I was amused by the new terminology of "exercise-related
transient abdominal pain" for stitch. It seems a shame
that a more creative approach wasn't taken to use
STITCH as a mnemonic!
I used to get this fairly frequently as a child exploring the
countryside. It was annoying but, since I usually had a
pressing need to get from A to B rapidly, I tended not to let
it deflect me very often. I...
I was amused by the new terminology of "exercise-related
transient abdominal pain" for stitch. It seems a shame
that a more creative approach wasn't taken to use
STITCH as a mnemonic!
I used to get this fairly frequently as a child exploring the
countryside. It was annoying but, since I usually had a
pressing need to get from A to B rapidly, I tended not to let
it deflect me very often. I simply resorted to a method I
knew would lessen the discomfort. This involved carrying on
running (or hobbling!) while clutching a handful of freshly
picked grass, using the hand on the same side as the pain.
I have no idea why it worked or, indeed, if it really did!
The article by Noakes and Speedy [1] has provoked ferocious arguments [2-7]. It appears that, while the aetiology of hyponatraemia is clear, the
main argument is over the ACSM guidelines, which tell athletes “to learn
to drink fluids during exercise, in volumes that approximate sweat loss in
an effort to prevent both extremes – dehydration and hyponatremia” [2].
There are several difficulties....
The article by Noakes and Speedy [1] has provoked ferocious arguments [2-7]. It appears that, while the aetiology of hyponatraemia is clear, the
main argument is over the ACSM guidelines, which tell athletes “to learn
to drink fluids during exercise, in volumes that approximate sweat loss in
an effort to prevent both extremes – dehydration and hyponatremia” [2].
There are several difficulties.
1) It is difficult for the athlete and
non-athlete in the field to know how much sweat is being lost.
2) There
are several figures quoted in guidelines for fluid intake and, because, in
most of the literature, dehydration is apparently closely linked with poor
performance and the danger of heatstroke, the non-scientist tends to
assume that the higher figure is better.
3) There is great disagreement
over the importance of dehydration. However the possibility that the
two sides are in fact comparing two different physiological states has
been suggested [8]. The comparisons are summarised below.
The evaporation of sweat is essential to minimize the increase in
core temperature during exercise in hot conditions. While the evaporation
of sweat facilitates cooling, the production of sweat also promotes fluid
loss, which can have a detrimental effect on the circulation, body-cooling
capability, and exercise performance. The volume of sweat loss during high-intensity exercise may be as much as 2ltr/hour. It is unlikely that the
exerciser will be able to consume fluids at this rate to compensate. Fluid
losses of this magnitude may be essential to limit the rise in core
temperature via evaporative sweat loss, but such sweat rates will lead to
progressive dehydration and a loss of electrolytes.
To study the effects of dehydration Armstrong et al [9] used a diuretic
to dehydrate their subjects by ~2 per cent of body weight. The 5k times
for hydrated and dehydrated (1.6 per cent of body weight) were 18.2 and
19.5 minutes respectively. The 10k times for hydrated and dehydrated (2.1
per cent of body weight) were 38.9 and 41.5 minutes respectively. This
research shows that large decrements in performance occur when subjects
are dehydrated. Since races are often won in less than half a second,
these data suggest that, purely on the basis of performance, the exerciser
should avoid dehydration in endurance events.
However results from an Ironman triathlon, where the athletes were
divided into groups based on the weight loss during the triathlon, suggest
that large weight losses may not have a great influence on endurance
performance. Despite one group having an average 6 per cent (range 5.0 - 10.7%) body weight loss (due to dehydration) compared with -3.9% and -2.1% weight loss in the other two groups, endurance performance was not
related to decreases in body weight [10]. Athletes who had large weight
losses apparently did not have a marked reduction in performance. In fact,
those losing most weight tended to have the fastest times. According to
some laboratory studies this 6-10% body weight decrease through
dehydration [10] would be expected to cause result in 58% to 125% decrease
in performance. It should be highlighted, however, that the race took
place in ‘mild environmental conditions’.
The fact, that messages from laboratory studies often seem to
contradict findings made “in the field’, may simply be because, though the
situations may seem the same, there may in fact be differences in the
tests. For example, in some laboratory studies athletes are asked to
maintain a given speed, whereas in actual events the athletes vary speeds,
and are likely to slow down in very hot conditions. Noakes [11] highlights
that trials at a given intensity are less reproducible than when the
athletes are able to select their own intensity. In a “hot” laboratory,
the only heat loss mechanisms are evaporation plus some pendulum
convective heat loss through limb movement. By contrast in the “hot”
field, in addition to the above heat loss routes, there is air movement
over the whole body. This convective cooling effect is more marked in
cycling compared with running, due to the higher speeds over the ground.
This convective cooling would reduce the requirement for sweat production.
Increased air movement over the body would also be conducive to more
efficient evaporation of sweat, again reducing the requirement for sweat
production. The limited convective cooling in the laboratory may result in
a higher sweat rate than in the field, through increased need for
evaporative heat loss and also through greater wastage of sweat, with more
liquid sweat running off the body. These factors may produce sweat loss
values that may not occur in competition. Thus, there may be greater
levels of dehydration and more emphasis placed on the need for fluid
intake as a result of these laboratory studies. An anecdotal observation
is that after exercise involving running or cycling, in cold and heat
(35°C), liquid sweat has only appeared on the skin after stopping,
especially if going straight indoors. This illustrates the importance of
convective heat loss, and is almost the equivalent of going from the
"field" into a "laboratory". (It also has possible implications for the
onset of heat stroke when exercise movement stops.) A possible distortion
in results from the field may be an over-estimate of dehydration, since
the runners may start hyperhydrated, or there may be limitations in the
accuracy of the weighing. It is salutary to remember that the Bushmen of
the Kalahari, exercise in extremely hot conditions, do not carry water on
their hunting expeditions and do not seem to have a high incidence of heat
stroke.
