In their paper [1], McDowell and Ciocco conclude that "BBS values in slowpitch softball exceed recommended safety limits imposed on the sport" and their "findings indicate that softball is perhaps more dangerous then most coaches, players and parents think." Had this paper been published in an American journal it might have attracted considerable attention from the news media due to its alarming conclusion...
In their paper [1], McDowell and Ciocco conclude that "BBS values in slowpitch softball exceed recommended safety limits imposed on the sport" and their "findings indicate that softball is perhaps more dangerous then most coaches, players and parents think." Had this paper been published in an American journal it might have attracted considerable attention from the news media due to its alarming conclusions. However, it is also possible that if this paper had been submitted to an American journal, reviewers more familiar with the current status of performance testing in softball might have identified some fatal flaws.
Had this paper been published five years ago, the conclusions drawn would have been relevant to the game of softball. Unfortunately the performance standards referenced in this study were already out of date, and several of the softball bats tested in this study had already been banned from play by the time this paper was accepted for publication. Furthermore, the references quoted by the authors include television news stories and websites, while ignoring a serious body of recent research on bat performance.
Outdated performance standards. The performance standard used to test softball bats, referenced by McDowell and Ciocco [1], is ASTM F1890. This test specifies that an initially stationary bat is impacted with a ball fired from a cannon at a speed of 26.8 m/s. The ball rebounds from the bat while the bat swings away about a pivot to which the handle is clamped. The ratio of rebounding to initial ball speeds is used to determine the Bat Performance Factor and the Batted-Ball Speed. However, there are two critical flaws in this test, which are completely ignored by McDowell and Ciocco. The first is that the F1890 test standard specifies that the ball must impact the bat at its centre-of-percussion (COP) relative to a pivot point 6-inches (15.24 cm) from the handle end of the bat. Research has shown [2] that the COP is not the location where the ball rebounds from the bat with the greatest speed.
Secondly, several field studies have shown that the relative speed between an actual pitched ball and swung bat in a typical slow-pitch softball game is approximately 49m/s, not 26.8m/s as dictated by F1890. Increasing the speed with which the ball is fired from the cannon causes measured bat performance to increase significantly beyond values obtained by the slower speed F1890 standard.[3-4] Because of both of these reasons, many bats which passed F1890 (BPF or BBS) have been found to perform significantly better in the field than test results predicted.
Sometime around 2002 the ASTM F1890 test standard was revised requiring that location of ball impact be scanned along the barrel in order to determine the bat's actual "sweet spot" before conducting the test, although the ball speed has been kept at 26.8 m/s. The USSSA has been using this modified BPF test for the last couple of years, and several bats which passed the original BPF test have since been banned from USSSA play. In January, 2004, the ASA abandoned the F1890 test altogether and adopted a new bat performance standard, ASTM F2219. This new test fires balls at the higher speed of 49 m/s, and uses the ratio of ball rebound/incoming speeds along with the impact location and the moment-of-inertia to calculate a Batted-Ball Speed representative of what a skilled player in the field would actually produce. The inclusion of the moment-of-inertia is to account for the manner in which the bat-swing speed depends on the inertial properties of the bat [5-7] as found by several recent field tests.
The ASA has set a maximum Batted-Ball Speed limit of 43.8 m/s (157.7 km/h) using the high-speed impact test F2219. While this speed is higher than the 38 m/s (137 km/h) value from the older F1890 test, the current test standard is actually a much more stringent test, is more representative of actually playing conditions, and results in a safer game. Many bats which passed the old F1890 test will not pass the ASA implementation of F2219. Unfortunately, the paper by McDowell and Ciocco does not reflect the recent and current performance standards for testing bat performance.
Illegal and banned bats. A second fatal flaw with this paper is that three of the softball bats which the authors state pose a safety threat to pitchers have long been banned for league and tournament play by both the ASA and USSSA. As a side note, the Miken Velocit-E is not an aluminium multi-wall bat as the authors state, but is in reality a composite bat.
I find it somewhat amazing that the authors included a titanium bat in their study since the Louisville Slugger TPS Titanium bat (along with Worth Titanium and Easton Typhoon Titanium models) was quickly banned by all softball organizations back in 1993, just a few months after it was introduced into the market. Since 1993 (which is 7 years before ASA adopted performance standards) it has always been illegal to use titanium bats in ASA or USSSA league play. ny conclusions regarding the safety of the game which are drawn from results obtained for titanium bat are irrelevant since these bats have been banned from play for the last 12 years.
In addition, since 2002, both the Easton Synergy and Miken Ultra II composite bats have both been banned for use by the ASA and USSSA. Both bats fail to pass the USSSA BPF test when the ball impact location is scanned along the barrel instead of testing only at the COP. Both bats also fail to pass the ASA 2004 test as per ASTM F2219 which uses the higher ball impact speed and accounts for the bat's inertia and impact location. Again, any conclusions drawn from the data for these bats is irrelevant since players cannot legally use them in ASA and USSSA sanctioned games.
The two remaining bats in this study, the DeMarini Doublewall Classic and the DeMarini Ultimate Weapon single wall bat both pass the 43.8 m/s (157.7 km/h) limits imposed by the current ASA F2219 test and are both considered legal bats, though the double-wall bat does outperform the single-wall bat. The warnings presented by McDowell and Ciocco regarding the performance of titanium and high performance composite bats are rendered somewhat irrelevant since these bats are not allowed to be used in play.
