I now better appreciate Prof. Noakes' reasons for using the words he
used following his response to my eletter posted on the BJSM Blog, and
consider the issue of "data exclusion" settled. However, I would like to
make the following points to clarify my position and respond to Noakes'
interpretation of the physiology:
1. I do not consider myself "wedded to the Hill model" because the
"Hi...
I now better appreciate Prof. Noakes' reasons for using the words he
used following his response to my eletter posted on the BJSM Blog, and
consider the issue of "data exclusion" settled. However, I would like to
make the following points to clarify my position and respond to Noakes'
interpretation of the physiology:
1. I do not consider myself "wedded to the Hill model" because the
"Hill model" as presented by Noakes bears no relationship to my
understanding of the physiological response to exercise. It is my
contention that the "Hill model" is an erroneous caricature of the
physiology of exercise that Noakes uses as a straw man in contrast to his
central governor model. Few scientists are likely to defend the view that
cardiac output and VO2 must always be identical at exhaustion, for the
evidence against this proposition is overwhelming! In short, the “Hill
model” is not a contemporary model of exercise physiology, it is a vehicle
invented by Noakes.
2. “Oxygen consumption" or, more correctly, pulmonary oxygen uptake,
is not a "surrogate measure of cardiac output and the state of muscle
oxygenation". To claim this indicates a misunderstanding or
misrepresentation of basic physiological measurements. Pulmonary VO2 is
useful because in both the non-steady state and the steady state it
closely reflects muscle VO2, which itself reflects energetic events
occurring in the cell. If one accepts that the rate of energy transfer is
an important consideration during exercise, then measuring the most
quantitatively significant energy transfer process is worthwhile.
Furthermore, the phrase “state of muscle oxygenation” is hopelessly vague.
Does Noakes mean “muscle O2 extraction”, “arterio-venous oxygen
difference” or “intracellular [or mitochondrial] PO2”? The first two
measures are difficult to make, whilst the latter is currently impossible
to make during whole-body exercise.
3. I do not “believe” that exhaustion occurs before VO2max is
attained during "extreme" exercise, it is an experimental fact: exercise
is terminated whilst VO2 is still rising in a futile attempt to meet the
energetic demand.[1] Exercise under these conditions is terminated
because the subject is no longer able to sustain the power requirements of
the task (in my experience not because the subject is unwilling), but this
says little of the mechanism. Classic works on the aetiology of muscle
fatigue acknowledge that fatigue processes occur at a number of sites
within the neuromuscular system,[2,3] and I certainly embrace this.
Exhaustion at these “extreme” work rates is attended by falling [PCr] and
pH and rising [Pi] and [ADP], amongst other derangements known to cause a
fall in tension produced by the myocyte.[4] However, measurements of
these processes in whole-body exercise are presently too spatially or
temporally crude to be definitive – but that is certainly not a reason to
reject the periphery as a plausible or even pivotal contributor to task
failure (exhaustion). Note also that the identification of metabolites
involved in substrate-level phosphorylation does not imply that the
conditions within the cell are “anaerobic”: the concentrations of these
metabolites will change progressively during exercise above the so-called
“critical power”[5] irrespective of cellular PO2.[6]
4. Noakes argues that the “simulaneous [sic] measurement of muscle
activation” is required to test the alternate (central governor) theory
“that maximal exercise always terminates before there is 100% activation
of all the available motor units in the exercising limbs”. However, this
is impossible to verify with current technology. Even if
electromyographic recordings are taken from the surface of a large number
of muscles and normalised to some measure of maximal voluntary muscle
function (such as an MVC), this will not provide an estimate of the
fractional number of motor units that are active. The EMG signal is
determined, in part, by the number of active muscle fibres in the region
of interrogation, their firing frequency, and the conductivity of the
tissues between the fibres and the electrodes, not simply by the number of
active motor units. A method of determining the total number of active
motor units during whole-body exercise would be very useful but does not
currently exist.
The processes leading to additional motor unit recruitment during
rhythmic whole-body exercise are far from understood. However, it is
logical that in conditions where the rate of O2 delivery is maximal (i.e.,
when cardiac output is maximal) the recruitment of additional motor units
will lead to worsening metabolic conditions within the exercising muscles,
as those newly recruited fibres will also extract O2 from the
microvasculature. The consequent fall in microvascular PO2 will make the
appropriate matching of O2 demand and supply (essential for the
continuance of exercise) increasingly difficult. Additional motor unit
recruitment is thus likely to yield diminishing returns in terms of
sustaining the required power output. In this scenario, task failure will
occur before all motor units are activated even in the absence of a
“governor”.
In summary, Prof. Noakes’ representation of the physiology of
exercise could be charitably described as inaccurate. The “Hill model” is
not one that any physiologist is “wedded” to because it does not exist.