There are other physiological reasons for possible differences
between laboratory and field findings.
Some laboratory studies have induced dehydration by using a diuretic
[9], which removes the fluid from the intravascular space, leaving the
subject with a relative hypovolaemia at the start of the exercise. When
the exercise starts, because of the reduced volume, the heart has to work
harder than normal to provide circulation to the working muscles, and to
the skin, to allow for the increased blood flow needed for heat loss and
for fluid to the sweat glands. The reduced circulating volume could result
in impairment of the mechanism for removing the excess heat from the
cells, and also the mechanism for heat loss from the skin by having
insufficient fluid to fill all the available skin capillaries, and
insufficient fluid to allow the sweat glands to function at their best. It
has become accepted that the reduced skin blood flow from dehydration also
reduces sweating thus increasing the risk of heatstroke. However Noakes
& Speedy [1] cite evidence that sweating is regulated independently of
skin blood flow, but requires an intact neural supply to supply the sweat
glands. The absence of sweating in some cases of heatstroke is usually
attributed to dehydration but alternatively it may be due to the high core
temperature affecting the neural control of sweating, as well as other
cerebral functions. Whatever the mechanism the pre-induced dehydration
would mean that the core temperature would tend to rise faster than it
would with a full circulating volume.
In the field situation the athlete normally starts with a full
circulating volume. As fluid is gradually lost from the circulation
through sweating, the exercise itself causes fluid transfer, first from
the interstitial space into the intravascular space to replace the fluid
loss [12]. If fluid loss continues, the exercise causes fluid to be
transferred from inside the cells to the interstitial space [12]. Thus the
endurance runner would finish the event with some loss of fluid from the
interstitial space, and possible slight dehydration of the cells, but with
minimal depletion of the circulating fluid volume. This loss would mean
that the mechanism for removing the excess heat from the cells would not
be too impaired. The heart would also be under less stress.
Dehydration, and the consequent reduction in body weight, would
decrease the oxygen cost of the activity. However, the combination of
dehydration and hyperthermia is likely to reduce cardiovascular function
[13]. Given that dehydration and hyperthermia combined will synergistically
promote fatigue, it is difficult to make a case for voluntary dehydration
to reduce body weight and lower energy costs. A strategy that results in
the early attainment of a fatiguing core temperature as a result of
voluntary dehydration is not sound.
It is likely that fast runners will find it difficult to take fluid
on board at high speed, and, along with the limited gastric empting (due
to high intensity), this could result in a marked level of dehydration.
Coyle [13] concludes that there is reasonable consensus that dehydration
should not exceed 2 per cent in most athletic contests. Noakes [11] however
counsels that more research is needed on the effects of dehydration. He
stresses that studies should focus on dehydration in a long-duration
competitive setting, and that the statement that athletes should not lose
more than 2 per cent body weight during exercise should be assessed.
Cade et al [14] proposed that fluid loss from sweating during exercise
causes a loss in blood volume, which adversely affects the ability of the
body to dissipate heat, and may, indeed, be of major importance in the
genesis of heat stroke. However, despite one group having an average 6
per cent (range 5.0 -10.7%) body weight loss (due to dehydration) after an
Ironman triathlon, increases in core temperature were not related to
decreases in body weight as compared with others who lost less weight [10].
Athletes did not experience exceptionally high core temperatures or an
increased risk for medical treatment as a result of heat illness. Noakes
[11] stresses that a number of studies using field trials have found no
meaningful association between the degree of dehydration, and the end-of-race core temperature.
Heatstroke appears to be common when vigorous exercise is undertaken
with inappropriate clothing, as happened with an overdressed man
shovelling snow and as happened with military personnel who had to run
across mudflats on a hot day wearing wetsuits. In fact runners are at
most danger of heat injury in races that last from 15 to 60 minutes
(between 5 and 21k for elite performers, who run at ~ 85 per cent of their
VO2max, and above [11]. Alberto Salazaar was a onetime fastest male
marathoner who, after running very fast in a 7-mile race in very hot
conditions, was covered in ice and given the last rights. However, he did
recover and was able to compete again.
The main determinant of core temperature during exercise in heat is
exercise intensity, and the combination of a high metabolic and
environmental heat stress can result in an increased core temperature.
This would inevitably mean that fast finishers had higher core
temperatures, which fits in with Coyle’s [13] observation that, despite
running in cool conditions, runners who were dehydrated (often fast
finishers) sometimes had core temperatures in the region of 40°C. This
does not necessarily mean that this higher core temperature is dangerous.
A rise in core temperature will result in an increase in the
temperature of the blood circulating through the skin. This in turn will
increase the temperature differential between the skin and the ambient
air, and increase the rate of heat loss. This will have a marginal effect
in a laboratory but may have more effect in the field because of
convective heat loss resulting from the athlete’s movement over the
ground.
It is probably important to remember that, in all branches of medicine,
results from the laboratory may not be totally applicable to the field,
and vice versa.
It is also important to remember that “concensus” does not always
equate to "fact". When I started research into Hypothermia there was a
total concensus on the physiology and management of hypothermia. This
has now been totally turned around [15]. Also at one time there was
concensus that the world was flat!
