With regard to the Leader by ADG Baxter-Jones and N Maffulli [1] we would
like to extend our appreciation to the authors for their interest in this
never ending “hot debate”.
The authors clearly point out difficulties and
potential pitfalls of exercise testing, exercise prescription and the
interpretation of acute responses and of the chronic adaptation to
exercise training during growth and ma...
With regard to the Leader by ADG Baxter-Jones and N Maffulli [1] we would
like to extend our appreciation to the authors for their interest in this
never ending “hot debate”.
The authors clearly point out difficulties and
potential pitfalls of exercise testing, exercise prescription and the
interpretation of acute responses and of the chronic adaptation to
exercise training during growth and maturation.[1] We totally support the
conclusion that appropriate endurance training in children and adolescents
lowers blood lactate levels (BLC) at given workload and improves peak
oxygen uptake and performance at anaerobic threshold (AT). However, we
strongly feel that the comments on AT especially with respect to so called
“lactate criteria” do not consider the current state of knowledge in this
field of science.
There are a huge number of different concepts of AT that use BLC,
ventilatory measures or the combination of both.[2] In theory the BLC based
concepts of AT are supposed to identify the highest exercise intensity at
which a steady state of BLC can be identified during a prolonged constant
workload. The corresponding steady state BLC is defined as the maximal
lactate steady state (MLSS).[3,4] Depending on the testing condition AT
measurements determine a workload which correlates with the MLSS workload
but which may not be identical to the latter.[3]
Therefore behaviour of the BLC during prolonged constant workload exercise
conditions has been systematically analysed for individuals aged between 9
and 32 years.[5-11] Differences in experimental methods have been
analysed [5] and the procedures were validated against methods previously
established and exclusively used in the adult population.[12] The results
show that at given exercise intensities up to the level of the workload
corresponding to the MLSS the BLC appears to be independent of age across
the whole range of maturation from pre-puberty to adulthood.
We agree totally that the acute response and chronic adaptation to
exercise of young athletes is not yet fully understood. However, based on
the current state of knowledge there is no evidence for the statement: “In
general, BLC levels are lower in children and adolescents than in adults
at any given exercise intensity”
and in fact experimental results support
the opposing view point.
References
(1) Baxter-Jones ADG and Maffulli N. Endurance in young athletes: it can be trained. Br J Sports Med 2003; 37: 96-97.
(2) Loat CE, Rhodes EC. Relationship between the lactate and ventilatory
thresholds during prolonged exercise. Sports Medicine 1993;15(2):104-115.
(3) Beneke R. Anaerobic threshold, individual anaerobic threshold, and
maximal lactate steady state in rowing. Med Sci Sports Exerc 1995;27(6):863-867.
(4) Heck H, Mader A, Hess G, et al. Justification of the 4-mmol/l lactate
threshold. Int J Sports Med 1985;6:117-130.
(5) Beneke R, Schwarz V, Leithäuser R et al. Maximal lactate steady state
in children. Ped Exerc Sci 1996;8(4):328-336.
(6) Beneke R, Heck H, Schwarz V, et al. Maximal lactate steady state during
the second decade of age. Med Sci Sports Exerc 1996;28(12):1474-1478.
(7) Beneke R, Leithäuser RM, Schwarz V, et al. Maximales Laktat-Steady-
State bei Kindern und Erwachsenen. Dtsch Z Sportmed 2000;51:100-104.
(8) Heck H. Laktat in der Leistungsdiagnostik. Wissenschaftliche
Schriftenreihe des deutschen Sportbundes. Schorndorf: Verlag Karl Hofmann, 1990.
(9) Mocellin R, Heusgen M, Korsten-Reck U. Maximal steady state blood
lactate levels in 11-year-old-boys. Eur J Pediatr 1990;149: 771-773.
(10) Mocellin R, Heusgen M, Gildein HP. Anaerobic threshold and maximal
steady-state blood lactate in prepubertal boys. Eur J Appl Physiol
1991;62:56-60.
(11) Williams JR, Armstrong N. Relationship of maximal lactate steady state
to performance at fixed blood lactate reference values in children. Ped
Exer Sci 1991;3: 333-341.
(12) Beneke R. Methodological aspects of maximal lactate steady state –
implications for performance testing. Eur J Appl Physiol 2003;89:95-99.
The Ernst and Sran commentary [1]
about 'chiropractic manipulation' is not consistent with the majority of
systematic reviews, nor national guidelines. It is, however, highly
consistent with the previous and prolific writings of the first author
himself on this topic. Surely, the significance of this pattern is an
obvious one, and the suggestion that if anyone else but a chiropractor
performs a ma...