The alarming conclusions McDowell and Ciocco make regarding the dangers inherent to the game of softball are not representative of the current state of the game. The bats which this study declares to be dangerous are not representative of bats currently used by slow-pitch softball players playing by ASA or USSSA rules. And, the performance standards used in this study to classify bats as being dangerous had either been modified or abandoned before this paper was accepted, and do not represent the current state of the game.
Respectfully,
Daniel A. Russell, Ph.D.
Associate Professor of Applied Physics
Kettering University, Flint, MI, USA
References
1. M McDowell and M V Ciocco, A controlled study on batted ball speed and available pitcher reaction time in slowpitch softball. Br J Sports Med 2005; 39: 223-225.
2. L.V. Smith and J.T. Axtel, "Mechanical Testing of Baseball Bats," J. Testing Eval., 31(3), 210-214 (2003).
4. A.M. Nathan, "Characterizing the performance of baseball bats," Am. J. Phys., 71(2), 134-143 (2003).
5. L. Smith, J. Broker and A. Nathan, "A Study of Softball Player Swing Speed," in: Sports Dynamics Discovery and Application, Edited by A. Subic and F. Alam (RMIT University, Melbourne Australia, 2003), 12-17.
6. G. Fleisig, N. Zheng, D. Stodden and J. Andrews, "Relationship between bat mass properties and bat velocity," Sports Engineering, 5(1), 1-8, (2002).
7. K. Koenig, N. Mitchel, T. Hannigan, and J. Clutter, "The influence of moment of inertia on baseball/softball bat swing speed," Sports Engineering, 7(2), 105-118 (2004).
Thank you for the help on the topic of hand washing. I
have been studying the importance of hand washing for
about three weeks, with no success. This article
helped me out a lot. I know how it is to have snotty kids,
I babysit, and the spreading of germs is deadly. I
recently spoke to a young woman who after her daycare
job, each day would throw all toys and such into a
bucket of bleach. We are d...
Thank you for the help on the topic of hand washing. I
have been studying the importance of hand washing for
about three weeks, with no success. This article
helped me out a lot. I know how it is to have snotty kids,
I babysit, and the spreading of germs is deadly. I
recently spoke to a young woman who after her daycare
job, each day would throw all toys and such into a
bucket of bleach. We are desperately trying to help get
rid of the deadly diseases.
Together I feel that all women with children could in
fact help teach good hand washing.
The altitude training study of Friedmann et al. reported a 6%
increase in haemoglobin mass (Hbmass), but this result warrants close
scrutiny, particularly without a corroborating measure of augmented
VO2max, nor of corresponding measures in a matched control group. The
authors’ contend that “there exist no studies in which the changes in
total haemoglobin mass following treatment with recombinant...
The altitude training study of Friedmann et al. reported a 6%
increase in haemoglobin mass (Hbmass), but this result warrants close
scrutiny, particularly without a corroborating measure of augmented
VO2max, nor of corresponding measures in a matched control group. The
authors’ contend that “there exist no studies in which the changes in
total haemoglobin mass following treatment with recombinant human were
measured…”. But in 2001, we reported increased Hbmass after 4 weeks of
injections with recombinant human EPO (r HuEPO) at doses of 50 IU/kg,
thrice weekly [1]. When combined with weekly iron supplements either intra-muscularly or orally, the mean (SD) increase in Hbmass was 7 (2)% and 12
(2)%, respectively [1]. In comparison, by interpolating from Friedmann’s
Figure 2A, we calculate a mean (SD) expansion of Hbmass of 6 (7)%,
reinforcing the authors’ conclusion of large individual variability.
Although we commend the authors for providing individual percent
changes in Hbmass, rises of 24, 18 and even 13% (interpolation from their
Figure 2A) after 3 weeks at 2100-2300m are disconcerting. Collectively,
these three subjects contribute more than half of the overall group
increase in Hbmass. Moreover, perturbations as large as these are extreme
given the relatively attenuated EPO response of altitude compared with r
HuEPO injections [2]. What else might contribute to such large increase in
Hbmass? From our experience, the most common source of error with the CO-
method is a leak by a subject around the mouthpiece or noseclip, or a leak
in the rebreathing apparatus itself. An inadvertent leak substantially
increases, never decreases, the estimated Hbmass. Secondly, a small
rebreathing volume and large dose of CO (~1.5 ml.kg-1 for men and 1.25
ml.kg-1 for women) ameliorate the magnitude of error for Hbmass, but the
smaller dose used by Friedmann (0.85 ml.kg-1) and the larger rebreathing
volume (5L) are sub-optimal [3].
References
1. Parisotto R, Gore CJ, Emslie KR, et al. A novel method utilising
markers of altered erythropoiesis for the detection of recombinant human
erythropoietin abuse in athletes. Haematologica 2000;85:564-72.
2. Ashenden MJ, Hahn AG, Martin DT, et al. A comparison of the
physiological response to simulated altitude exposure and r-HuEpo
administration. J Sports Sci 2001;19:831-7.
3. Burge CM, Skinner SL. Determination of hemoglobin mass and blood
volume with CO: evaluation and application of a method. J Appl Physiol
1995;79:623-31.
I would like to thank you for your time and interest to read and
comment our article. I do not agree with some of your comments, but I
think that the disagreement is the beginning in order to continue research
in a topic.
Lateral epicondylitis (LE), commonly referred to as tennis elbow
(TE), is a tendon problem. Although the terms TE and LE are not
appropriate, I will use these two terms in...
I would like to thank you for your time and interest to read and
comment our article. I do not agree with some of your comments, but I
think that the disagreement is the beginning in order to continue research
in a topic.