Therein lay the “misleading interpretations” to which I referred in my
first letter. One final point needs to be made:
If the “absence of any such catastrophe [myocardial ischaemia or
rigor during exercise] suggests the presence of an anticipatory, complex,
regulatory control system”[7], then surely the presence of myocardial
ischaemia during exercise[8] suggests the absence of an anticipatory,
complex regulatory control system? How long can the central governor
theory survive with this elephant in the room?
“It does not make any difference how beautiful your guess is. It does
not make any difference how smart you are, who made the guess, or what his
name is - if it disagrees with experiment it’s wrong. That’s all there is
to it.” Richard P. Feynman.
References
1. Hill DW, Poole DC, Stevens JC. The relationship between power and
the time to achieve VO2max. Med Sci Sports Exerc. 2002;34:709-714
2. Bigland-Ritchie B, Woods JJ. Changes in muscle contractile
properties and neural control during human muscular fatigue. Muscle Nerve.
1984;7:691-699.
3. Gandevia SC. Spinal and supraspinal factors in human muscle
fatigue. Physiol Rev. 2001;81:1725-1789.
4. Fitts RH. The cross-bridge cycle and skeletal muscle fatigue. J
Appl Physiol. 2008;104:551-558.
5. Jones AM, Wilkerson DP, DiMenna F, Fulford J, Poole DC. Muscle
metabolic responses to exercise above and below the “critical power”
assessed using 31-PMRS. Am J Physiol Regul Integr Comp Physiol.
2008;294:R585-R593.
7. Noakes TD. Peer review/fair review: How did A.V. Hill understand
the VO2max and the “plateau phenomenon”? Still no clarity? Brit J Sports
Med, in press. DOI: 10.1136/bjsm.2008.046771.
8. Bogaty P, Poirier P, Boyer L, Jobin J, Dagenais GR. What induces
the warm-up ischemia/angina phenomenon: exercise or myocardial ischemia?
Circulation. 2003;107:1858-1863.
Tennis elbow – impingement at the common extensor origin?
Case report
We thank Dr Knobloch and colleagues for raising questions of the
influence of elbow position on the area with high blood flow seen in the
common extensor origin and outcome measurement in patients with painful
tennis elbow. The first question raised is if the grip strength with 900
elbow flexion might change as well as th...
Tennis elbow – impingement at the common extensor origin?
Case report
We thank Dr Knobloch and colleagues for raising questions of the
influence of elbow position on the area with high blood flow seen in the
common extensor origin and outcome measurement in patients with painful
tennis elbow. The first question raised is if the grip strength with 900
elbow flexion might change as well as the grip strength with extended
elbow changes in response to the intratendinous injection treatment.[1]
This question will be answered in an original article in the future.
The other question raised is if the area with high blood flow inside the
area of structural changes seen on ultrasound examination is influenced by
elbow position. One of the findings on ultrasound examinations of the
common extensor origin is “tendon thickening”.[2] We believe that this
thickening in some cases is exposed to internal compressive forces. This
belief is based on the findings we have made when we have performed
ultrasound and colour Doppler examinations during elbow movement. When the
elbow is flexed 70-80 degrees there is plenty of space between the head of the
radial bone and the lateral epicondyle but during extension of the elbow,
the radius makes a movement towards the lateral epicondyle and there will
be impingement of the area with structural changes and high blood flow
(Figure 1a and 1c). The raised pressure in the thickened tendon due to
impingement at the extensor origin will diminish the high blood flow (not
detectable), and like on palpation (applying external compressive force),
the patient will experience pain. To perform an intratendinous injection
targeting the area with high blood flow, the blood flow must be visible on
colour Doppler examination which is the case when the elbow is flexed 70-
800, not when the elbow is extended (Figure 1b and 1d). This theory of
impingement at the common extensor origin in tennis elbow might be the
explanation behind good results in arthroscopic debridement of the
area.[3] Other authors have also noted impingement during elbow
arthroscopy, Mullet and colleagues classified their findings as
degenerative capsular fold.[4]
We hope this case rapport is an acceptable answer to the question at the
time being. Further studies of the biomechanical prosperities of the elbow
and the effect on the soft tissue are highly indicated. Are some
individuals more prone to develop recalcitrance painful tennis elbow?
References
[1] Zeisig E, Fahlstrom M, Ohberg L, et al. Pain relief after
intratendinous injections in patients with tennis elbow: results of a
randomised study. British journal of sports medicine. 2008 Apr;42(4):267-
71.
[2] Levin D, Nazarian LN, Miller TT, et al. Lateral epicondylitis of the
elbow: US findings. Radiology. 2005 Oct;237(1):230-4.
[3] Cummins CA. Lateral epicondylitis: in vivo assessment of arthroscopic
debridement and correlation with patient outcomes. The American journal of
sports medicine. 2006 Sep;34(9):1486-91.