The Ernst and Sran commentary [1]
about 'chiropractic manipulation' is not consistent with the majority of
systematic reviews, nor national guidelines. It is, however, highly
consistent with the previous and prolific writings of the first author
himself on this topic. Surely, the significance of this pattern is an
obvious one, and the suggestion that if anyone else but a chiropractor
performs a manipulation, it is likely to be much safer, speaks for itself?
The same considerations might be applied to journal editorial practice as
well, especially when the affected public may have seriously disabling
problems which could be pivotally changed by the correct treatment.
Reference
(1) Ernst E and Sran MM. Chiropractic spinal manipulation for back pain • Commentary. Br J Sports Med 2003;37:195-196.
We found the leader by Professor Ernst (Br J Sports Med 2003;37:195-196) to be rather disjointed, out of date and potentially misleading.
This is particularly evident in the initial paragraph. The author begins
by generally addressing sports medicine clinicians, including those who
are trained in mobilisation and manipulation, namely osteopaths,
physiotherapists and chiropractors and a...
We found the leader by Professor Ernst (Br J Sports Med 2003;37:195-196) to be rather disjointed, out of date and potentially misleading.
This is particularly evident in the initial paragraph. The author begins
by generally addressing sports medicine clinicians, including those who
are trained in mobilisation and manipulation, namely osteopaths,
physiotherapists and chiropractors and abruptly concludes, for no apparent
reason, that chiropractic manipulation will be the focus of the remainder
of the article. Our question is, "Why single out chiropractic manipulation
when similar forms of manipulation are routinely practised by all of the
other initially identified professions?".[1] This author has a long track
record of reporting the potential adverse reactions specifically related
to manipulation performed by chiropractors. Additionally, the author
chooses a different forum for each "letter". The current leader appears to
be simply rehashing old statements rather than adding new material to the
discussion. Each new forum tends to confuse the issue further, as new
groups of professionals are brought into the debate without all of the
information required to make an informed decision. This type of approach
requires the chiropractic profession to continually respond in a more
defensive fashion. This undermines co-operative research efforts and
thwarts any attempt at productive interprofessional debate.
Chiropractic manipulation is singled out, even though Assendelft et al,[2] concluded the minimum effectiveness of spinal manipulation
irrespective of the provider was not superior to other treatments for back
pain. Such results can also be interpreted as manipulation being at least
equivalent to other available treatments. This would naturally increase
the number of therapeutic options available for the management of a
complex clinical condition. Under these circumstances, clinical
utilisation and decision making should always take into account patient
centred factors such as side effects and patient satisfaction. Professor
Ernst clearly has reservations regarding the United Kingdom's current
national clinical practice guideline and evidence review. This states
that: "Within the first 6 weeks of acute or recurrent low back pain,
manipulation provides better short-term improvement in pain and activity
levels and higher patient satisfaction than the treatments to which it has
been compared" and "the risks of manipulation for low back pain are very
low, provided patients are selected and assessed properly and it is
carried out by a trained therapist or practitioner [3] "; i.e.,
chiropractors, manipulating physiotherapists and osteopaths.
With respect to the forces applied during a manipulation, the paper
quoted by Professor Ernst could appear misleading. The loads reported for
manipulation by Triano and Schultz [4] do not take into account the
surface area of contact and the dissipation of the forces by the local
tissues. This would reduce and dissipate the forces over a wider area.
Professor Ernst also misleads the reader by suggesting that these loads
are inordinately high when in fact, as pointed out by Triano and Schultz [4] "estimates of the loads transmitted were consistent with those observed
in common tasks requiring lifting and twisting movements". Furthermore,
researchers in this area would freely admit that it has been poorly
researched until more recently [5] with chiropractic manipulative forces
being the most extensively studied of all the professions mentioned.
Professor Ernst also appeared to be unaware of the recent publication by
the UK BEAM group.[1] This group, while formulating their methodology
concluded that chiropractic, osteopathic and physiotherapeutic
manipulation had more similarities than differences: this would be
expected to incorporate the potential risks as well as the potential
benefits.