Lateral epicondylitis (LE), commonly referred to as tennis elbow
(TE), is a tendon problem. Although the terms TE and LE are not
appropriate, I will use these two terms in the present report. LE is a
tendinosis--no tendonitis--condition, but the ideal term for clinical
diagnosis is the term tendinopathy (See articles Khan and his colleagues).
I do not know the article about Achilles tendonitis that you referred in
your letter, but I think that the example with Achilles tendonitis is not
appropriate for a condition, which is not inflammatory. If you mean
Achilles tendinosis or tendinopathy, I apologise for this comment.
Our review was the first review that studied the effectiveness of
extracorporeal shock-wave therapy (ESWT) for LE (See our article for more
details). You wrote in you letter that there are several well-designed
studies with ESWT for LE. I disagree with the previously opinion since the
well designed randomized controlled trials (RCTs) are few (My opinion is
supported by the introduction section of Chung and Willey, 2004 study). We
evaluated only the published RCTs. Therefore the Patronne et al. RCT was
not considered in our review. In addition, the majority of included RCTs
had methodological shortcomings (this opinion is supported by the
discussion section of Chung and Willey, 2004 study) and therefore we
cannot draw definite conclusions for the effectiveness of ESWT for LE.
You tried to explain the different results between your study and
Haake et al. (2002) RCT through the mechanism of action for ESWT. However,
reading your letter I see that the evidence of mechanism of action is
still conflicting. Moreover, these studies have only been performed in
either healthy animals or animals with artificially created tendinopathy
and we cannot be confirmed that these reported effects from animals could
be translated to the humans (My opinion is supported by the introduction
section of Chung and Willey, 2004 study).
The mechanism of pain in tendinopathies such as LE is still unknown.
You also tried to explain the analgesic effects of ESWT via the mechanism
of pain of LE, which is still uncertain (see Khan and his colleagues
articles). Besides, the literature on LE failed to define acute and
chronic LE (Trinh et al., 2004)
Furthermore, you tried to explain the different results between your
study and Haake et al. (2002) RCT via the anesthesia. However there are
studies without anesthesia (Crowther et al., 2002; Speed et al., 2002;
Chung and Willey, 2004; Melikyan et al., 2003) that showed that ESWT is not
an effective for LE or ESWT is a less effective treatment than sham or
other conservative treatment for LE. In contrast, there are studies that
showed that ESWT under anesthesia is an effective treatment for LE (Mehra
et al., 2005). We can argue that all the previously reported studies had
differences in outcome measures, protocols, follow ups and etc. Thus
definite conclusions about the effectiveness of ESWT for LE cannot be
drawn.
In conclusion, we support our finding that the results of this review
reveal conflicting findings about the effectiveness of ESWT in the
management of tennis elbow. Further research with well designed RCTs is
needed to establish its absolute and relative effectiveness.
I read with interest the Stasinopoulos/johnson article on ECWST for
"tennis elbow". I would like to bring to the author's attention our double
-blinded, randomized (placebo vs. active treatment groups) study
previously presented at the AAOS annual meeting 2003 with 6 month results
and at the 2004 meeting with 12 month results. This study has been
accepted for publication in the JBJS.
I read with interest the Stasinopoulos/johnson article on ECWST for
"tennis elbow". I would like to bring to the author's attention our double
-blinded, randomized (placebo vs. active treatment groups) study
previously presented at the AAOS annual meeting 2003 with 6 month results
and at the 2004 meeting with 12 month results. This study has been
accepted for publication in the JBJS.
Our study involved 114 patients non-responsive to two of three
conventional therapies including physical therapy, NSAIDS, and steriod
injections. Active treatment consisted of 3 weekly treatments of low-dose
shock wave therapy. without anaesthetic. Patients were evaluated with
radiographs and physical examination omcluding provocative testing and
dynamometry. A visual analog scale was used to evaluate pain and an upper
extremity functional scale was used to assess function. Evaluations of
patients were performed prior to treatment and at 1, 4, 8, 12 weeks, 6
months and 12 twelve months.
A stistically sighnificant difference (p=0.001) in pain reduction
was observed at 12 weeks in the active cohort with 61% (34/56) of active
treated patients showing at least 50% improvement in pain , compared to
29% (17/58) in the placebo group. This was found to persist for one year.
These results demonstrated ECSWT to be a safe and effective treatment
for chronic lateral epicondylitis. Interestingly, our results mirror those
of Rompe (AJSM 2004;32:734-43). Hence, in combination, provide additional
weight of evidence to this conclusion. Clearly, the effectiveness is dose
related and some consistency of methodology must be achieved to be able to
objectively evaluate differing studies.
I read with interest the review of Stasinopuolos and Johnson on the
“Effectiveness of extracorporeal shock wave therapy for tennis elbow” (Br
J Sports Med 2005; 39:132-139).
I acknowledge their evaluation in terms that the trials from Haake et
al. [1] and from our group [2] are by far the highest-ranking publications
in this field, while other studies show various major flaws in study
desi...
I read with interest the review of Stasinopuolos and Johnson on the
“Effectiveness of extracorporeal shock wave therapy for tennis elbow” (Br
J Sports Med 2005; 39:132-139).
I acknowledge their evaluation in terms that the trials from Haake et
al. [1] and from our group [2] are by far the highest-ranking publications
in this field, while other studies show various major flaws in study
design.
Unfortunately, Stasinopoulos and Johnson failed to provide a sensible
explanation for the different clinical outcomes of these two easily
comparable randomized controlled trials. To understand the discrepancy of
results of these two trials it is necessary to have insight into the most
recent results of experimental work on the mechanism of action of low-
energy ESWT.
