcome measure, there is still no significant effect of ESWT as a
treatment for LE. We were unable to include Chung and Wiley in this
pooled analysis because of differences in timing of outcome measure and
differences in presentation of data within the paper. Since Chung and
Wiley reported non-significant results, the pooled representation of pain
severity as reported herein is likely to be an overestimate of the effect
of ESWT on the measure of pain.
We also identified a paper by Stasinopoulos and Johnson[15] which
was a systematic review on the effects of ESWT on LE. This review
concluded that further research was required due to conflicting results
across current RCTs. Differences in outcome measures between studies
continues to be a major barrier to the pooling of data and potentially
limits conclusions that can be drawn by a systematic review.
It appears that Rompe continues to ignore the evidence that
highlights the lack of benefit of ESWT for Lateral Epicondylalgia. Rompe
would have the reader embrace ESWT as a treatment of choice for LE, but
the conflicting evidence of high quality clinical trials suggests that no
conclusions can currently be drawn as to its efficacy. Furthermore, an
expert opinion, as expressed in the Rompe letter, represents the lowest
level on the hierarchy of evidence and as such, should be interpreted with
caution.
References
1. Bisset L, Paungmali A, Vicenzino B, Beller E. A systematic review
and meta-analysis of clinical trials on physical interventions for lateral
epicondylalgia. Br J Sports Med 2005; 39: 411-22.
2. Speed C, Nichols D, Richards C, Humphreys H, Wies J, Burnet S, et
al. Extracorporeal shock wave therapy for lateral epicondylitis - A double
blind randomised controlled trial. J Orthop Res 2002; 20: 895-898.
3. Clarke M, Oxman A, editors. Cochrane Reviewers’ Handbook 4.2.0
[updated March
2003]. Update Software. Updated quarterly. ed. In: The Cochrane Library.
Issue 2. Oxford; 2003.
4. Smidt N, Lewis M, Hay E, van der Windt D, Bouter L, Croft P. A
comparison of two primary care trials on tennis elbow: issues of external
validity. Ann. Rheum Dis published online 30 Mar 2005
doi:10.1136/ard.2004.029363 2005.
5. Haake M, Konig I, Decker T, Riedel C, Buch M, Muller H.
Extracorporeal shock wave therapy in the treatment of lateral
epicondylitis: A randomized multicenter trial. J Bone Joint Surg-Am Vol
2002; 84(A): 1982-1991.
6. Rompe J, Decking J, Schoellner C, Theis C. Repetitive low-energy
shock wave treatment for chronic lateral epicondylitis in tennis players.
Am J Sports Med 2004; 32: 734-43.
7. Pettrone F, McCall B. Extracorporeal shock wave therapy without
local anesthesia for chronic lateral epicondylitis. J Bone Joint Surg-Am
Vol 2005; 87: 1297-1304.
8. Kent P, Keating J. Classification in nonspecific low back pain:
What methods do primary care clinicians currently use? Spine 2005; 30:
1433-1440.
9. Kent P, Keating J. Do primary-care clinicians think that non-
specific low back pain is one condition? Spine 2004; 29: 1002-31.
10. Moher D, Fortin P, Jadad A, Juni P, Klassen T, Le Lorier J, et
al. Completeness of reporting of trials published in languages other than
English: implications for conduct and reporting of systematic reviews.
Lancet 1996; 347: 363-6.
11. Gregoire G, Derderian F, LeLorier J. Selecting the language of
the publications included in a meta-analysis: is there a tower of Babel
bias? J Clin Epidemiol 1995; 48: 159-63.
12. Egger M, Zellweger-Zahner T, Schneider M, Junker C, Lengeler C,
Antes G. Language bias in randomised controlled trials published in
English and German. Lancet 1997; 350: 326-9.
13. Juni P, Holenstein F, Sterne J, Bartlett C, Egger M. Direction
and impact of language bias in meta-analyses of controlled trials:
empirical study. Int J Epidemiol 2002; 31: 115-23.