With respect to the statement that "dramatic complications have been
noted with some degree of regularity" Professor Ernst abruptly switches
the argument to cervical manipulation. This statement apparently refers to
the potential yet unproven association made between stroke and cervical
spine manipulation. Although this is out of direct context with the theme
of the leader, namely osteoporosis and back pain, it would suggest there
have been many incidences and that the manipulation was a causative factor
in the production of vertebrobasilar artery accidents. There is
experimental evidence which would argue to the contrary.[6] However, in
the relative absence of direct evidence there exists an alternative, yet
equally plausible hypothesis for this association: namely, that those
people who already have problems with their vertebrobasilar artery
(dissection or plaque) develop symptoms, which would lead them to seek out
a chiropractor for treatment. This is made more evident in a society where
chiropractic is more commonly available, such as Canada and USA. Such
problems in diagnosing a patient in this situation are not unique to
chiropractic. A recent case report in the Lancet [7] presented details of
a patient with acute onset neck pain attending a hospital based emergency
department. This patient was given analgesics and discharged. She returned
(24 hours later) with more advanced symptoms suggestive of an acute
anterior spinal artery syndrome. It is interesting to note that
chiropractic manipulation had been ruled out, as had rapid head movement
and head trauma, however, no mention of ruling out visits to other
practitioners of manipulation was made. Although this is only one isolated
report, it is probable that there are many such incidences that go
unreported in all health care professions.
With respect to the osteoporotic patient, chiropractors are fully
aware of the potential risks involved with the application of manual
forces with respect to relative osseous fragility. As a result,
osteoporosis has been on the British chiropractors list of relative
contraindications for manipulation for years, hence it appears rather
surprising that a Professor of complementary therapies would appear to be
unaware of this fact. We disagree with the statement by Professor. Ernst,
that there is no reliable diagnostic method available to chiropractors.
Many chiropractors have alternative methods available to them for
determining the potential presence of this condition. None more powerful
than a comprehensive case history, which is a fundamental statutory
competency. Furthermore, many chiropractors have alternatives to
radiographs (DEXA, ultrasound) present in their offices or within a
referral service, available for confirmatory objective quantification.
With respect to Professor Ernst's statement concerning information
available to the patient; in Britain it is now necessary (indeed
incorporated in the educational infrastructure) to inform all patient of
the potential risks (benign and potentially serious) as well as expected
therapeutic benefits. This is done under the umbrella term of "evidence
based medicine" which has been the subject of both undergraduate and
postgraduate education in UK chiropractic for at least 10 years. Patients
are advised of all the treatment options, including referral to other
practitioners. Furthermore they are informed about the use of Xrays and
the limitations of plain film Xray to demonstrate the presence or absence
of osteoporosis. They are also informed that osteoporosis is a relative
contraindication to manual interventions and what that means to the
patient in terms of overall case management.
So in conclusion the article by Professor Ernst does not appear to be
well informed or well researched. It appears to target chiropractic
because there is less information available about the other manipulating
disciplines. The chiropractic profession has sought to engage Professor
Ernst in constructive dialogue for at least 5 years. However, he still
appears to have ignored the steps being taken by professions such as
chiropractic whose clinical focus is guided by statutory regulation aimed
at protecting the patient and raising standards of care and education.
References
1. Harvey E, Burton AK, Moffett JK, Breen A; UK BEAM trial team.
Spinal manipulation for low-back pain: a treatment package agreed to by
the UK chiropractic, osteopathy and physiotherapy professional
associations. Man Ther. 2003; 8 (1):46-51.
2. Assendelft WJ, Morton SC, Yu EI, Suttorp MJ, Shekelle PG. Spinal
manipulative therapy for low back pain. A meta-analysis of effectiveness
relative to other therapies. Ann Intern Med. 2003; 138 (11):871-81.
3. Waddell G, Feder G, McIntosh A, Lewis M, Hutchinson A. Clinical
guidelines for the management of acute low back pain: clinical guidelines
and evidence review. London: Royal College of General Practitioners ,
1996.
4. Triano J, Schultz AB. Loads transmitted during lumbosacral spinal
manipulative therapy. Spine 1997;22:1955–64.
5. Herzog W. Clinical Biomechanics of spinal manipulation. Ed W
Herzog. Pub Churchill Livingston, London, 2002
6. Symons BP, Leonard T, Herzog W. Internal forces sustained by the
vertebral artery during spinal manipulative therapy. J Manipulative
Physiol Ther. 2002; 25(8):504-10.
7. Latronico N, Fassini P, Antonini B, Gasparotti R. A pain in the
neck. Lancet. 2002; 359 (9313):1206.
McCarthy, Byfield [1] and Breen [2] make a number of comments which require a brief reply. I wrote the article on this specific subject because I was invited to do so by the British Journal of Sports Medicine. All three correspondents seem to oppose my "long track record" of writing about adverse effects of spinal manipulation. I do this simply because it is my job. I try to apply the rules of science to al...