The rationale for ESWT in clinical use is stimulation of soft tissue
healing and inhibition of pain receptors.
Haake et al., as usual, failed to provide any evidence for a specific
biological response when evaluating changes in the activity of local
nociceptive afferent nerve fibers or of spinal cord neurones in a rat
model after shock wave application (1000 impulses, Energy Flux Density
(EFD) = 0.13mJ/mm² - 0.33 mJ/mm²). The authors concluded that it was
unlikely that ESWT could trigger stimulation-induced analgesic response
via activation of peripheral nerves, and that analgesic effects of ESWT
were endogenous opioid – dependent. The authors further negated that ESWT
could trigger the endogenous pain control system. [3-5]
Others showed that Haake et al. were completely wrong!
Wang et al. [6] investigated the effect of low-energy shock wave
therapy on neovascularization at the tendon-bone junction in rabbits. The
results showed that low-energy shock wave treatment (500 impulses, EFD=
0.12 mJ/mm²) produced a significantly higher number of neo-vessels and
angiogenesis-related markers including endothelial nitric oxide synthase
(eNOS), vessel endothelial growth factor (VEGF) and proliferating cell
nuclear antigen (PCNA) than the control without shock wave treatment.
Chen et al. [7] reported that only an optimal ESW treatment promoted
healing of Achilles tendintis by inducing TGF-beta1 and IGF-I. Rats with
the collagenease-induced Achilles tendinitis were given a single shock
wave treatment (EFD= 0.16 mJ/mm²) with 0, 200, 500 and 1000 impulses. 200
impulses restored biomechanical and biochemical characteristics of healing
tendons 12 weeks after treatment. However, ESW treatments with 500 and
1000 impulses elicited inhibitory effects on tendinitis repair.
Histological observation demonstrated that ESW treatment resolved edema,
swelling, and inflammatory cell infiltration in injured tendons. The
proliferation of tenocytes adjunct to hypertrophied cell aggregate and
newly formed tendon tissue coincided with intensive TGF-beta1 and IGF-I
expression. Together, low-energy shock wave effectively promoted tendon
healing.
Meirer et al. [8] investigated the effect of low-energy ESWT on
compromised skin flaps. For this purpose, the epigastric skin flap model
in rats, based solely on the right inferior epigastric vessels was used.
20 rats were divided into an ESWT-group (2500 impulses, EFD= 0.15 mJ/mm²),
and a control group. Necrotic zones relative to total flap surface area
were measured and expressed as percentages. Overall, there was a
significant reduction in the surface area of the necrotic zones of the
flaps in the ESWT group compared to the control group (2.2% versus
control: 17.4%). Low-energy ESWT represented a feasible and cost effective
method to improve blood supply in ischemic tissue.
To investigate the analgesic properties of low-energy shock wave
application, Ohtori et al. [9] demonstrated that low-energy shock waves
(1000 impulses, EFD= 0.08 mJ/mm²) produced morphologic changes in
cutaneous nerve fibers. The number of sensory fibers decreased
significantly following shock wave application as indicated by the loss of
immunoreactivity for calcitonin gene related peptide (CGRP) compared to
the untreated skin. CGRP is a marker of sensory neurons, regarded as the
primary afferent peptide with the strongest evidence of a role in pain
perception, and has immunohistochemically been co-localized with substance
P. Reinnervation of the epidermis started 2 weeks after treatment. Ohtori
concluded that low-energy ESWT was able to temporarily destroy the sensory
free nerve endings in the rat skin.
When repeating shock wave application after 14 days in another
experiment, the same authors described delay of re-innervation for as long
as 42 days, significantly longer than after single shock wave
application. [10]
Takahashi et al. [11] investigated the analgesic properties of low-
energy shock wave application (1000 impulses, EFD= 0.08 mJ/mm²). They
analyzed changes in CGRP-immunoreactive (ir) neurons in the dorsal root
ganglion (DRG). In the nontreated group, 61% of fluorogold-labeled dorsal
root ganglion neurons innervating the most middle foot pad of hind paw
were CGRP-ir. However, in the shock wave-treated group, the percentage
decreased to 18%.
The described effect on CGRP-positive nociceptive nerve fibers is of
particular importance. Ljung et al. [12] studied the muscle origin in
patients suffering from tennis elbow. Immunohistochemistry and antibodies
to substance P (SP) and CGRP as well as the general nerve marker PGP 9.5
were used. Specific immunoreactions were observed in nerve bundles and as
free nerve fibers, the observations constituting a morphological correlate
for the occurrence of nerve mediated effects in this region. Their study
gave further evidence to previous suggestions that tennis elbow is not an
inflammatory process in the sense of involving inflammatory cells.
Frequent mechanical involvement obviously affected sensory innervation.
Substance P and calcitonin gene-related peptide were suggested to have
various important efferent effects in the etiology of tennis elbow.
From neurophysiological studies it is well known that nociceptive C-
fiber nerve endings release CGRP and substance P which result in protein
extravasation and vasodilation. This neurogenic inflammation has been
implicated in the pathophysiology of various human diseases with uncertain
etiology such as arthritis or tendinosis. Most important, beyond its
primarily inflammatory character neurogenic inflammation was regarded as a
mechanism that activates protective responses, thus bringing about a first
line of defence to maintain the integrity of the tissue and to contribute
to tissue repair. [13] Application of a local anesthetic effectively
inhibits this CGRP-induced healing cascade. [14]
Being aware of this fact a critical focus has to be on the use of
local anesthetics in the various trials. And the use of local anesthesia
happens to be the most decisive difference between the two highest-ranking
trials in Stasinopoulos´ analysis.