References
1. Noakes, T., Speedy, D. Case proven: exercise associated
hyponatraemia is due to overdrinking. So why did it take 20 years before
the original evidence was accepted? Br J Sports Med; 2006; 40, 567–72
2. Murray, B. Manufactured arguments: turning concensus into
controversy does not advance science. Br J Sports Med; 2007; 41, 106-7.
3. Noakes, T.D , Speedy,D.B. Lobbyists for the sports drink industry:
an example of the rise of “contrarianism” in modern scientific debate. Br
J Sports Med; 2007; 41, 107-9.
4. Roberts, W.O. Fractured fairy tales: hyponatraemia and the
American College of Sports Medicine fluid recommendations. Br J Sports
Med; 2007; 41, 109.
5. Noakes, T.D , Speedy,D.B. Time for the American College of Sports
Medicine to acknowledge that humans, like all other earthly creatures, do
not need to be told how much to drink during exercise. Br J Sports
Med; 2007; 41, 109-10.
6. Epstein, Y., Cohen-Sivan, Y. Exercise-associated hyponatraemia:
facts and myths. . Br J Sports Med; 2007; 41, 111.
7. Noakes, T.D , Speedy,D.B. The aetiology of exercise-associated
hyponatraemia is established and is not “mythical”. Br J Sports Med; 2007;
41, 111-3.
8. Grant, S., Lloyd, E. Training and Performance in Difficult
Environments. A guide for competitive athletes. The Crowood Press Ltd,
Marlborough, Wiltshire. (2006) ISBN 1-86126-881-5.
9. Armstrong, L. E., Costill, D. L. and Fink, W. J. Influence of
diuretic-induced dehydration on competitive running performance, Med Sci
and Sport and Exercise ;1985; 17, 456–61
10. Sharwood, K. A., Collins, M., Goedecke, J. H. et al. Weight
changes, medical complications, and performance during an Ironman
triathlon, Br J Sports Med; 2004; 38, 718–24
11. Noakes, T., The Lore of Running, Human Kinetics, Champaign,
Illinois (2001) ISBN 0-87322-959-2
12. Tappan, D. V., Jacey, M. J., Heyder, E. and Gray, P. H. Blood
volume responses in partially dehydrated subjects working in the cold,
Aviat Sp and Environ Med; 1984; 55, 296–301
13. Coyle, E. (2004) Fluid and fuel intake during exercise, J Sports
Sci; 2004; 22, 39–56
14. Cade, J. R., Free, H. J., De Quesada, A. M., et al. Changes in
body fluid composition and volume during vigorous exercise by athletes, J
Sports Med and Phys Fit; 1971; 11, 172–78
We have seen and treated a series of four of these patients.
None of the lesions were deemed to be suitable for liposuction and hence
they were removed surgically, under general anaesthetic.
All were found to be vascular and un-encapsulated which necessitated
sharp dissection to facilitate excision. Excess overlying skin was also
taken in two cases to ensure cosmetic correction. Vacuum drai...
We have seen and treated a series of four of these patients.
None of the lesions were deemed to be suitable for liposuction and hence
they were removed surgically, under general anaesthetic.
All were found to be vascular and un-encapsulated which necessitated
sharp dissection to facilitate excision. Excess overlying skin was also
taken in two cases to ensure cosmetic correction. Vacuum drainage was
used in all cases and removed on the first post-operative day.
Postoperative healing was uneventful.
All lesions were diagnosed histologically to be fibrolipomata,
consisting mainly of mature adipose tissue admixed with benign
fibrocartilaginous connective.
It is our opinion that these lesions should be removed by specialists
with an interest in soft tissue management to maximise the patients
outcome.
We read with great interest the randomized-controlled trial performed
by Mayer and coworkers focussing a four-week treatment interval for
running athletes suffering Achilles mid-portion tendinopathy. Time is of
critical importance in rehabilitation of all sport-related injuries as
pointed out by the authors and we fully agree with them. Given a
professional soccer player suffering mid-portion Achilles t...
We read with great interest the randomized-controlled trial performed
by Mayer and coworkers focussing a four-week treatment interval for
running athletes suffering Achilles mid-portion tendinopathy. Time is of
critical importance in rehabilitation of all sport-related injuries as
pointed out by the authors and we fully agree with them. Given a
professional soccer player suffering mid-portion Achilles tendinopathy, he
most likely will prefer the treatment options which will reduce his pain
and improve his function as early as possible. A 12-week-therapeutic
regimen such as proposed for eccentric training therefore has certain
limitations given the time to spent in this perspective, since at the
beginning one cannot be sure whether the athlete will respond or not
following the three months. Surgical procedures therefore seem attractive
in this perspective since a single procedure might cure the athlete with
tendinopathy. Nonathletic patients with Achilles tendinopathy yield worse
results following open surgery for Achilles tendinopathy than athletes
[7]. In this perspective, the initial report on 11 patients (mean age 41
years) undergoing ultrasound-guided electrocoagulation of the mid-portion
Achilles tendon appears very interesting with good results even at 6-months follow-up in 10 patients [3].