McCarthy, Byfield [1] and Breen [2] make a number of comments which require a brief reply. I wrote the article on this specific subject because I was invited to do so by the British Journal of Sports Medicine. All three correspondents seem to oppose my "long track record" of writing about adverse effects of spinal manipulation. I do this simply because it is my job. I try to apply the rules of science to all areas of complementary medicine. To exclude therapeutic safety from this strategy would be unforgivable. I have certainly published more on the adverse effects of herbal medicine than on spinal manipulation. To assume that I have singled out spinal manipulation is therefore pure fantasy.
I disagree with McCarthy and Byfield about their assumption that the safety of cervical manipulation is not directly related to osteoporosis and back pain. Contrary to these authors, I also think that “a comprehensive case history” is not a specific and sensitive diagnostic tool for osteoporosis. However, I do agree with McCarthy and Byfield that many adverse effects of manipulation go unreported. In our own case series under-reporting was precisely 100%.[3] Finally, I am not aware that "the chiropractic profession has sought to engage [me] in constructive dialogue for at least 5 years".
I believe Breen [2] is wrong in stating that 2the majority of systematic reviews" do not agree with my article. We have recently evaluated all reviews of spinal manipulation for back pain published in the last 10 years.[4] Sixteen reviews met our inclusion criteria; 9 reached a positive and 7 a negative conclusion about the effectiveness of spinal manipulation. An overall positive conclusion was most significantly associated with low methodological quality of the review and first authorship by a chiropractor or osteopath.
In summary, I feel that my article was as evidence-based as it could be given its brevity while the comments of McCarthy, Byfield and Breen seem to bear the hallmarks of an emotional ad hominem attack.
References
(1) McCarthy PW and Byfield DC. Observations concerning chiropractic spinal manipulation for back pain a reply [electronic response to Ernst and Sran Chiropractic spinal manipulation for back pain - Commentary] bjsports.com 2003http://bjsm.bmjjournals.com/cgi/eletters/37/3/195#38
(2) Breen AC. The "war" on chiropractors [electronic response to Ernst and Sran Chiropractic spinal manipulation for back pain - Commentary] bjsports.com 2003http://bjsm.bmjjournals.com/cgi/eletters/37/3/195#38
(3) Stevinson C, Honan W, Cooke B, Ernst E. Neurological complications of cervical spine manipulation. J Roy Soc Med 2001; 94: 107-10.
(4) Canter PH, Ernst E. Sources of bias in reviews of spinal manipulation for back pain. Submitted 2003.
There are a number of interesting points raised by this case report,
as well as some fundamental and misleading errors.
I would be very interested to know what the authors actually mean by
the term “shin splints”
They state that “Exercise-induced compartment syndrome is the least
common” (cause of lower leg pain). Perhaps exercise-induced acute
compartment syndromes are very rare, bu...
There are a number of interesting points raised by this case report,
as well as some fundamental and misleading errors.
I would be very interested to know what the authors actually mean by
the term “shin splints”
They state that “Exercise-induced compartment syndrome is the least
common” (cause of lower leg pain). Perhaps exercise-induced acute
compartment syndromes are very rare, but certainly not chronics. It is
debatable as to whether CCS (Chronic Compartment Syndrome) or MTSS (Medial
Tibial Stress Syndrome)is the most common cause of exercise-induced lower
leg pain, and it is impossible to prove either way. However CCS is at
least 100 times more common in athletes than either venous diseases or
obliterative arterial diseases. This is supported by both common sense and
the literature. For example, in the April 2004 issue of the Journal, Cunningham & Spears
maintain that CCS is the most common form of leg pain in athletes
EICS is a misleading term because it does not distinguish between
Chronic and Acute, which is a very important difference in terms of
possible sequelae and urgency of treatment. CCS is better, exercise is
implicit in the name as, unlike acutes, which can have many causes, there
is no other cause of a CCS.
Why was the Superficial posterior compartment decompressed, when it
was clearly shown by the pressure tests to be completely normal?
The most common causes of acute compartment syndrome must certainly
include tibial fractures and crush injuries, but muscle ruptures and blood
diseases are extremely rare causes. External compression and burns are far
more common. But are these facts really relevant in a paper about CCS.
Bilateral involvement is much more common than unilateral (as per
Detmer (5) 82/94 patients), it is not just an occassional finding as
implied here.
Fascial defects have only ever been reported in the Anterior
compartment, so are not relevent to Deep Posterior compartments.
Many of the surgical techniques, e.g. fibulectomy are only ever used
in acute cases, so mentioning them here is purely padding.
The reference to a 20% decrease in strength of the compartment
following surgery (Mozan & Keagy) is misleading. This is an isolated
paper on frog’s legs. There is no in-vivo evidence to suggest any long-
term detrimental effects of surgery for CCS, although several
investigations have been undertaken.