Accordingly, in the trial by Haake et al. [1] applying low-energy ESWT
under local anesthesia, the success rate was 26% in the verum group,
compared to 25% in the sham group.
In the study doing low-energy ESWT without local anesthesia, the success
rate was 65% in the verum group, compared to 33% in the sham group. [2]
And, those results have been supported by a US multicenter trial using an
identical study design. [15]
What is more, the same discrepancy of study results may be observed
when treating patients with chronic plantar fasciitis.
Again, Haake et al. [16] used a low-energy treatment under local
anesthesia, and again the results were unfavorable, with a success rate of
34% in the verum group, and of 30% in the sham group.
In the study doing low-energy ESWT without local anesthesia, the success
rate was 60% in the verum group, compared to 27% in the sham group. [17,18]
In an upcoming publication, Rompe et al. [19] evaluated the effect of local
anesthesia on the clinical outcome after repetitive low-energy ESWT for
chronic plantar fasciitis. 86 patients with chronic plantar fasciitis were
randomly assigned to receive either low-energy ESWT without local
anesthesia, given weekly for three weeks (3 x 2000 pulses, EFD= 0.09
mJ/mm2) or identical ESWT with local anesthesia. At 3 months,
significantly more patients achieved ≥ 50% reduction of pain
after low-energy ESWT without compared to low-energy ESWT with local
anesthesia (67% vs. 29%).
Together, I contradict the conclusion by Stasinopoulos and Johnson.
There are well designed trials providing meaningful evidence on the
effectiveness of ESWT for the management of tennis elbow. US and German
groups [2,15] have independently shown a treatment design leading to
successful outcome in close to 70% of patients with recalcitrant lateral
elbow tendinosis.
As always it is much easier to achieve unfavorable results with various
treatment regimes than to develop a successful treatment strategy. One
recent example is the trial by Chung and Wiley [20] who adopted the
treatment parameters of the above mentioned US and German trials, but
focused on patients with acute, not previously treated patients with a
tennis elbow, instead of chronic recalcitrant cases. As could be expected
from several other randomized controlled trials evaluating conservative
treatment methods for acute tennis elbow they found it impossible to beat
the self-limiting course of acute tendinosis at 8-week follow-up.
References
1. Haake M et al. Extracorporeal shock wave therapy in the treatment
of lateral epicondylitis. J Bone Joint Surg 2002; 84-A:1982-1991.
2. Rompe et al. Repetitive low-energy shock wave treatment for
chronic lateral epicondylitis in tennis players. Am J Sports Med 2004;
32:734-743.
3. Haake M et al. Absence of spinal response to extracorporeal shock
waves on the endogenous opioid systems in the rat. Ultrasound Med Biol
2001; 27:279-284.
4. Haake M et al. No influence of low-energy extracorporeal shock
wave therapy (ESWT) on spinal nociceptive systems. J Orthop Sci 2002; 7:97
-101.
5. Haake M et al. Unchanged c-Fos expression after extracorporeal
shock wave therapy: an experimental investigation in rats. Arch Orthop
Trauma Surg 2002; 122:518-521.
6. 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 2004; 22: 854-861.
7. Wang CJ et al. Shock wave therapy induces neovascularization at
the tendon-bone junction. A study in rabbits. J Orthop Res 2003; 21:984-
989.
8. Meirer R et al. Extracorporeal shock wave may enhance skin flap
survival in an animal model. Br J Plast Surg 2005; 58:53-57.
9. Ohtori S. et al. Shock wave application to rat skin induces
degeneration and reinnervation of sensory nerve fibres. Neurosci Lett
2001; 315:57-60.
10. Takahashi N et al. Application of shock waves to rat skin
decreases calcitonin gene-related peptide immunoreactivity in dorsal root
ganglion neurons. Auton Neurosci 2003; 107:81-84.
11. 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.
12. Ljung BO et al. Neurokinin-1 receptors and sensory neuropeptides
in tendon insertion of the medial and lateral epicondyles of the humerus.
Studies on tennis elbow and medial epicondylalgia. J Orthop Res 2004;
22:321-327.
13. Herbert MK, Holzer P. Neurogenic inflammation. II.
pathophysiology and clinical implications. Anasthesiol Intensivmed
Notfallmed Schmerzther 2002; 37:386-394.
14. Zimmermann M. Neuronal mechanism of chronic pain. Orthopade 2004;
33: 515-524.
15. Pettrone F, McCall B. Low-energy shock wave treatment for chronic
lateral epicondylitis. Journal Bone Joint Surg 2005; 87-A: in press.
16. Haake M et al. Extracorporeal shock wave therapy for plantar
fasciitis: randomised controlled multicentre trial. BMJ 2003; 327:75-85.
17. Rompe JD et al. Evaluation of low energy extracorporeal shock
wave application and treatment in chronic plantar fasciitis. J Bone Joint
Surg 2002; 84-A:335-341.
18. Rompe JD et al. Shock wave application for chronic plantar
fasciitis in running athletes - a prospective, randomized, placebo-
controlled trial. Am J Sports Med 2003; 31:268-275.
19. Rompe JD et al. Repetitive low-energy shock wave application
without local anesthesia is more efficient than repetitive low-energy
shock wave application with local anesthesia in the treatment of chronic
plantar fasciitis. J Orthop Res 2005; 23: in press (available online 7
December 2004).
20. 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; 32:1660-1667.