Sclerosing therapy as proposed by the Alfredson group from Umea is
another current option in tendinopathy with reasonable results at 2-year follow-up [6]. However, since at mean three injections of polidocanol are
suggested to be performed under colour Doppler-control with 6-8-week
intervals in between, at least 12-16 weeks have to be calculated for this
treatment option to assess the full response of a given athlete with mid-portion Achilles tendinopathy. Interestingly, some patients even respond
not earlier than following 6 weeks following initial sclerosing therapy
[2], a time point which is beyond the four weeks tested in the recent
study by Mayer. It would be interesting to speculate, and by far better to
know, how the running athletes treated with either combined physiotherapy
including eccentric training, proprioceptive training and cryotherapy and
deep friction massage or those with insoles will behave in the 2nd and 3rd
month following therapy in contrast to the control group.
Interestingly, Alfredson reported that following polidocanol
sclerosing therapy there is initially (during 1–3 weeks) an increased
intratendinous vascularity, which might be a response to the colour
Doppler based sclerosing therapy, which can be encountered following the
first three weeks of eccentric training as well [1]. They stated: “In
successfully treated patients, we have found that after both eccentric
training and sclerosing injections, there is already at day 1 after
instituted treatment an increased vascularity in the region with
structural tendon changes and neovessels. In the majority of tendons, this
increased vascularity remains during 2–3 weeks and then in the
successfully treated cases, gradually decreases.”
Unfortunately given the small number of patients (n=31) in the
randomized trial by Mayer, only the combined application of deep friction
massages at the midsubstance of the Achilles tendon, local pulsed
ultrasound (1.5W/cm2), ice application and sensory motor training with 3
sets of 15 repetitions of balance and stabilization exercises on a
stability pad and eccentric exercises (loading of the calf muscles by
lowering the heel standing with the forefoot on stairs, drop-jumps and
counter-movement-jumps) has been tested. It would be at least in our view
by far more interesting to elucidate the impact of prioprioceptive
training in addition to eccentric training alone, since in the literature
we could not identify such a comparison. It is worthwhile to speculate
that besides its injury preventing effect proprioceptive training on
balance pads might have an effect in Achilles tendinopathy.
Furthermore, we do not know whether or not all the different
modalities of treatment might counteract and limit themselves in the
effect sizes since we do not know the effect size of each treatment alone
besides the eccentric training. Another critical issue in the treatment
group is the cryotherapy: How long was it applied and how often
(intermittent or single shot), since intermittent cryotherapy for 3x10min
has been demonstrated to decrease mid-portion Achilles tendon capillary
blood flow significantly by 65% [4], which might at least in part be
effective in Achilles tendinopathy.
Mayer did not perform any ultrasound, colour Doppler or MRI at all in
their 4-week trial, so we can only speculate on the structural response in
the given running athletes with mid-portion tendinopathy quoting Karim
Khan: “12-month clinical outcome cannot be predicted using ultrasound.
Power and color Doppler sonography did not improve performance [5]. ” The
recent published comparison in patellar tendinopathy found the combination
of grey-scale and colour Doppler Sonography to be more accurate than
magnetic resonance imaging in confirming clinically diagnosed patellar
tendinopathy [8].
Based on these recent findings and given the long rehabilitation
times in tendon disorders at the Achilles level, we believe that
substantial changes in tendon structure and function will at least take 8-12 weeks to be sustained, since Achilles tendon rupture is to be prevented
as the worst case scenario in athletes suffering Achilles tendinopathy.
References
(1) Alfredson H, Ohberg L. Increased intratendinous vascularity in
the early period after sclerosing injection treatment in Achilles
tendinosis: a healing response? Knee Surg Sports Traumatol Arthrosc
2006;14(4):399-401.
(2) Alfredson H. Personal communication, 2007, Jan 30 via email.
(3) Boesen MI, Torp-Pedersen S, Koenig MJ, Christensen R, Langberg H,
Holmich P, Nielsen MB, Bliddal H. Ultrasound guided electrocoagulation in
patients with chronic non-insertional Achilles tendinopathy: a pilot
study. Br J Sports Med 2006;40(9):761-6.
(4) Knobloch K, Grasemann R, Spies M, Vogt PM. Intermittent KoldBlue®
cryotherapy of 3x10min changes mid-portion Achilles tendon
microcirculation. Br J Sports Med 2006, Nov 30 (Epub).
(5) Khan KM, Foster BB, Robinson J, Cheong Y, Louis L, Maclean L et
al. Are ultrasound and magnetic resonance imaging of value in assessment
of Achilles tendon disorders? A two year prospective study. Br J Sports
Med 2003;37:149-153
(6) Lind B, Ohberg L, Alfredson H. Sclerosing polidocanol injections
in mid-portion Achilles tendinosis: remaining good clinical results and
decreased tendon thickness at 2-year follow-up. Knee Surg Sports Traumatol
Arthrosc 2006;14(12):1327-32.
(7) Maffulli N, Testa V, Capasso G, Oliva F, Sullo A, Benazzo F,
Regine R, King JB. Surgery for chronic Achilles tendinopathy yields worse
results in nonathletic patients. Clin J Sports Med 2006;16(2):123-8.
(8) Warden SJ, Kiss ZS, Malara FA, Oui AB, Cook JL, Crossley KM.
Comparative accuracy of magnetic resonance imaging and ultrasonography in
confirming clinically diagnosed patellar tendinopathy. Am J Sports Med
2007, Jan 29 (Epub).
If my understanding of tissue energetics is correct then a rate-limiting factor in athletes might well be the adequacy of hepatic
oxygenation [1]. If so the presence of celiac axis stenosis might be a
contributing and reversible factor.
Celiac axis stenosis, which may be caused by a contricting band of
fibrous tissue, was found in 1.7% of 3449 patients from 0 to 18 years
examined with abdomi...