14. Chung B,Wiley JP. Effectiveness of extracorporeal shock wave
therapy in the treatment of previously untreated lateral epicondylitis: a
randomized controlled trial. Am J Sports Med 2004; 32: 1660-7.
15. Stasinopoulos D, Johnson M. Effectiveness of extracorporeal shock
wave therapy for tennis elbow (lateral epicondylitis). Br J Sports Med
2005; 39: 132-136.
Smith in his recent article in the Br J Sports Med
highlights the
importance of aggressively cooling heat stroke victims to improve
prognosis.[1] The paper extensively reviews the major cooling methods, and
the author advocates the immersion in an ice-cold bath as the method of
choice. Whereas this conclusion might be true for young patients who may
tolerate aggressive treatment with ice water (1–5°C...
Smith in his recent article in the Br J Sports Med
highlights the
importance of aggressively cooling heat stroke victims to improve
prognosis.[1] The paper extensively reviews the major cooling methods, and
the author advocates the immersion in an ice-cold bath as the method of
choice. Whereas this conclusion might be true for young patients who may
tolerate aggressive treatment with ice water (1–5°C), the more vulnerable
patients and those with prior cardiovascular illnesses should not be
exposed to unnecessary risks. Therefore, the more conservative technique
that has been proven effective, the pouring of large volumes of tepid
water (12–16°C) and fanning, should be used instead (especially under
field conditions, where ice is not available).[2]
It should also be emphasized that the use of antipyretics
in the
treatment of heat stroke is contraindicated.[3] In heat stroke the
accumulated body heat is not a result of a change in the thermoregulatory
set-point, as is the case in fever. Thus, antipyretics are not effective
in lowering body temperature. Furthermore, certain antipyretics can cause
additional damage; i.e. temperature-induced hepatic dysfunction may worsen
from the use of paracetamol (acetaminophen), administration of
nonsteroidal anti-inflammatory drugs may reduce potassium excretion, and
aspirin (acetylsalicylic acid) may aggravate bleeding diathesis.
References
1. Smith JE. Cooling methods used in the treatment of
exertional heat
illness. Br J Sports Med 2005; 39:503-7.
2. Hadad E, Rav-Acha m, Heled Y, Epstein Y, Moran DS. Heat
stroke: a
review of cooling methods. Sports Med 2004; 34:501-11.
3. Heled Y, Rav-Acha m, Shani Y, Epstein Y, Moran DS. The "golden
hour"
for heatstroke theatment. Mil Med 2004; 169:184-6.
There is a long history of doping in sport. Since the ancient Greco-
Roman times, ergogenic aids in form of natural products, bland chemicals
and animal extracts, have been commonplace in the attempt to push human
performances to the limit. In recent times, remarkable advances in science
and biotechnology have favoured the introduction of synthetic molecules,
recombinant hormones and genetic manipulatio...
There is a long history of doping in sport. Since the ancient Greco-
Roman times, ergogenic aids in form of natural products, bland chemicals
and animal extracts, have been commonplace in the attempt to push human
performances to the limit. In recent times, remarkable advances in science
and biotechnology have favoured the introduction of synthetic molecules,
recombinant hormones and genetic manipulation of athletes.[1]
Doping in sports should be energetically opposed, employing effective
strategies, but definitive tools are yet to be identified. The recent
article of Somerville and colleagues, provides an interesting view and
induces further reflections on this topic.[2] The conclusion is rather
frustrating, as the need to modify the educational process of elite
sportspeople to the doping laws clearly emerged. However, such a
consideration can be extended to the whole problem of the availability of
unfair products to athletes.