I read your editorial 'The power of placebo' with some relief. It
would seem that all too often, 'advances' in practice and even research
are relegating the placebo effect to the status of quackery. Certainly, I
am not a great fan of many therapies or technologies that claim
scientifically dubious healing or performance-enhancing qualities (I am to
be honest even less of a fan of those who sell them...
I read your editorial 'The power of placebo' with some relief. It
would seem that all too often, 'advances' in practice and even research
are relegating the placebo effect to the status of quackery. Certainly, I
am not a great fan of many therapies or technologies that claim
scientifically dubious healing or performance-enhancing qualities (I am to
be honest even less of a fan of those who sell them). However, by
dismissing the power of such artefacts/interventions to bring about a wide
range of positive effects, we are also dismissing the power of the mind to
bring about these very same effects.
Certainly the placebo effect, based essentially on the twin processes
of conditioning and expectancy (i.e. human beliefs), may be more easily
elicited in the more suggestible individual, and certainly may not be
powerful enough to operate in a wide range of conditions in which various
authors have made some fairly extreme claims. However, evidence, both
empirical and anecdotal, suggests that it is very much alive and well, if
hidden from view much of the time. It will remain hidden until the sports
science community adopts methodologies that allow it to demonstrate its
power. For example, the use of no-placebo control groups alongside placebo
and experimental groups (allowing not only the comparison of placebo and
experimental conditions but placebo and no-placebo conditions) might
reveal placebo effects of a far greater magnitude than one would imagine.
In fact, a recent meta analysis indicated that placebo effects may account
for up to 75% of the overall therapeutic effect of anti-depressant drugs
[1]. Certainly, such methodologies are complex and require a
high degree of control over variables, but they provide a far better
picture of what is really going on when, for example, an athlete takes a
tablet to reduce pain or sits on a treatment table.
What is all too often forgotten by practitioners is that the placebo
effect does not operate in isolation; it sits alongside many other
processes (e.g. pharmacological or biomechanical) and, if utilised
effectively, may augment many intervention significantly. On this basis
alone, it warrants far greater exploration in sport.
For those sceptics among us, or those who would like an informed
debate as opposed to the often emotional and opinionated rhetoric on this
subject, I strongly recommend Dylan Evans’ recent book on the subject [2]. Evans proposes a sound physiological basis for the placebo effect, and on
this basis, offers a strong case for a range of conditions being either
placebo responsive or not. A very useful starting point for practitioners
interested in the phenomenon.
Yours
Dr Chris Beedie
Canterbury, UK
No competing interests
References
1. Kirsch, I. Sapirstein, G., 1998, Listening to Prozac but Hearing Placebo.
A Meta-Analysis of Antidepressent Medication. Prevention and Treatment.
1(2): 1 – 15.
2. Evans, D., 2003, Placebo: The Belief Effect. London: Harper Collins.
Having worked in sport's injury prevention with children for the last
15 years and having monitored their evolution in a representative group of
about 160 adolescent girls and boys competing in various sports, I can but
express a certain amount of frustration as to the results of injury
prevention.
Having contributed to introduce and observed changes in, nutritional
and psychological counse...
Having worked in sport's injury prevention with children for the last
15 years and having monitored their evolution in a representative group of
about 160 adolescent girls and boys competing in various sports, I can but
express a certain amount of frustration as to the results of injury
prevention.
Having contributed to introduce and observed changes in, nutritional
and psychological counselling, stretching, interaction with coaches and
clubs, school timetable adaptation and physiological evaluation, I would
have expected to see at least part of the 75% injury reduction proposed by
Ekstrand in 1982 [1] even though their study only concerned football
players.
Over the last 15 years the incidence of sport injuries in our group
of adolescents has stayed constant at about 0.28 +/- .066 injuries / pupil
/ school year or 1.08 x 10-3 +/- 2.6 x10-4 injuries / pupil / 100 hours of
sport practised. The proportion of boys and girls and the type of sports
staying relatively constant through time. There was however a decrease in
overuse injuries, that seems to have been compensated by non-overuse
injuries.
Over the same period, the mean average increase in training time was
18 min./week.
Should we be finding a decrease in the incidence of injuries with
preventive measures, or does prevention merely permit athletes to practice
more and/or harder and reach higher levels of performance? Might it be
more pertinent to monitor the increase in performance (if possible)to get
an idea of the effectiveness of prevention?
To measure a change in incidence, attributable to prevention, would
imply that the training load and absolute performance objectives stay
constant through time. This, as one imagines, is contrary to the concept
of competitive sports, where the objective is to challenge our limits may
they be physical, mental or other.
I therefore believe that it might be difficult to measure the overall
efficacy of injury prevention in a constantly changing paradigm based on
performance and challenging limits. Improving records and performances
over time might confirm this.
References
1. Ekstrand J., A training program for the prevention of injuries to
reduce soccer injuries by 75 per cent. Nord Med. 1982 Jun;97(6-7):164-5
Dr P.B. Mahler,
Centre de Médecine d'Exercice,
Service de Santé de la Jeunesse,
11 Glacis de Rive, CP 3682,
1211 Genève 3,
Switzerland,
Tel: 41-22-3276157,
Fax: 41-22-3276171,
per.mahler@etat.ge.ch http://www.geneve.ch/ssj/
Huang and colleagues have prepared an estimate of the cost-
effectiveness of the Victorian, Active Script Programme, which they
conclude indicates a successful program and one suitable for wider
adoption. Confidence in a cost effectiveness estimate depends on
confidence in the evidence on effectiveness and costs.
The Active Script Program evaluation was designed to determine up-
take of the...