Taken together these points would give the inexperienced reader a
rather false and misleading picture of the incidence, diagnosis and
treatment of a Chronic Compartment Syndrome.
Our reply to the comments raised by an author is submitted as follows.
Author Comment (AC):I would be very interested to know what the authors
actually mean by the term “shin splints”
Reply: Shin splints, which we cited in our article as one of the main
causes of recurrent lower leg pain, refers to a condition that produces
pain and discomfort in the leg owing to repetitive running or hiki...
Our reply to the comments raised by an author is submitted as follows.
Author Comment (AC):I would be very interested to know what the authors
actually mean by the term “shin splints”
Reply: Shin splints, which we cited in our article as one of the main
causes of recurrent lower leg pain, refers to a condition that produces
pain and discomfort in the leg owing to repetitive running or hiking.
Further, the condition is limited to musculotendinous inflammations and
should exclude stress fractures and ischemic disorders. Although the term
shin splint syndrome is out of date its common usage in classical
textbooks ensures its survival. (Andrish JT: The leg DeLee and Drez's
Orthopaedic Sports Medicine, 2nd ed. WB Saunders 2003, OKU Sports Medicine
2 1999 Ed. Arendt EA)
AC: They state that “Exercise-induced compartment syndrome is the
least common” (cause of lower leg pain). Perhaps exercise-induced acute
compartment syndromes are very rare, but certainly not chronics. It is
debatable as to whether CCS (Chronic Compartment Syndrome) or MTSS (Medial
Tibial Stress Syndrome)is the most common cause of exercise-induced lower
leg pain, and it is impossible to prove either way. However CCS is at
least 100 times more common in athletes than either venous diseases or
obliterative arterial diseases. This is supported by both common sense and
the literature. For example, in the April 2004 issue of the Journal,
Cunningham & Spears maintain that CCS is the most common form of leg
pain in athletes
Reply: We stated EICS as the least common among the causes of lower
leg pain in normal population, on the contrary to athletes.Detmer et al.
reported that only three cases per year came from a university population
of 40000 students. (Detmer D, Sharpe K, Sufit R, et al. Chronic
compartment syndrome: diagnosis, management and outcomes. Am J Sports Med
1985;13:162–70.) Since the vast majority of EICS cases are treated with
conservative procedures successfully, we as orthopaedic surgeons, rarely
encounter such cases.
AC: EICS is a misleading term because it does not distinguish between
Chronic and Acute, which is a very important difference in terms of
possible sequelae and urgency of treatment. CCS is better, exercise is
implicit in the name as, unlike acutes, which can have many causes, there
is no other cause of a CCS.
Reply: In our case report, we actually mention a case with exercise
induced chronic compartment syndrome by stating EICS in our paper. We
aggree with the comments of the author.
AC: Why was the Superficial posterior compartment decompressed, when
it was clearly shown by the pressure tests to be completely normal?
Reply: In our case, the soleus was bulky and wrapped around the deep
compartment. Therefore we performed partial fasciotomy to the soleus
fascia in order to gain access to the deep compartment.
AC: The most common causes of acute compartment syndrome must
certainly include tibial fractures and crush injuries, but muscle ruptures
and blood diseases are extremely rare causes. External compression and
burns are far more common. But are these facts really relevant in a paper
about CCS.
Reply: Since the case in our paper was exercise induced chronic
compartment syndrome, we mentioned only some causes of acute compartment
syndrome as a general statement. External compression and burns may be
added to the article.
AC: Bilateral involvement is much more common than unilateral (as per
Detmer (5) 82/94 patients), it is not just an occassional finding as
implied here.
Reply: We did not imply unilateral involvement as an occasional
finding in our paper. Moreover we cited the study of Detmer et al. in our
discussion section by giving the same ratio as bilateral involvement being
much more common.
AC: Fascial defects have only ever been reported in the Anterior
compartment, so are not relevent to Deep Posterior compartments.
Reply: The author is right on this matter. However we implied not
only deep posterior compartment syndrome, but also a general approach to
physical examination findings of the exercise induced chronic compartment
syndrome.
AC: Many of the surgical techniques, e.g. fibulectomy are only ever
used in acute cases, so mentioning them here is purely padding.
Reply: We do know that fibulectomy is only applied in acute cases
however this was stated only among the different surgical treatment
alternatives.
AC: The reference to a 20% decrease in strength of the compartment
following surgery (Mozan & Keagy) is misleading. This is an isolated
paper on frog’s legs. There is no in-vivo evidence to suggest any long-
term detrimental effects of surgery for CCS, although several
investigations have been undertaken.