Over the past decades, athletes received or purchased doping products from
colleagues, team managers, unfair physicians and black market.[1]
However, the situation is possibly evolving towards more uncontrollable
scenarios. The World Wide Web is the most striking example. So far, there
are plenty of resources and virtual stores on the Web, offering several
doping products, from anabolic steroids to recombinant hormones.[3]
Accordingly, anyone can easily order through the Internet whatever
substance is required to enhance a specific athletic performance. From a
medical view, this is unacceptable. Firstly, as most of these
manufacturers are not forced to strict or certified production procedures,
the claimed products may be unsure and harmful. Sadly, they may even be
unhelpful to the athlete, as there is little warranty that they contain
the supposed ergogenic agent.[3]
Then, there is no effective legal control and virtual stores can not be identified and pursued. Finally, the hazard of this form of cheating is low, as banned products can be shipped
anonymously to the buyer. The scientific community must be aware that
antidoping testing is an effective repressive tool, but it will lead to
much wasted efforts unless appropriate preventive strategies against this
obscure scenario of providing doping to athletes will be established.
References
1. Lippi G, Guidi GC. Gene manipulation and improvement of athletic
performances: new strategies in blood doping. Br J Sports Med 2004;38:641.
2. Somerville SJ, Lewis M, Kuipers H. Accidental breaches of the
doping regulations in sport: is there a need to improve the education of
sportspeople? Br J Sports Med 2005;39:512-6.
3. Dumestre-Toulet V, Kintz P. 19-norsteroids: doping, Internet,
toxicology and analysis. Eur J Emerg Med 2001;8:80.
We appreciate Russell's comments and additional analyses. While there
may be minor points where we still disagree, it is clear from Russell's
comments that he supports our general hypothesis that there is indeed a
safety concern in the sport of slow-pitch softball. We continue to stand
by our field-testing research as well as published human response time
studies that support our claims that the sp...
We appreciate Russell's comments and additional analyses. While there
may be minor points where we still disagree, it is clear from Russell's
comments that he supports our general hypothesis that there is indeed a
safety concern in the sport of slow-pitch softball. We continue to stand
by our field-testing research as well as published human response time
studies that support our claims that the sport of softball is unsafe and
will continue to conduct research studies using human subjects as the
ideal metric for predicting safety in the sport of softball and baseball.
Your diagnosis of rhabdomyolysis appears warranted on the basis of the "dark urine" and "muscle aches combined with massive elevation of creatine kinase. However, I cannot accept the report that there was no myoglobinuria present in these individuals. The urine is dark due to the myoglobin and in view of the CK increase in the thousands, myoglobin must have been present. Many laboratories use outdated and...
Your diagnosis of rhabdomyolysis appears warranted on the basis of the "dark urine" and "muscle aches combined with massive elevation of creatine kinase. However, I cannot accept the report that there was no myoglobinuria present in these individuals. The urine is dark due to the myoglobin and in view of the CK increase in the thousands, myoglobin must have been present. Many laboratories use outdated and insensitive methods and myoglobin deteriorates fairly rapidly in acidic urine. Immunoassay methods are preferred. Additional relevant references are listed.
1: Wu AH, Laios I, Green S, et al. Immunoassays for serum and urine myoglobin: myoglobin clearance assessed as a risk factor for acute renal failure.
Clin Chem. 1994 May;40(5):796-802.
2: Loun B, Astles R, Copeland KR, Sedor FA. Adaptation of a quantitative immunoassay for urine myoglobin. Predictor in detecting renal dysfunction. Am J Clin Pathol. 1996 Apr;105(4):479-86.
3: Chen-Levy Z, Wener MH, Toivola B, et al. Factors affecting urinary myoglobin stability in vitro.
Am J Clin Pathol. 2005 Mar;123(3):432-8.
I was interested to read your recent article in the British Journal of Sports Medicine on a sequential AIIS avulsions in an adolescent long jumper. I have recently had a young patient who was a soccer player, with two sequential avulsions on the right side of the AIIS within a shorter
time frame. I would just like to point out, however, that on the xray, especially in Figure 1, it appears as if the injur...