Huang and colleagues have prepared an estimate of the cost-
effectiveness of the Victorian, Active Script Programme, which they
conclude indicates a successful program and one suitable for wider
adoption. Confidence in a cost effectiveness estimate depends on
confidence in the evidence on effectiveness and costs.
The Active Script Program evaluation was designed to determine up-
take of the program by GPs. For the crucial evidence on patient physical
activity levels, the authors draw on the results of a different physical
activity intervention reported in a non-peer reviewed, unpublished
conference presentation by Bull (1999), which on inspection appears to
indicate a just significant 20% difference in activity levels between
control and intervention group at 6 months, which had fallen to a small
(<_5 non="non" significant="significant" difference="difference" in="in" the="the" percent="percent" active="active" between="between" intervention="intervention" and="and" control="control" groups="groups" at="at" _12="_12" months.="months." huang="huang" colleagues="colleagues" assume="assume" model="model" a="a" _20="_20" increase="increase" physical="physical" activity="activity" levels="levels" associated="associated" with="with" script="script" which="which" is="is" thus="thus" likely="likely" to="to" be="be" overstated="overstated" not="not" varied="varied" sensitivity="sensitivity" analysis.="analysis." fifty="fifty" of="of" this="this" group="group" presumed="presumed" maintain="maintain" their="their" long="long" enough="enough" accrue="accrue" health="health" benefit="benefit" unreferenced="unreferenced" consistent="consistent" data="data" by="by" bull="bull" shows="shows" that="that" months="months" there="there" has="has" been="been" _75="_75" reduction="reduction" observed="observed" _6="_6" p="p"/> Another more intensive active script type intervention demonstrated
an increase in the proportion of people physically active from baseline of
<_10 for="for" the="the" intervention="intervention" group="group" compared="compared" to="to" control="control" elley="elley" et="et" al="al" _2002="_2002" which="which" is="is" considerably="considerably" less="less" than="than" that="that" assumed="assumed" in="in" huang="huang" _2004="_2004" evaluation.="evaluation." p="p"/> The key effectiveness figure is likely to be overstated in the Huang
et al (2004) model. We find the step taken in the economic analysis from
GP awareness, knowledge and behaviour (which was measured) to patient
behaviour (which was not rigorously measured) to be beyond the scope of
the original data. It is likely that the estimates of cost effectiveness
would be higher and less certain than those presented, and that it may
have been more useful to highlight gaps in existing data.
References
(1). Bull F. Physical activity and General Practice: overview of the evidence.
Prepared for the participants of Active Australia Symposium on Physical
Activity in General Practice. Canberra, 1999.
(2). Elley CR, Kerse N, Arroll B, Robinson E. Effectiveness of counselling
patients on physical activity in general practice: cluster randomised
controlled trial. BMJ 2003;326:793.
Prompted by Lippi & Guidi [1] and their discussion that drugs
which modulate hypoxia inducible factors (HIFs) should soon be included in
antidoping legislation, is an old argument from my undergraduate days.
They state that HIFs stimulate red cell production and so could be used as
an athletic stimulant or to treat pathological conditions that involve
altered oxygen metabolism. On the flipside of...
Prompted by Lippi & Guidi [1] and their discussion that drugs
which modulate hypoxia inducible factors (HIFs) should soon be included in
antidoping legislation, is an old argument from my undergraduate days.
They state that HIFs stimulate red cell production and so could be used as
an athletic stimulant or to treat pathological conditions that involve
altered oxygen metabolism. On the flipside of the coin HIFs stimulate
genes encoding proteins involved in cell division and survival which could
ultimately promote the development of cancer [2].
This brings to mind an ongoing debate with an old lecturer.
Silicosis is a group of lung diseases that develop following the
inhalation of crystalline silica dust (SiO2)[3,4]. While for coal miners
this may simply be an occupational hazard, should the side effects of
steroids (or in this case gene manipulation) be an occupational hazard for
athletes?
Every drug is potentially toxic if administered in high enough doses
and drug use has increased in prevalence as athletes will “do anything,
take anything, short of killing themselves in order to improve
performance” [5]. In ancient Greece it was hallucinogenic mushrooms, 19th
century boxers used heroin as a painkiller, amphetamines and cocaine were
used together in the 50’s [6] and today athletes are using an even wider
range of drugs and genetic manipulation.
This historical view raises the point that drug use is not new, so we
cannot attribute it’s increase to financial rewards or increased media
scrutiny. In reality there is no justification for cheating, the
pressures and temptations are equal for all and any problem is of morality
and ethical justification. So what if the aspect of cheating was removed
and only the cost and availability limited the use of performance
enhancing techniques?
The mere seeking of an advantage is not implicitly unfair, nor is the
gaining of an advantage implicitly unfair [7]. In most cases any advantage
comes from an external source (e.g. sharkskin swimming suits), so why
should drugs or genetic manipulation be any different? So long as
athletes are informed of the risks, then why not allow (for example)
steroid use, it would certainly level the playing field. It would allow
those athletes who have to work harder to acquire an advantage through
training to easily achieve the same level as those who can gain a training
advantage with less effort.
The side-effects provide a sufficient basis for prohibition alone,
but is stopping competent adults from doing something an unwarranted
intrusion of privacy? There is in comparison little or no debate about
banning high-risk sports such as rugby or boxing and there is little
difference between athletes who risk their health by competing when
injured and those who risk their health to drugs. We admire those
competing dosed up to the eyeballs with painkillers and then condemn them
for taking other drugs to build muscle and relax after they have pushed
their bodies too far. If we are prepared to accept concern for an
athlete’s health as a basis to intervene over drug-use then logically we
should look at other aspects of certain high-risk sports. Allowing
performance-enhancing techniques may even decrease the risk for
athletes [8]. Banning them places a reliance on black market operations
(whose quality could not be guaranteed), there would be no advice on
dosages and hygiene could be compromised. If a ban is lifted then these
techniques could be controlled.