Reply: Even though the author is right in his concern, two
experimental studies revealed such a decrease in muscle strength and this
was cited in Surgery of the Foot and Ankle eds Coughlin MJ, Mann RA.
Seventh edition 1999.
AC: Taken together these points would give the inexperienced reader a
rather false and misleading picture of the incidence, diagnosis and
treatment of a Chronic Compartment Syndrome.
Reply: We believe that the author is too rigid in his judgement by
this statement. We never want to mislead any of the readers. However, many
debateable terms are still used for these cases. As we mentioned
previously, the incidence is very different in regular population and the
athletes. Our diagnosis is certainly correct and debateable uses of
different terms for this case is nonsense. The treatment performed to the
patient is also very appropriate even though the route of approach to the
deep compartment may be debateable and the complaints of the patient were
relieved completely and he continues his professional football career.
I read with great interest the recently published study by Shave et
al.[1] in the February, 2004 issue of the British Journal of Sports Medicine. The authors found that
exercise training in hypoxic environment did not affect cardiac systolic
and diastolic functions. However, it is known that the characteristics of the
study population (broad age range, aerobic exercise capacity) may cause
significantl...
I read with great interest the recently published study by Shave et
al.[1] in the February, 2004 issue of the British Journal of Sports Medicine. The authors found that
exercise training in hypoxic environment did not affect cardiac systolic
and diastolic functions. However, it is known that the characteristics of the
study population (broad age range, aerobic exercise capacity) may cause
significantly different diastolic Doppler parameters in subjects.
Furthermore, I believe that exercise duration is important for cardiac
functions and fatigue as much as exercise distance. It should be also
explained how the authors found lower E wave velocity, while higher
cardiac stroke volume and output in hypoxic group before exercise.
On the other hand, Bailey et al. [2] reported that the stimulus of
intermittent normobaric hypoxia invoked an additive cardioprotective
effect. Although anticipated, they found a decreased power output for a
given submaximal heart rate during hypoxic training because of an
increased sympathoadrenerjik drive and that the hypoxic inspirate
did not influence the submaximal heart rate and power output relationship.
It has been explained that the prevailing arterial hypoxemia would
decrease absolute training intensity and subsequent oxygen flux and thus
mask the potentially synergistic effects of hypoxic training [3]. The authors
proposed that physiological adaptation to intermittent hypoxemia could
have upregulated vascular reactivity, in particular, if the hypoxic
stimulus was of sufficient magnitude to induce morphological changes in
the endothelium.
I also believe that increased cardiovascular functional adaptations to
regular exercise in athletes [4] in normobaric normoxic conditions are
prevent cardiovascular injury and fatigue in hypoxic environment.
References
(1). Shave RE, Dawson E, Whyte G, George K, Gaze D, Collinson P. Effect of
prolonged exercise in a hypoxic environment on cardiac function and
cardiac troponin T. Br J Sports Med 2004;38:86-8.
(2). Bailey DM, Davies B, Baker J. Training in hypoxia: modulation of
metabolic and cardiovascular risk factors in men. Med Sci Sports Exerc
2000;32:1058-66.
(3). Levine BD, Stray-Gundersen J. Living high-training low: effect of
moderate-altitude acclimatization with low-altitude training in
performance. J Appl Physiol 1997;83:102-12.
(4). Kasikcioglu E, Kayserilioglu A, Oflaz H, Akhan H. Aortic distensibility
and left ventricular diastolic functions in endurance athletes. Int J
Sports Med 2004;25 (In press)
Judging from our animal studies, there is an opportunity to improve
performance by supplementing hepatic oxygenation from an enteric or even a
peritoneal source.
The idea might be especially appealing to the armed
forces but might conceivably be applied in a manner conducive to endurance
sports. In our study oxygenating just half of the gut eliminated the
compensatory increase in cardiac outp...
Judging from our animal studies, there is an opportunity to improve
performance by supplementing hepatic oxygenation from an enteric or even a
peritoneal source.
The idea might be especially appealing to the armed
forces but might conceivably be applied in a manner conducive to endurance
sports. In our study oxygenating just half of the gut eliminated the
compensatory increase in cardiac output induced by hypoxaemia [1].
Reference
(1). Gross BD, Sacristan E, Peura RA, Shahnarian A, Devereaux D, Wang HL,
Fiddian-Green R. Supplemental systemic oxygen support using an intestinal
intraluminal membrane oxygenator.
Artif Organs. 2000 Nov;24(11):864-9.
This a very interesting, but curious,paper.The novel theory
presented, enhanced the CNS as the more important center regulatory of
exercise fatigue, resembles all the research that occupied the minds of
clinical and experimental neuroscience people in regard of pain.