If my understanding of tissue energetics is correct then a rate-limiting factor in athletes might well be the adequacy of hepatic
oxygenation [1]. If so the presence of celiac axis stenosis might be a
contributing and reversible factor.
Celiac axis stenosis, which may be caused by a contricting band of
fibrous tissue, was found in 1.7% of 3449 patients from 0 to 18 years
examined with abdominal color duplex sonography [2]. "Their symptoms
included, abdominal pain (71%), nausea (29%), thoracic pain (22%),
heartburn (17%), weight loss (15%), vomiting (15%), systolic murmur (15%),
postprandial accentuation of symptoms (15%), diarrhea (14%), respiratory
discomfort (14%), and syncope (12%). Many of these symptoms are
experienced by athletes and exercise is a very good stress test in the
diagnosis of chronic visceral ischaemia [3]. More importantly the results
of stenting or surgical correction are very good.
It would be interesting to screen athletes for the presence of celiac
axis stenosis or compression using abdominal color duplex sonography and
considering correcting the abnormality. What of the possibility of
enhancing athletic performance by increasing hepatic arterial inflow with
a jump graft? Not a step one would necessarily recommend but an
interesting theoretical corollary.
References
1. Should screening for occlusive coelic axis disease be included in
goal-directed therapy?
Richard G Fiddian-Green (5 March 2006) eLetter re: Stephen Trzeciak, R.
Phillip Dellinger, Nicole L. Abate, Robert M. Cowan, Mary Stauss, J. Hope
Kilgannon, Sergio Zanotti, and Joseph E. Parrillo
Translating Research to Clinical Practice: A 1-Year Experience With
Implementing Early Goal-Directed Therapy for Septic Shock in the Emergency
Department,*
Chest 2006; 129: 225-232
2. Scholbach T. Celiac artery compression syndrome in children,
adolescents, and young adults: clinical and color duplex sonographic
features in a series of 59 cases. J Ultrasound Med. 2006 Mar;25(3):299-
305
We read with great interest the editorial from Dr. Meyer regarding
the question: Should aqua training and swimming be allowed for patients
with left ventricular dysfunction and heart failure. We fully agree with
the author that care should be taken when prescribing aqua exercise and
swimming to patients with a deteriorated cardiac function. Furthermore,
Dr. Meyer asks for more studies of patients invo...
We read with great interest the editorial from Dr. Meyer regarding
the question: Should aqua training and swimming be allowed for patients
with left ventricular dysfunction and heart failure. We fully agree with
the author that care should be taken when prescribing aqua exercise and
swimming to patients with a deteriorated cardiac function. Furthermore,
Dr. Meyer asks for more studies of patients involved in a swimming
programme, but the methods to detect cardiac output remain unclear.
Furthermore, detailed numbers regarding the change of stroke volume, heart
rate and cardiac output and cardiac index as well as regarding the
afterload are pending in the recent editorial. We would like to add some
of these numbers pending.
Schmid and coworkers reported recently their experience regarding the
hemodynamic changes induced in water, which is of special interest among
patients with deteriorated cardiac function (Schmid). Schmid used an inert
gas rebreathing method using an infrared photoacustic gas analyser, which
has been validated in land situations only by the references given by the
authors. Schmid reported significant stroke volume changes from 60ml to
more than 100ml among healthy subjects with consecutive increase of
cardiac index from 2.3l/min/m2 to 5l/min/m2 in the healthy subjects.
Systemic vascular resistance decreased significantly in immersion using
the rebreathing method.
We tested thirteen cardiac healthy swimming athletes using a
different method to detect cardiac output, the real-time continuous wave
(CW) Doppler based hemodynamic monitoring using the USCOM device at rest
at land, at immersion and following a swimming endurance protocol [1]. In
contrast to rest at land whole body immersion increased heart rate from
94±17/min to 100±14/min, stroke volume from 42±18ml to 81±18/ml, and
cardiac output from 4.0±0.9l/min to 8±1.6l/min (cardiac index 2.17±0.6l/min/m2 vs. 4.3±0.9l/min/m2), which is somehow in line with the
data presented by Schmid using the rebreathing method. Systemic vascular
resistance declined from 2053±469 to 986±249dyne*s*cm-5 significantly in
our small study which also is in line with the reported data from Schmid.
The endurance swimming test lead to significant upregulation of heart rate
to 160±12/min, stroke volume (95±9ml), cardiac output (15.4±1.6l/min), and
cardiac index (8.3±1.0l/min/m2).
Therefore, based on the results of Schmid using the rebreathing
method and our direct ultrasound cardiac monitoring using the USCOM in
healthy swimming athletes, significant changes of hemodynamics are
encountered in immersion especially regarding the upregulation of the
stroke volume rather than heart rate increase. How cardiac failure
patients respond to swimming exercise is currently still to be determined
with direct cardiac output monitoring by either indirect gas rebreathing
technique or direct cardiac output measurement using CW Doppler ultrasound
in the swimming pool with the ideal ultrasound circumstances being under
water with the probe.
References
(1) Knobloch K, Lichtenberg A, Winterhalter M, Rossner D, Pichlmaier
M, Phillips R. Non-invasive cardiac output determination by two-dimensional independent Doppler during and after cardiac surgery. Ann
Thorac Surg 2005;80:1479-83.
(2) Schmid JP, Noveanu M, Morger C, Gaillet R, Mauro C, Anderegg M,
Saner H. Influence of water immersion, water gymnastics, and swimming on
cardiac output in patients with heart failure. Heart 2006, Dec 12.