[4] Mullett H, Sprague M, Brown G, et al. Arthroscopic treatment of
lateral epicondylitis: clinical and cadaveric studies. Clinical
orthopaedics and related research. 2005 Oct;439:123-8.
LEGENDS TO THE FIGURE
Figure 1 a-d: Patient clinically diagnosed to have tennis elbow. The
common extensor origin is shown in a longitudinal view a. Grey-scale
ultrasonography (US) with the elbow flexed 70-800. b. Colour Doppler (CD)
shows high blood-flow inside the area with structural changes in the
extensor origin with the elbow flexed 70-800. c. US of the same patient
with extended elbow. Note the narrowing space between the lateral
epicondyle (*) and the head of the radial bone (**) compared to figure a.
d. CD shows no blood-flow inside the area with structural changes in the
extensor origin with the elbow extended.
I have read with interest the article by Wilson et al (in the March
edition of the British journal of Sports Medicine) regarding their support
for using an ECG in screening for sudden cardiac death in the young.
Furthermore I note that there is considerable support from many sporting
governing bodies for the above recommendation.
I note the comments of Dr Richard Page (in the Warm up section o...
I have read with interest the article by Wilson et al (in the March
edition of the British journal of Sports Medicine) regarding their support
for using an ECG in screening for sudden cardiac death in the young.
Furthermore I note that there is considerable support from many sporting
governing bodies for the above recommendation.
I note the comments of Dr Richard Page (in the Warm up section of the
March edition) where he argued that in the USA alone, mass ECG screening
of young athletes would exclude 2000 children from sport for every life
saved.
Dr Page's comments have very much caught my eye. By trying to save one
life in an issue that is highly media motivated for the obvious dramatic
nature of sudden cardiac death in a young person, we prison a further 2000
children to a potentially life threatening sedentary life style. Hence,
ironically we may increase these childrens risk of death from a cardiac
cause later in life.
Are we really doing whats best for these children or are we dancing
to the tune of the media? Have we thought about the long term
repercussions that such a screening programme may have on our childrens
physical and psychological wellbeing?
I read with concern the recent review of Noakes[1] accepted for
publication in the journal. Noakes suggests that there is no
“biologically plausible explanation” for the observation of lower oxygen
uptake (VO2) values in supramaximal exercise compared to incremental
exercise.[2] Noakes further argues that those supramaximal data are
therefore questionable and should be excluded, thus resul...
I read with concern the recent review of Noakes[1] accepted for
publication in the journal. Noakes suggests that there is no
“biologically plausible explanation” for the observation of lower oxygen
uptake (VO2) values in supramaximal exercise compared to incremental
exercise.[2] Noakes further argues that those supramaximal data are
therefore questionable and should be excluded, thus resulting in the
conclusions of the original authors being disproved. Noakes’ first
assertion (biological implausibility) is incorrect. His second assertion
is at best biased, and at worst could be viewed as endorsing unethical
practices.
The observation of lower VO2 values at exhaustion during supramaximal
exercise could be attributed to normal biological variation (random
error). However, the kinetics of VO2 dictates the rate at which VO2 rises
to meet the energetic demand. In situations where exhaustion occurs
before the kinetics drive VO2 to the maximum (so-called “extreme intensity
exercise”[3]), VO2 will be lower than that measured in an incremental test
performed to exhaustion. The boundary between “severe intensity exercise”
(wherein VO2 reaches VO2max before exercise termination) and “extreme
exercise” has been estimated to be ~110-135% VO2max,[3,4] providing the
“biologically plausible explanation” Noakes wishes to deny.
To argue exclusion of the supramaximal data is ethically troubling.
Such exclusion, in this case solely for the purpose of interpretation,
results in grossly biased conclusions. For any scientist, particularly
one as influential as Noakes, to adopt such an approach does a disservice
to students of exercise science. It would be tragic indeed if these
impressionable proto-scientists use Noakes’ precedence to endorse
unethical data manipulation techniques to promote their own subjective
opinions. Accordingly, I call upon Noakes to retract these statements to
prevent further misleading interpretations from entering the literature.
References
1. Noakes TD. Peer review/fair review: How did A.V. Hill understand
the VO2max and the “plateau phenomenon”? Still no clarity? Brit J Sports
Med, in press. DOI: 10.1136/bjsm.2008.046771.
2. Hawkins MN, Raven PD, Snell PG, Stray-Gundersen J, Levine BD.
Maximal oxygen uptake as a parametric parameter of cardiorespiratory
capacity. Med Sci Sports Exerc. 2007;39:103-107.
3. Hill DW, Poole DC, Stevens JC. The relationship between power and
the time to achieve VO2max. Med Sci Sports Exerc. 2002;34:709-714.
4. Wilkerson DP, Koppo K, Barstow TJ, Jones AM. Effect of work rate
on the functional ‘gain’ of Phase II pulmonary O2 uptake response to
exercise. Respir Physiol Neurobiol. 2004;142: 211-223.