I was interested to read your recent article in the British Journal of Sports Medicine on a sequential AIIS avulsions in an adolescent long jumper. I have recently had a young patient who was a soccer player, with two sequential avulsions on the right side of the AIIS within a shorter
time frame. I would just like to point out, however, that on the xray, especially in Figure 1, it appears as if the injury in your athlete is more to the anterior superior iliac spine (ASIS), where the sartorius muscle attaches.
In fact, it is identified as this in the caption for Figure 1, but not for the other Figures. I have also seen avulsion injuries to the superior part of the iliac crest where the gluteus medius muscle attaches.
Sincerely,
Connie Lebrun
Director Primary Care Sport Medicine
Fowler Kennedy Sport Medicine Clinic
Dear Editor
It was a pleasure to read Paul McRory championing the cause of comparative animal and human physiology, and of his equine example.(1) To the latter he might have added that, because the horse is entirely a nasal breather, attempts were made, from 1800 BC in Egypt to 17th century Europe, to increase its ventilation by slitting the nostrils, paralleling the (equally futile) attempts of modern runners with nas...
Dear Editor,
We thank Mitchell and Hayen for their criticisms of our consensus definition of cricket injuries. We agree that our “injury” definition is based on maintenance of high level function (i.e., ability to continue playing at elite level) rather than physical tissue damage. We accept that this introduces a certain bias into the definition, namely that some players may be able to continue to play with a cert...
Dear Editor,
While Orchard and colleagues[1,2] should be congratulated for their attempt at developing an international consensus on the definition of a cricket-related injury, a broader look at the literature on definitions of injury might have provided a more robust definition of a cricket injury.
Orchard et al.[1, 2] define a cricket injury (or significant injury) as “any injury or other medical conditio...
Dear Sir
Much of the controversy about the cooling methods used in hyperthermia arises because of a failure to consider the underlying physiology. There are two distinct mechanisms for the development of hyperthermia, SLOW and FAST, and each requires a different method of cooling.
The SLOW hyperthermia involves exposure to heat with only mild physical activity. In this situation the hyperthermia develo...
Dear Editor,
It is with interest we read the comments by Rompe, regarding our systematic review and we take this opportunity to respond.
1. Rompe found it ‘annoying’ that our systematic review showed no benefit in the use of extracorporeal shock wave therapy (ESWT) for lateral epicondylalgia (LE) and did not include recent evidence. The census date of our comprehensive database searches was clearly stated...
Dear Editor,
Smith in his recent article in the Br J Sports Med highlights the importance of aggressively cooling heat stroke victims to improve prognosis.[1] The paper extensively reviews the major cooling methods, and the author advocates the immersion in an ice-cold bath as the method of choice. Whereas this conclusion might be true for young patients who may tolerate aggressive treatment with ice water (1–5°C...
Dear Editor,
There is a long history of doping in sport. Since the ancient Greco- Roman times, ergogenic aids in form of natural products, bland chemicals and animal extracts, have been commonplace in the attempt to push human performances to the limit. In recent times, remarkable advances in science and biotechnology have favoured the introduction of synthetic molecules, recombinant hormones and genetic manipulatio...
Dear Editor,
We appreciate Russell's comments and additional analyses. While there may be minor points where we still disagree, it is clear from Russell's comments that he supports our general hypothesis that there is indeed a safety concern in the sport of slow-pitch softball. We continue to stand by our field-testing research as well as published human response time studies that support our claims that the sp...
Dear Editor,
Your diagnosis of rhabdomyolysis appears warranted on the basis of the "dark urine" and "muscle aches combined with massive elevation of creatine kinase. However, I cannot accept the report that there was no myoglobinuria present in these individuals. The urine is dark due to the myoglobin and in view of the CK increase in the thousands, myoglobin must have been present. Many laboratories use outdated and...
Dear Editor,
I was interested to read your recent article in the British Journal of Sports Medicine on a sequential AIIS avulsions in an adolescent long jumper. I have recently had a young patient who was a soccer player, with two sequential avulsions on the right side of the AIIS within a shorter time frame. I would just like to point out, however, that on the xray, especially in Figure 1, it appears as if the injur...
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