Pain is a reality, an alarm signal. Of course there are many pain
syndromes as diseases by thereselfes, as migraine, cluster h...
This a very interesting, but curious,paper.The novel theory
presented, enhanced the CNS as the more important center regulatory of
exercise fatigue, resembles all the research that occupied the minds of
clinical and experimental neuroscience people in regard of pain.
Pain is a reality, an alarm signal. Of course there are many pain
syndromes as diseases by thereselfes, as migraine, cluster headache,
trigeminal neuralgia, thalamic pain post-stroke, etc., and very important
pain due to other diseases, especially in cancer patients.
Nothing new about the typical pain neurosurgery, as cingullectomy, to
give a better quality of life in terminal oncology people: they continue
to refer pain, but without the limbic system information as these stimulus
is a nociceptive one, the suffering disappear – they points and describe
pain when questioned, but this symptom don’t cause any distress: the
emotional aspect of this form of sensibility was removed.
In another example, people with trigeminal neuralgia can survive many
years with good control of the pain with carbamazepine and perhaps (after
more controlled studies and evidence-based guidelines) gabapentin.However,
the total control of the disease is based in an anatomical question, the
vascular loop around the trigeminal pathway, and the definitive treatment
is the surgery, first performed by Janetta, from Pittsburgh, many years
ago.
After these considerations, the theory explained could reach a danger
level: fatigue is a periphery nociceptive sensation, an alarm signal.
Techniques to reduces or control the CNS role are, in thesis, something
like doping: the athlete could perform better marks, however could be
present a potential risk of damage in the muscles, bones, peripheral
nerves and even in central nervous structures.
The whole thing resembles a different way of Pavlov’s conditioning
methods, with a plausible cause of disease risk to people in good health.
I read with interest the article “Extracorporeal shock wave therapy
for plantar fasciitis: randomised controlled multicentre trial” by John
Ogden (Br J Sports Med 38: 382, 2004).
I strongly contradict his suggestion that multiple dosed, low-energy,
non-anaesthetically based treatments [9] cannot accomplish the same
clinical outcome and patient satisfaction as single dosed, high-energy,
ana...
I read with interest the article “Extracorporeal shock wave therapy
for plantar fasciitis: randomised controlled multicentre trial” by John
Ogden (Br J Sports Med 38: 382, 2004).
I strongly contradict his suggestion that multiple dosed, low-energy,
non-anaesthetically based treatments [9] cannot accomplish the same
clinical outcome and patient satisfaction as single dosed, high-energy,
anaesthetically based treatments [1,7,14].
Not a single study has been published directly comparing high-energy
with low-energy treatment protocols for chronic plantar fasciitis!
What is more the alleged efficacy of these single dosed, high-energy,
anaesthetically based treatments have already been discussed in an
exhaustive way by Buchbinder [2]:
Regarding the HealthTronics sponsored FDA trial [7] Buchbinder critizised
that the presence of plantar fasciitis was determined solely on clinical
grounds. It was uncertain whether the 2 groups in the trial were
comparable at baseline. In the “results” section none of 4 success
criteria was statistically significant in favor of the active treatment.
Regarding the Dornier sponsored FDA trial [1,14] Buchbinder wrote while a
statistical significant difference favoring the active group in
improvement of morning pain was reported to be evidence of efficacy of
ESWT, it could be argued that a difference of 0.7 on a 10-cm VAS pain
scale may not be clinically significant. And, there was no statistically
significant difference between groups in the proportion of participants
with at least 60% improvement in morning pain, AOFAS Ankle-Hindfoot-Scale,
and SF12 Health Status Questionnaire.
When discussing a possible working mechanism of shock wave
application it is important to focus not only on differences of shock wave
devices in clinical use. There are also different pathways for the effects
of high- versus low-energy shock waves.
It is important to know that the current literature [5,6,12,13]
indicates that shock waves may selectively lead to dysfunction of
peripheral sensory unmyelinated nerve fibers without affecting nerve
fibers responsible for motor function (large myelinated fibers).
For high-energy treatment with 0.9 mJ/mm², this selective destruction
of unmyelinated sensory nerve fibers within the focal zone of ESWT may
contribute to clinically evident long-term analgesia (5).
For low-energy application with 0.1 mJ/mm², analgesia may be a result
of a shock wave-induced release of neuropeptides, such as CGRP, resulting
in a local neurogenic inflammation in the focal area with subsequent
prevention of sensory nerve endings from reinnervating this area [6,12]. A
second application accentuated these inflammatory changes and therefore
prevented reinnervation [13].