I read the recent article by Paul Boyle [1] regarding the
longevity of English test cricketers with interest. In this paper the
authors linked length of international cricket career (‘success’) with
lifespan, suggesting that a successful life lead to a longer life. The
hypothesis that quality of life grants one a physiological advantage and
therefore increases length of life is well accepted in the...
I read the recent article by Paul Boyle [1] regarding the
longevity of English test cricketers with interest. In this paper the
authors linked length of international cricket career (‘success’) with
lifespan, suggesting that a successful life lead to a longer life. The
hypothesis that quality of life grants one a physiological advantage and
therefore increases length of life is well accepted in the medical field
and its mechanisms deserve closer examination.
However, I feel that the author has potentially overreached with this
conclusion by dismissing the effect of physical activity on lifespan. The
author states that the increased levels of physical fitness we would
expect in world class athletes are unlikely to affect lifespan because
“cricket is not a sport which requires physical strength”. In this
conclusion the author has incorrectly regarded fitness as musculoskeletal
strength alone, ignoring the important aerobic component. Cricket is
primarily an aerobic sport, and the fitness of its players is often
underestimated [3]. Several studies in both animals
and humans have demonstrated a link between aerobic activity and lifespan.
Rats subjected to only 10 minutes walking a day live 25% longer than
sedentary littermates [4]. The classic London busmen
study [2] and several others [5] all demonstrated that people who worked in physically active
positions lived significantly longer then workmates who had more sedentary
positions.
It is reasonable to assume that those who were honored to represent
their country for longer had a higher level of physical activity for a
longer period of time than those who did not, therefore likely having an
effect on longevity.
Bradley Elliott,
Centre de recherche de l'Hôpital Laval, Québec, Canada
bradley.elliott@crhl.ulaval.ca
References
[1] Boyle, P. J. (2008). "Does occupational success influence longevity
among England test cricketers?" Br J Sports Med: bjsm.2007.041566.
[2]Heady, J. A., J. N. Morris and P. A. Raffle (1956). "Physique of London
busmen; epidemiology of uniforms." Lancet 271(6942): 569-70.
[3]Noakes, T. D. and J. J. Durandt (2000). "Physiological requirements of
cricket." J Sports Sci 18(12): 919-29.
[4]Retzlaff, E., J. Fontaine and W. Furuta (1966). "Effect of daily exercise
on life-span of albino rats." Geriatrics 21(3): 171-7.
[5]Warburton, D. E., C. W. Nicol and S. S. Bredin (2006). "Health benefits of
physical activity: the evidence." Cmaj 174(6): 801-9.
Germonpré et al. have presented the possible mechanisms of a new
technique to equalize middle ear and sinus cavities during extreme-depth
apnoea diving by passive flooding of these cavities with surrounding
water. Even though their measures were not made in water, they demonstrate
that it is possible to flood the middle ear in order to better compensate
during very deep apnoea diving. In addition to the...
Germonpré et al. have presented the possible mechanisms of a new
technique to equalize middle ear and sinus cavities during extreme-depth
apnoea diving by passive flooding of these cavities with surrounding
water. Even though their measures were not made in water, they demonstrate
that it is possible to flood the middle ear in order to better compensate
during very deep apnoea diving. In addition to the risks of degeneration
and/or infections, the supplementary risk of decompression sickness (DCS)
must be underlined. There are two main limiting factors in very deep
apnoea dives: cranial cavity compensation and apnoea duration. PM, by
drowning his cranial cavities, succeeded in liberating himself from the
first factor while playing on the second and thus limiting the risk of
hypoxia. But he also considerably raised the ascent and descent speed (2
m.s-1), thus potentially increasing the risk of DCS. Although the exact
mechanisms of DCS in breath-hold divers (BHDs) are not well known (Schipke
2005), DCS has already been observed after only one shallower apnoea dive
(120 m) made using the same type of material (Magno et al., 1999). The
concerned BHD had nausea, dizziness, fatigue, visual disturbance and
hemiplegic symptoms that were resolved after a hyperbaric chamber session
of some hours. PM experienced mainly extreme fatigue after his dive to 209
m; he also was transported to the hospital and treated in a hyperbaric
chamber. This extremely fast ascent could disturb the evacuation of blood
present around the lung, which would encourage the passage of bubbles into
the arterial circulation and lead to DCS. For these reasons, I don't think
that one can affirm with certainty that this technique increases the
security of BHDs. It certainly permits them to reach greater depths, but
the corresponding immersion dangers remain unknown.
References
Magno L, Lundgren CEG, Ferrigno M. Neurological problems after breath
-hold diving. Undersea Hyper Med 1999;26:28-29.
Schipke JD. Decompression sickness following breath-hold diving. Res
Sports Med 2006;14:163-178.