We read with great interest the case series from Bhatia and coworkers
describing the “Bench-presser’s shoulder” as an overuse insertional
tendinopathy of the pectoralis minor muscle. We fully agree with the
authors that tendinopathy is often times underdiagnosed as it is at the
pectoralis minor muscle. However, we would like to comment on some issues.
We read with great interest the case series from Bhatia and coworkers
describing the “Bench-presser’s shoulder” as an overuse insertional
tendinopathy of the pectoralis minor muscle. We fully agree with the
authors that tendinopathy is often times underdiagnosed as it is at the
pectoralis minor muscle. However, we would like to comment on some issues.
Body-building athletes seem to be the predominant athletes’ entity
suffering pectoralis tendinopathy and pectoralis tendon ruptures [6].
About 25% to 30% of all elite weight and power lifters report an injury
sufficiently severe to seek medical attention [5]. Power lifting injuries
most often involve shoulder injuries with an injury rate of 0.57 to
0.71/1000 hours of power lifting. Upper limb injuries account for ¼ of all
power lifting injuries. Often two contributing factors causing wrist
injuries are encountered:
(a) loss of balance causing the barbell to drift
back behind the head of the power lifter, which hyperextends the wrist and
(b) the maximal weight.
Songraphic evaluation was performed including the assessment of the
rotator cuff, the biceps tendon and the bicipital groove. Furthermore the
integrity of the muscle-tendon-unit was examined. However, unfortunately
only conventional grey scale Sonography has been performed by the authors.
Neovascularisation, which is often times encountered in tendinopathy all
over the body might be detected by colour Doppler, which is not addressed
in the current study. However, currently no published evidence regarding
the potential neovascularisation in pectoralis tendinopathy is given.
Therefore, we advocate using the colour Doppler on the future patients
encountered with this tendinopathy and report on that.
In analogy to the Achilles tendon, one might speculate that at the
pectoralis level a continuum from the healthy tendon via the painful,
tendinopathic tendon towards the pectoralis tendon rupture is evident. As
shown by Maffulli [2], only degenerated tendons rupture, which might be
the same for the pectoralis muscle rupture [4].
MRI might add evidence to the colour Doppler Sonography results as
stated by Carrino using thin (3-4mm) axial sections with a variety of
sequences combined for anatomical delineation (T1-weighted SE or PD SE)
and fluid detection (T2-weighted SE, T2-weighted FSE with fat suppression,
or STIR). Zvijac and coworkers stated in 2006 that clinical impression
often times appeared to be overestimate the severity, location and the
grade of the pectoralis injury [8]. Magnetic resonance imaging provided in
their view a more accurate assessment. However, the current report on the
seven patients with pectoralis minor tendinopathy did not comment on MRI
findings, which might be of interest at least in our view.
Regarding the therapy used – a single ultrasound-guided injection of
a corticosteroid to the enthesis - we have reasonable concerns, since
evidence is accumulating that a single dose of a corticosteroid does not
alter the acute phase response in tendinopathy at all [7, 3]. We rather
recommend to implement – in analogy to the patellar and the Achilles
tendon – an eccentric training in case of pectoralis minor tendinopathy,
which hypothetically might decrease the suspected neovascularisation in
analogy to the Achilles and patellar tendon.
References
(1) Carrino JA, Chandnanni VP, Mitchell DB, Choi-Chinn K, DeBerardino
TM, Miller MD. Pectoralis major muscle and tendon tears: diagnosis and
grading using magnetic resonance imaging. Skeletal Radiol 2000;29(6):305-
13.
(2) Maffulli N, Testa V, Capasso G, Ewen SW, Sullo A, Benazzo F, King
JB. Similar histopathological picture in males with Achilles and patellar
tendinopathy. Med Sci Sports Exerc 2004;36(9):1470-5.
(3) Nichols AW. Complications associated with the use of
corticosteroids in the treatment of athletic injuries. Clin J Sports Med
2005;15(5):370-5.
(4) Potter BK, Lehman RA Jr, Doukas WC. Pectoralis major ruptures. Am
J Orthop 2006;35(4):189-95.
(5) Powell KE, Heath GW, Kresnow MJ, Sacks JJ, Branche CK. Injury
rates from walking, gardening, weightlifting, outdoor bicycling, and
aerobics. Med Sci Sports Exerc 1998;30: 1246-1249.
(6) Roller A, Becker U, Bauer G. Rupture of the pectoralis major
muscle: classification of injuries and results of operative treatment. Z
Orthop Ihre Grenzgeb 2006;144(3):316-21.
(7) Wei AS, Callaci JJ, Juknelis D, Marra G, Tonino P, Freedman KB,
Wezeman FH. The effect of corticosteroid on collagen expression in injured
rotator cuff tendon. J Bone Joint Surg Am 2006;88(6):1331-8.
(8) Zvijac JE, Schurhoff MR, Hechtman KS, Uribe JW. Pectoralis major
tears: correlation of magnetic resonance imaging and treatment strategies.
Am J Sports Med 2006;34(2):289-94.
We read with great interest the randomized trial of de Vos and
coworkers regarding the additional value of night splinting to eccentric
training in Achilles mid-portion tendinopathy. Functional improvement
assessed using the VISA-score and patient satisfaction were not different
between sole eccentric training and the combination of eccentric training
and the night splint.
We read with great interest the randomized trial of de Vos and
coworkers regarding the additional value of night splinting to eccentric
training in Achilles mid-portion tendinopathy. Functional improvement
assessed using the VISA-score and patient satisfaction were not different
between sole eccentric training and the combination of eccentric training
and the night splint.