Any game is defined by its specific rules and if the rules are broken
you are not really playing that game. For example if a soccer player
picks up the ball and runs it is no longer soccer but branches off to
become rugby union, by the same token if one lone athlete takes drugs or
modifies their genes to express hypoxia tolerant characteristics then they
are playing a different game. A more effective way to ensure maximum
fairness may be to allow the free use of drugs. Consequently though, if
unrestricted access to drugs was allowed would that be fair? Inequalities
would exist between users themselves as well as users and non-users [9]. No
two people can be guaranteed to respond in the same way to the same drug
due to their individual physiology and no matter what drugs are used,
someone is always going to be first to use those that are newly developed.
Whatever route is taken to justify or oppose drug-use they all seem
to lead to a cul-de-sac of ambiguity and counter argument and therefore
the answer to the original question is not simple. It is down to the
individual athlete to consider all the risks involved and only then can
they decide if using performance enhancing techniques is just an
occupational hazard.
References
(1). Lippi, G, Guidi, G. Gene manipulation and improvement of athletic
performance: new strategies in blood doping. Br J Sports Med 2004;38: 641.
(2). Marx J. How cells endure low oxygen. Science 2004;303: 1454-6.
(3). Beckett, W, Abraham, J, Becklake, M, Christiani, D, Cowie, R,
Davis, G, Jones, R, et al. Adverse effects of crystalline silica exposure.
Am J Respir Crit Care Med 1997;155: 761-765.
(4). Mossman, B, Churg, A. Mechanisms in the pathogenesis of
asbestosis and silicosis. Am J Respir Crit Care Med 1998;157: 1666-1680.
(5). Connelly, H. cited in J.J. Coakley. Sport in Society: Issues and
Controversies. Mosby, St Louis, Missouri, USA. 1994; 151.
(6). Todd, T. Anabolic Steroids: the gremlins of sport. J Sport Hist
1987;14(1): 87-107.
(7). Fost, N.C. Ethical and Social Issues in Anti-doping Strategies in
Sport. In Landry, F., Landry M.,& Yerles, M. (eds.) Sport... The Third
Millenium. Sainte-Foy, Les Presses de l’Universite de Laval. 1991.
(8). Black, T, Pape, A. The Ban on Drugs in Sport, The Solution or the
Problem? J Sport Soc Iss 1997;21(1): 83-92.
(9). Gardner, R. On Performance-enhancing Substances and the Unfair
Advantage Argument J Phil Sport 1989;XVI: 59-73.
Dear Editor,
In their paper [1], McDowell and Ciocco conclude that "BBS values in slowpitch softball exceed recommended safety limits imposed on the sport" and their "findings indicate that softball is perhaps more dangerous then most coaches, players and parents think." Had this paper been published in an American journal it might have attracted considerable attention from the news media due to its alarming conclusion...
Dear Editor,
Thank you for the help on the topic of hand washing. I have been studying the importance of hand washing for about three weeks, with no success. This article helped me out a lot. I know how it is to have snotty kids, I babysit, and the spreading of germs is deadly. I recently spoke to a young woman who after her daycare job, each day would throw all toys and such into a bucket of bleach. We are d...
Dear Editors,
The altitude training study of Friedmann et al. reported a 6% increase in haemoglobin mass (Hbmass), but this result warrants close scrutiny, particularly without a corroborating measure of augmented VO2max, nor of corresponding measures in a matched control group. The authors’ contend that “there exist no studies in which the changes in total haemoglobin mass following treatment with recombinant...
Dear Editor,
I would like to thank you for your time and interest to read and comment our article. I do not agree with some of your comments, but I think that the disagreement is the beginning in order to continue research in a topic.
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Dear Editior,
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Our s...
Dear Editor,
I read with interest the review of Stasinopuolos and Johnson on the “Effectiveness of extracorporeal shock wave therapy for tennis elbow” (Br J Sports Med 2005; 39:132-139).
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Dear Editor,
I read your editorial 'The power of placebo' with some relief. It would seem that all too often, 'advances' in practice and even research are relegating the placebo effect to the status of quackery. Certainly, I am not a great fan of many therapies or technologies that claim scientifically dubious healing or performance-enhancing qualities (I am to be honest even less of a fan of those who sell them...
Dear Editor,
Having worked in sport's injury prevention with children for the last 15 years and having monitored their evolution in a representative group of about 160 adolescent girls and boys competing in various sports, I can but express a certain amount of frustration as to the results of injury prevention.
Having contributed to introduce and observed changes in, nutritional and psychological counse...
Dear Editor,
Huang and colleagues have prepared an estimate of the cost- effectiveness of the Victorian, Active Script Programme, which they conclude indicates a successful program and one suitable for wider adoption. Confidence in a cost effectiveness estimate depends on confidence in the evidence on effectiveness and costs.
The Active Script Program evaluation was designed to determine up- take of the...
Dear Editor,
Prompted by Lippi & Guidi [1] and their discussion that drugs which modulate hypoxia inducible factors (HIFs) should soon be included in antidoping legislation, is an old argument from my undergraduate days. They state that HIFs stimulate red cell production and so could be used as an athletic stimulant or to treat pathological conditions that involve altered oxygen metabolism. On the flipside of...
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