In a recent letter,[7] Noakes reminded us that the brain estimates
the maximal exercise duration that can be sustained (maybe even before the
exercise begins), and then uses the ratings of perceived exertion (RPE) to
inform the body when the exercise will and must terminate. I agree with
this suggestion. RPE attests to the exercise intensity, but also to the
duration.[3] Therefore, according to Noake...
In a recent letter,[7] Noakes reminded us that the brain estimates
the maximal exercise duration that can be sustained (maybe even before the
exercise begins), and then uses the ratings of perceived exertion (RPE) to
inform the body when the exercise will and must terminate. I agree with
this suggestion. RPE attests to the exercise intensity, but also to the
duration.[3] Therefore, according to Noakes,[7, 8] RPE is a predictor of
the exercise duration that remains until exhaustion. However, RPE is not
the only perceptual tool that informs us of the exercise end point, and
perhaps not the most effective.
Drawing from the “teleoanticipation” concept,[9] prior to, or early
in an exercise period, the brain estimates the time limit (i.e., Tlim)
that can safely sustained.[8] Then, this predicted Tlim is associated with
the maximal RPE that can be tolerated. During exercise, the brain provides
RPE, which increases as a function of the percentage of the predicted
Tlim, until the attainment of the corresponding tolerated maximal RPE.[8]
Garcin and Billat confirmed that RPE attests to both exercise
intensity and duration.[3] However, these authors[3] found similar results
for a second scale (Estimated Time Limit scale, ETL). This scale predicts
how long the current exercise level can be maintained (i.e., the
estimation of exhaustion time). Therefore, as suggested by Noakes,[7] if
humans may accurately predict the exercise duration that they are or will
be able to sustain at any exercise intensity, ETL may be considered as the
conscious interpretation of the Tlim predicted by teleoanticipation, and
may be more effective than RPE in predicting the time remaining before
exhaustion.
The reliability of ETL scale is established.[1, 5] Moreover, although
the accuracy of this scale must be improved, no significant difference was
found between the Tlim predicted from this scale and those that were
actually measured.[1, 2, 4] Therefore, ETL scale may be associated with
the RPE scale (or substituted for the RPE scale, if the accuracy
improves), not to precisely measure the Tlim predicted by
teleoanticipation, but to provide an estimation of this latter, as
recently suggested.[6]
There are no competing interests.
References
1. Coquart, J. B. J. and M. Garcin. Validity and reliability of
perceptually-based scales during exhausting runs in trained male runners.
Percept Mot Skills. 2007;104:254-266.
2. Coquart, J. B. J., M. Garcin, S. Robin, and R. Matran. Prediction of
exhaustion time from a perceptually-based scale. In 12th International
Congress of the Association des Chercheurs en Activités Physiques et
Sportives. Leuven, Belgium, p. 68, 2007.
3. Garcin, M. and V. Billat. Perceived exertion scales attest to both
intensity and exercise duration. Percept Mot Skills. 2001;93:661-671.
4. Garcin, M., L. Mille-Hamard, and V. Billat. Influence of aerobic
fitness level on measured and estimated perceived exertion during
exhausting runs. Int J Sports Med. 2004;25:270-277.
5. Garcin, M., M. Wolff, and T. Bejma. Reliability of rating scales of
perceived exertion and heart rate during progressive and maximal constant
load exercises till exhaustion in physical education students. Int J
Sports Med. 2003;24:285-290.
6. Joseph, T., B. Johnson, R. A. Battista, G. Wright, C. Dodge, J.P.
Porcari, J. J. De Koning, and F. Foster. Perception of fatigue during
simulated competition. Med Sci Sports Exerc. 2008;40:381-386.
7. Noakes, T. D. RPE as a predictor of the duration of exercise that
remains until exhaustion. Br J Sports Med Oneline [eLetter] 8 January
2008. http://bjsm.bmj.com/cgi/content/abstract/bjsm.2007.043612v1
8. Noakes, T. D., R. J. Snow, and M. A. Febbraio. Linear relationship
between the perception of effort and the duration of constant load
exercise that remains. J Appl Physiol. 2004;96:1571-1573.
9. Ulmer, H. V. Concept of an extracellular regulation of muscular
metabolic rate during heavy exercise in humans by psychophysiological
feedback. Experientia. 1996;52:416-420.
The injected agent with color Doppler– does it matter in tennis
elbow?
We read with great interest the recent randomised, double-blinded
controlled cross-over trial by Dr. Zeisig and colleagues evaluating
ultrasound and color Doppler guided injections in the proximal forearm in
tennis elbow. We would like to comment on some issues.
Grip strength was considered as “the best objective...
The injected agent with color Doppler– does it matter in tennis
elbow?
We read with great interest the recent randomised, double-blinded
controlled cross-over trial by Dr. Zeisig and colleagues evaluating
ultrasound and color Doppler guided injections in the proximal forearm in
tennis elbow. We would like to comment on some issues.