Roos found in 2004 in a randomized trial with 44 patients no further
pain reduction when using a night splint in mid-portion Achilles
tendinopathy [3]. Based on this two randomized trial it seems that there
is no place for the night splint as a passive and rigid orthesis in the
therapy of Achilles tendinopathy. But not only in the Achilles region,
also in the plantar region the night splint does not seem to be beneficial
above placebo.
A randomized study published in 1999 with 116 patients with plantar
fasciitis, where the addition of a night splint to antirheumatic
medication, stretching exercise and shoe recommendations was not superior
[2]. Therefore, the rigid night splint does not seem to play a role in
tendinopathy.
A second important question is raised by the authors: the critical
compliance. As with each physiotherapy which is performed without direct
supervision it is mandatory to convince the trainees. De Vos reported that
more than a quarter of the patients in both groups reported performing
less than 50% of the prescribed intensity. We agree with de Vos that the
compliance should be point out in detail in all studies in tendinopathy,
which is pending in the majority of published studies.
In a randomised trial comparing eccentric training and eccentric
training plus a pneumatic Achilles wrap (dj ortho AirHeel™, [1] with 112
randomized patients, 91 patients completed the study over the 12-week
period (81% compliance). In case the patients did not fulfill an 80%
compliance regarding the daily eccentric training and/or the Achilles
wrap, subjects were addressed to the drop out group. The 21 participants
not fulfilling the study were 50% male with a mean age of 51 years and a
body mass index of 25.2. 32% of the drop out patients were active smokers
of 20 cigarettes a day or more at the time of the study. The major
drawbacks among these drop patients were overwhelming pain, recommendation
to quit the study by orthopaedic surgeons or osteopaths or moving the
city. One patient underwent surgery for bilateral mid-portion Achilles
tendinopathy in a 61-year-old secretary (BMI 22). No Achilles tendon
rupture or partial tear happened among the participants.
Regarding compliance issues all physicians prescribing eccentric
training have to further enhance patients’ attitude towards tendinopathy
and the possible painful eccentric training regimen. We should try to work
out exactly why non-compliance occurs in our studies and report in detail
about these drop out patients to learn out more how we might get them in
the future, since eccentric training seems to be a reasonable non-invasive
treatment option in tendinopathy.
References
[1] Knobloch K, Schreibmueller L, Jagodzinski M, Zeichen J, Vogt PM,
Krettek C. Tendon and paratendon Achilles microcirculation in eccentric
training and an Achilles wrap in insertional and mid-portion tendinopathy
– a randomized trial. Br J Sports Med 2006, Oct 11.
[2] Probe RA, Baca M, Adams R, Preece C. Night split treatment for
plantar fasciitis. A prospective randomized study. Clin Orthop Relat Res
1999;358:190-5.
[3] Roos EM, Engstrom M, Lagerquist A, Soderberg B. Clinical
improvement after 6 weeks of eccentric exercise in patients with mid-
portion Achilles tendinopathy-a randomized trial with 1-year follow-up.
Scand J Med Sci Sports 2004;14(5):286-95.
We read with great interest the recent work of Dr. Algafly und Dr.
George regarding the effect of sole cryotherapy on nerve conduction
velocity, pain threshold and pain tolerance in healthy volunteers. We
would like to thank the authors for their important contribution, but we
would further appreciate commenting on some issues raised by the authors.
We read with great interest the recent work of Dr. Algafly und Dr.
George regarding the effect of sole cryotherapy on nerve conduction
velocity, pain threshold and pain tolerance in healthy volunteers. We
would like to thank the authors for their important contribution, but we
would further appreciate commenting on some issues raised by the authors.
The ankle was focussed in this study using crushed ice, which was
applied on average for 26min (range 20-31min) to achieve a skin
temperature of 10°C. For each 1 degree fall in skin temperature, the
authors found a decrease of sensory nerve conduction velocity of 0.4m/s
among their subjects. We fully agree with the authors that further studies
are mandatory. Especially, since the RICE regimen incorporates not only
cryotherapy, but also compression, elevation and rest, we do not know to
what extent sole cryotherapy works in this mosaic. Actually, besides the
neurological point of view, we found tissue microcirculation to be
modified tremendously following sole cryotherapy, if applied intermittent
for 3x10min [1]. Among thirty volunteers, superficial capillary blood
flow was reduced from 42 relative units (rU) to 6rU in the 1st, 5rU in the
2nd and 3rU in the 3rd cryotherapy period (-65%, p=0.0003) with no
significant capillary hyperaemia. Superficial tendon oxygen saturation
dropped significantly from 43% to 26/18/11% (p=0.0004) after repetitive
cryotherapy with persisting increase of tendon oxygenation during
rewarming (51/49/54%, p=0.077) up to +27% of the baseline level. Relative
postcapillary venous tendon filling pressures were favourably reduced from
41+/-11rU to 31/28/26rU (-36%, p=0.0004) superficially and deep from 56+/-
11rU to 45/46/48rU (-18%, p=0.0001) during cryotherapy facilitating
capillary venous clearance. Therefore a facilitation of postcapillary
venous outflow is associated with sole cryotherapy applied for 3x10min only
which might have a direct effect on pain level as well due to reduced
tissue tension. This data is supported by a recent controlled laboratory
study stating that prolonged cooling reduces microvascular dysfunction,
inflammation, and structural impairment [2].