Centrally, the common findings of a reduction in the number of
neurons immunoreactive to CGRP and substance P without a reduction of the
total number of neurons within the lower lumbar DRG probably are a
secondary effect following the (primarily induced) decrease of the number
of sensory nerve fibers in the focal zone of shock wave application. So
the peripheral and central nervous system may both play a pivotal role in
mediating shock wave induced long-term analgesia.
Recently, Wang [15] showed that low-energy shock wave application
resulted in increased neovascularization at the tendon-bone junction in
rabbits. Chen [4] treated rats with a collagenease-induced Achilles
tendinitis with a single low-energy shock wave treatment with 0, 200, 500
and 1000 impulses. Shock wave application with 200 impulses restored
biomechanical and biochemical characteristics of healing tendons 12 weeks
after treatment. However, shock wave treatments with 500 and 1000 impulses
elicited inhibitory effects on tendinitis repair. Together, low-energy
shock wave effectively promoted tendon healing.
In my view it is clear from these experimental data that with
increasing energy applied there is a chance of side effects that my well
inhibit healing of an already diseased fascia or tendon.
It is also clear that even low-energy shock waves may induce a
positive local reaction regarding down-regulation of pain transmitters,
and up-regulation of cell proliferation factors. I am not aware of any
such studies with regard to energy flux densities of about 0.3 mJ/mm² as
used by Ogden [7] or Theodore [14].
Accordingly, I cannot agree with Ogden´s [8] and Theodore´s [14]
statement that high energy shock waves initiate a more effective and
quicker clinical response than low-energy shock waves. I would like the
authors to support this statement with results from experimental studies
or from prospective controlled clinical trials.
I agree with Speed [11] that some regimes of ESWT are a potentially
helpful addition to the options for the management of soft-tissue
conditions such as chronic plantar fasciitis. Like Ogden [8] and Theodore
[14] I am opposed to the opinion of Buchbinder [3]. Contrary to her I
strongly recommend that these regimes of ESWT - producing virtually no
complications, allowing immediate full weight bearing without splints -
should be given priority before surgery [10].
References
(1). Buch M et al. Extracorporeal shockwave therapy in symptomatic heel
spurs. Orthopade 31:637-644, 2002.
(2). Buchbinder R et al. Ultrasound-guided extracorporeal shock wave
therapy for plantar fasciitis: a randomized controlled trial. JAMA
288:1364-1372, 2002.
(3). Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med
350:2159-2166, 2004.
(4). Chen YJ et al. Extracorporeal shock waves promote healing of
collagenase-induced Achilles tendinitis and increase TGF-beta1 and IGF-I
expression.J Orthop Res 22:854-861, 2004.
(5). Maier M et al. Substance P and prostaglandin E2 release after
shock wave application to the rabbit femur. Clin Orthop 406:237-245, 2003.
(6). Ohtori S et al. Shock wave application to rat skin induces
degeneration and reinnervation of sensory nerve fibres. Neurosci Lett
315:57-60, 2001.
(7). Ogden JA et al. Shock wave therapy for chronic proximal plantar
fasciitis.
Clin Orthop 387: 47-59, 2001.
(9). Rompe JD et al. Shock wave application for chronic plantar
fasciitis in running athletes – a prospective, randomized, placebo-
controlled trial. Am J Sports Med 31:268-275, 2003.
(10). Rompe JD. Letter to the editor. N Engl J Med 351: 834; 2004.
(11). Speed CA. Extracorporeal shock-wave therapy in the management of
chronic soft-tissue conditions. JBJS 86-B:165-171, 2004.
(12). Takahashi N et al. Application of shock waves to rat skin
decreases calcitonin gene-related peptide immunoreactivity in dorsal root
ganglion neurons. Auton Neurosci 107:81-84, 2003.
(13). Takahashi N et al. The mechanism of pain relief in extracorporeal
shock wave therapy. Poster # 448, AAOS Annual Meeting San Francisco, 2004.
http://www.aaos.org/wordhtml/anmt2004/poster/p448.htm.
(14). Theodore GH et al. Extracorporeal shock wave therapy for the
treatment of plantar fasciitis. Foot Ankle Int 25:290-297, 2004.
(15). Wang CJ. Shock wave therapy induces neovascularization at the
tendon-bone junction. A study in rabbits. J Orthop Res 21:984-989, 2003.
Dear Editor
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Dear Editor,
I read with interest the article “Extracorporeal shock wave therapy for plantar fasciitis: randomised controlled multicentre trial” by John Ogden (Br J Sports Med 38: 382, 2004).
I strongly contradict his suggestion that multiple dosed, low-energy, non-anaesthetically based treatments [9] cannot accomplish the same clinical outcome and patient satisfaction as single dosed, high-energy, ana...
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