Grip strength was considered as “the best objective outcome measure”
for tennis elbow by the authors. The maximum voluntary grip strength was
evaluated with the elbow straight and the wrist in a neutral position.
Interestingly, elbow position does play a role for grip strength in tennis
elbow [1]. An 8% difference in grip strength between flexion and extension
was found to be 83% accurate in distinguishing the affected from the
unaffected extremities. In other words, grip strength is used to
distinguish tennis elbow from a pain-free extremity based on flexed and
extended elbow position. ECRB’s unique anatomy with a sarcomere length
maximal with the elbow at 90° of flexion, and minimal between 30° of
flexion and 60° of flexion is considered to play a role in this regard. It
would be interesting to see whether the grip strength with 90° elbow
flexion might change as well in response to the injection therapy by
either polidocanol or lidocaine/adrenaline or any other agent.
This idea leads us to another suggestion. Colour Doppler sonography
was performed with the arm resting on a table in 70°-80° elbow flexion and
pronated wrist. On the other hand, as mentioned before, grip strength was
tested on the elbow extended. The area of neovascularisation inside the
area of structural changes in the extensor origin might be influenced by
elbow position as well. One is tempted to speculate that blood flow in the
area of neovascularisation might be changed by elbow extension. In
Achilles tendinopathy, the eccentric position of the ankle has been
reported to reduce the area of neovascularisation [3]. Therefore, it might
be worth considering elbow position for colour Doppler ultrasound as well,
since even in the pilot paper on neovascularisation in tennis elbow [5]
there is no mention why a 70° to 80° position was used and how
neovascularisation might be influenced as a function of elbow flexion.
The authors speculated that regardless of the type of substance
injected, the volume injected might have increased the intratendinous
pressure which might be responsible for the pain relieving effects. Dr.
Zeisig injected 0.5ml per injection with either polidocanol or
lidocaine/adrenaline. A recently published, case-only, blinded
intervention study among 62 patients with tennis elbow performed a colour
Doppler guided injection (90° elbow flexion) of 1ml methylprednisone
(40mg/ml) and 0.5ml lidocaine (1%) [4]. Within two weeks symptoms resolved
which corresponded to a reduction of the vascular activity in the common
extensor origin following the injection. In Achilles tendinopathy, color
Doppler guided injection of 1ml lidocaine (2%) and 1ml of 50% dextrose
yielded to to good clinical responses as far as pain at rest and during
tendon-loading activities was concerned [2].
Studies with various volumes injected by guided color Doppler
ultrasound with clinical outcome scores as well as functional data such as
tendon metabolism or tendon microcirculation might help in the future to
determine the appropiate amount and type of injected agent in tennis
elbow. We would like to thank the authors for their inspiring and
stimulating work.
References
[1] Dorf ER, Chhabra AB, Golish SR, McGinty JL, Pannunzio ME. Effect
of elbow position on grip strength in the evaluation of lateral
epicondylitis. J Hand Surg 2007;32:882-6.
[2] Maxwell NJ, Ryan MB, Taunton JE, Gillies JH, Wong AD.
Sonographically guided intratendinous injection of hyperosmolar dextrose
to treat chronic tendinosis of the Achilles tendon: a pilot study. AJR Am
J Roentgenol 2007;189:W215-20.
[3] Ohberg L, Alfredson H. Effects on neovascularisation behind the
good results with eccentric training in chronic mid-portion Achilles
tendinosis? Knee Surg Sports Traumatol Arthrosc 2004;12:465-70.
[4] Torp-Pedersen TE, Torp-Pedersen ST, Ovistgaard E, Bliddal H.
Effect of glucocorticosteroid injections in tennis elbow verified on
colour doppler ultrasound: evidence of inflammation. Br J Sports Med 2008
Mar 4 [Epub ahead of print].
[5] Zeisig E, Ohberg L, Alfredson H. Extensor origin vascularity
related to pain in patients with tennis elbow. Knee Surg Sports Traumatol
Arthrosc 2006;14:659-63.
Hegedus et al [1] used a fixed-effects model to pool diagnostic odds
ratios (DOR) for the Neer and the Hawkins-Kennedy tests for impingement.
In Figure 2 and in Figure 3 they display the natural logarithms of the DOR
for the individual and pooled results (the figures are inadvertently
labeled as DOR rather than as the logarithms). In each diagram, the null
value (natural logarithm of the DOR =0) is incl...
Hegedus et al [1] used a fixed-effects model to pool diagnostic odds
ratios (DOR) for the Neer and the Hawkins-Kennedy tests for impingement.
In Figure 2 and in Figure 3 they display the natural logarithms of the DOR
for the individual and pooled results (the figures are inadvertently
labeled as DOR rather than as the logarithms). In each diagram, the null
value (natural logarithm of the DOR =0) is included in the confidence
intervals of the pooled results, while it is not included in the
confidence intervals of any of the individual studies. The authors report
that the 95% confidence interval for the pooled DOR crosses 1
(corresponding to a log-odds of 0) indicating that neither test has
diagnostic utility for impingement.
In a fixed-effects model, a weighted average is taken of the odds
ratios of the individual studies. Different calculation methods may arrive
at slightly different confidence intervals for the pooled odds ratio, but
the standard error of the weighted sum is smaller than the standard errors
of the individual studies. It often happens that the confidence intervals
for individual studies may include the value for the null hypothesis,
while the pooled estimate confidence interval excludes that value; this is
one reason that meta-analyses are undertaken. If the converse occurs, a
computational mishap is likely to have occurred. Pooling several
statistically significant odds ratios will not yield a non-significant
odds ratio. In the present meta-analysis, extracting the data from the
four studies and pooling the results may yield a DOR of insufficient
magnitude to discriminate between cases and non-cases of impingement, but
the calculation yielding a DOR whose confidence interval includes 1 should
be re-examined.
References
1. Hegedus EJ et al. Physical examination tests of the shoulder: a
systematic review with meta-analysis of individual tests. Br J Sports Med
2008;42:80-91.
I read with great interest the recent review focussing the
pathophysiology, the diagnosis and the treatment of tennis elbow. However,
based on this report I would appreciate having the chance to comment on
some issues raised by the authors shortly.
Diagnosis: The role of neovascularisation determined by colour or
even better by Power Doppler sonography has been mentioned for several
sites...
I read with great interest the recent review focussing the
pathophysiology, the diagnosis and the treatment of tennis elbow. However,
based on this report I would appreciate having the chance to comment on
some issues raised by the authors shortly.
Diagnosis: The role of neovascularisation determined by colour or
even better by Power Doppler sonography has been mentioned for several
sites with painful tendons. Besides both, mid-portion and insertional
Achilles tendinopathy [8], patellar tendinopathy [6], supraspinatus
tendinopathy [1] as well as tennis elbow and wrist tendinopathy [7] have
been reported to be associated with neovascularisation which is closely
related to pain. Therefore the role of colour and Power Doppler sonography
can currently not be overestimated based on these reports, which is not
reflected in the review.
The effect of elbow position on grip strength as an easy measure in
the evaluation of tennis elbow should be mentioned here [4]. The grip
strength was tested in full extension of the elbow and in 90° flexion.
Strength was no different in flexion and extension for the healthy
extremity and 29% stronger in flexion than in extension for the affected
extremity. The affected arm averaged 50% of the strength of the healthy
arm in extension and 69% of the strength of the healthy arm in flexion.
These differences were statistically significant. An 8% difference in grip
strength between flexion and extension was found to be 83% accurate in
distinguishing the affected from the unaffected extremities.
Conservative treatment: A recent analysis of 383 patients suffering
tennis elbow from two randomized trials investigated wait-and-see policy,
corticosteroid injections and physiotherapy [2]. Based on individual
patient data from both trials, they found that corticosteroid injections
were statistically and clinically superior at 6 weeks, but significantly
worse at 52 weeks compared with both wait-and-see and physiotherapy.
I agree with the authors of the review that further randomized-
controlled trials are warranted focussing for example the use of eccentric
training in tennis elbow. However, given the results at the Achilles and
the patellar tendon level, one could speculate that an appropriate painful
eccentric training at the elbow and forearm level ameliorates recovery in
tennis elbow, but studies are pending.
Surgery: Recently a ten- to 14-year follow-up has been published
among 139 consecutive patients suffering tennis elbow which were operated
on by a single surgeon between 1991 and 1994 [5]. The overall improvement
rate was 97%. Patient satisfaction averaged 8.9 of 10. Ninety-three
percent of those available at a minimum of 10-year follow-up reported
returning to their sports.
Evidence-based medicine: Bottom line should be the recent reference
by Dr. Cowan and coworkers. They analysed the quality of prospective
controlled randomized trials [3]. The use of the gold-standard trial
design, the prospective randomized therapeutic study (Level-I or II
evidence), does not ensure quality research or reporting. Critical
analysis of scientific work is important regardless of the study design.
Clinical scientists should be familiar with the CONSORT criteria and
adhere to them when reporting clinical trials.
References
[1] Alfredson H, Harstad H, Haugen S, Ohberg L, Sclerosing
polidocanol injections to treat chronic painful shoulder impingement
syndrome-results of a two-centre collaborative pilot study. Knee Surg
Sports Traumatol Arthrosc. 2006;14(12):1321-6
[2] Bisset L, Smidt N, Van der Windt DA, Bouter LM, Jull G, Brooks P,
Vincenzino B. Conservative treatments for tennis elbow do subgroups of
patients respond differently? Rheumatology (Oxford) 2007;46(10):1601-5.
[3] Cowan J, Lozano-Calderon S, Ring D. Quality of prospective
controlled randomized trials. Analysis of trials of treatment for lateral
epicondylitis as an example. J Bone Joint Surg Am 2007;89:1693-9.
[4] Dorf ER, Chhabra AB, Golish SR, McGinty JL, Pannunzio ME. Effect
of elbow position on grip strength in the evaluation of lateral
epicondylitis. J Hand Surg [Am] 2007;32:882-6.
[5] Dunn JH, Kim JJ, Davis L, Nirschl RP. Ten- to 14-year follow-up
of the Nirschl surgical technique for lateral epicondylitis. Am J Sports
Med 2007 Nov 30 [Epub ahead of print].
[6] Gisslen K, Alfredson H. Neovascularisation and pain in jumper`s
knee: a prospective clinical and sonographic study in elite junior
volleyball players. Br J Sports Med 2005;39:423-8.
[7] Knobloch K, Spies M, Busch KH, Vogt PM. Sclerosing therapy and
eccentric training in flexor carpi ulnaris tendinopathy in a tennis
player. Br J Sports Med 2007;41:920-1.
[8] deVos RJ, Weir A, Cobben LP, Tol JL. The value of power Doppler
ultrasonography in Achilles tendinopathy: a prospective study. Am J Sports
Med 2007;35:1696-701.
Dear Editor:
I now better appreciate Prof. Noakes' reasons for using the words he used following his response to my eletter posted on the BJSM Blog, and consider the issue of "data exclusion" settled. However, I would like to make the following points to clarify my position and respond to Noakes' interpretation of the physiology:
1. I do not consider myself "wedded to the Hill model" because the "Hi...
Dear Editor
Tennis elbow – impingement at the common extensor origin? Case report
We thank Dr Knobloch and colleagues for raising questions of the influence of elbow position on the area with high blood flow seen in the common extensor origin and outcome measurement in patients with painful tennis elbow. The first question raised is if the grip strength with 900 elbow flexion might change as well as th...
Dear editor
I have read with interest the article by Wilson et al (in the March edition of the British journal of Sports Medicine) regarding their support for using an ECG in screening for sudden cardiac death in the young. Furthermore I note that there is considerable support from many sporting governing bodies for the above recommendation.
I note the comments of Dr Richard Page (in the Warm up section o...
Dear Editor
I read with concern the recent review of Noakes[1] accepted for publication in the journal. Noakes suggests that there is no “biologically plausible explanation” for the observation of lower oxygen uptake (VO2) values in supramaximal exercise compared to incremental exercise.[2] Noakes further argues that those supramaximal data are therefore questionable and should be excluded, thus resul...
Dear Editor
I read the recent article by Paul Boyle [1] regarding the longevity of English test cricketers with interest. In this paper the authors linked length of international cricket career (‘success’) with lifespan, suggesting that a successful life lead to a longer life. The hypothesis that quality of life grants one a physiological advantage and therefore increases length of life is well accepted in the...
Dear Editor
Germonpré et al. have presented the possible mechanisms of a new technique to equalize middle ear and sinus cavities during extreme-depth apnoea diving by passive flooding of these cavities with surrounding water. Even though their measures were not made in water, they demonstrate that it is possible to flood the middle ear in order to better compensate during very deep apnoea diving. In addition to the...
Dear Editor,
In a recent letter,[7] Noakes reminded us that the brain estimates the maximal exercise duration that can be sustained (maybe even before the exercise begins), and then uses the ratings of perceived exertion (RPE) to inform the body when the exercise will and must terminate. I agree with this suggestion. RPE attests to the exercise intensity, but also to the duration.[3] Therefore, according to Noake...
Dear Editor
The injected agent with color Doppler– does it matter in tennis elbow?
We read with great interest the recent randomised, double-blinded controlled cross-over trial by Dr. Zeisig and colleagues evaluating ultrasound and color Doppler guided injections in the proximal forearm in tennis elbow. We would like to comment on some issues.
Grip strength was considered as “the best objective...
Dear Editor
Hegedus et al [1] used a fixed-effects model to pool diagnostic odds ratios (DOR) for the Neer and the Hawkins-Kennedy tests for impingement. In Figure 2 and in Figure 3 they display the natural logarithms of the DOR for the individual and pooled results (the figures are inadvertently labeled as DOR rather than as the logarithms). In each diagram, the null value (natural logarithm of the DOR =0) is incl...
Dear editor,
I read with great interest the recent review focussing the pathophysiology, the diagnosis and the treatment of tennis elbow. However, based on this report I would appreciate having the chance to comment on some issues raised by the authors shortly.
Diagnosis: The role of neovascularisation determined by colour or even better by Power Doppler sonography has been mentioned for several sites...
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