The intermittent cryotherapy seems to be favourable to use, since the
superb Bleakley study, where they randomized 44 sportsmen and 45 general
public subjects with moderate ankle sprains for either 20min of single
cryotherapy or intermittent cryotherapy for 10 minutes with 10min of
rewarming and a second 10min of cryotherapy and 10min of reperfusion with
this cycle being repeated every two hours [3]. Subjects treated with the
intermittent protocol had significantly (p<0.05) less ankle pain on
activity
than those using a standard 20 minute protocol; however, one week after
ankle injury, there were no
significant differences between groups in terms of function, swelling, or
pain at rest. Therefore based on these results it would be appropriate to
examine the effects of only 10minutes of cryotherapy in an intermittent
regiment regarding the nerve conduction velocity to elucidate its value.
25 or even 30minutes of continuous ice application are in our personal
view not that effective at least both, from a microcirculatory and a
clinical point of view [1,2] and might lead to an adverse reaction, such
as a frostbite at the gym [4].
References
[1] Knobloch K, Grasemann R, Spies M, Vogt PM. Intermittent
KoldBlue(R) cryotherapy of 3x10min changes mid-portion Achilles tendon
microcirculation. Br J Sports Med 2006, Nov 30.
[2] Schaser KJ, Disch AC, Stover JF, Lauffer A, Bail JH, Mittlmeier
T. Prolonged superficial local cryotherapy attenuates microcirculatory
impairment, regional inflammation, and muscle necrosis after closed soft
tissue injury in rats. Am J Sports Med 2007;34(1):93-102.
[3] Bleakley CM, McDonugh SM, MacAuley DC. Cryotherapy for acute
ankle sprains: a randomised controlled study of two different icing
protocols. Br J Sports Med 2006;40:700-5.
[4] O'Toole G, Rayatt S. Frostbite at the gym: a case report of an
ice pack burn. Br J Sports Med 1999;33(4):278-9.
The authors of this study suggest that the 2d:4d ratio is an
important predictor of sporting ability in women. The interpretation is
based on the beta-coefficients and p-values from regression analyses of
different sports and the authors cite several works that hypothesize about
biological mechanisms.
I have several questions about the methods. First, if one is a high
level running athlete, th...
The authors of this study suggest that the 2d:4d ratio is an
important predictor of sporting ability in women. The interpretation is
based on the beta-coefficients and p-values from regression analyses of
different sports and the authors cite several works that hypothesize about
biological mechanisms.
I have several questions about the methods. First, if one is a high
level running athlete, then they might only play recreational soccer. Did
the authors include an elite runner as a recreational soccer player? It
would also be helpful for the authors to clarify whether subjects who
didn't participate in a sport were excluded from that particular analysis,
and if so, they should indicate the number of subjects for each sport.
Another concern regards the statistical analysis. Unfortunately, one
needs to know more than the beta coefficient and p-value from a
correlation to appropriately interpret the results. At the least, one
needs to know the r-squared value, and even more appropriate would be for
the authors to indicate that they conducted the appropriate tests showing
that the data fulfills the assumptions of linear regression. Actually
seeing the data in a scatter plot for each sport (or one scatter plot with
different symbols for each sport) would also be helpful but with so many
sports, this may have been limited by journal space.
Even assuming all of these are correct, one should examine the
relationships between sports. Why do soccer and running have large
negative correlations but gymnastics does not? How is golf similar to
soccer and running, but not cricket? How come there was no correlation for
skiing in this analysis whereas there was a correlation in the Manning
article cited by the authors (reference #11)? The requirements of
badminton are similar to those of squash but the correlations were quite
different. Given the proposed mechanisms by the authors, why would Martial
Arts have a reverse correlation?
I look forward to reading the authors' response.
Ian Shrier MD, PhD, Dip Sport Med, FACSM
Centre for Clinical Epidemiology and Community Studies
Lady Davis Institute for Medical Research, SMBD-Jewish General Hospital,
McGill University
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Dear Editor
We read with great interest the randomized-controlled trial performed by Mayer and coworkers focussing a four-week treatment interval for running athletes suffering Achilles mid-portion tendinopathy. Time is of critical importance in rehabilitation of all sport-related injuries as pointed out by the authors and we fully agree with them. Given a professional soccer player suffering mid-portion Achilles t...
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Dear Editor
We read with great interest the case series from Bhatia and coworkers describing the “Bench-presser’s shoulder” as an overuse insertional tendinopathy of the pectoralis minor muscle. We fully agree with the authors that tendinopathy is often times underdiagnosed as it is at the pectoralis minor muscle. However, we would like to comment on some issues.
Body-building athletes seem to be the pred...
Dear editor
We read with great interest the randomized trial of de Vos and coworkers regarding the additional value of night splinting to eccentric training in Achilles mid-portion tendinopathy. Functional improvement assessed using the VISA-score and patient satisfaction were not different between sole eccentric training and the combination of eccentric training and the night splint.
Roos found in 2004...
Dear editor,
We read with great interest the recent work of Dr. Algafly und Dr. George regarding the effect of sole cryotherapy on nerve conduction velocity, pain threshold and pain tolerance in healthy volunteers. We would like to thank the authors for their important contribution, but we would further appreciate commenting on some issues raised by the authors.
The ankle was focussed in this study usi...
Dear Editor
The authors of this study suggest that the 2d:4d ratio is an important predictor of sporting ability in women. The interpretation is based on the beta-coefficients and p-values from regression analyses of different sports and the authors cite several works that hypothesize about biological mechanisms.
I have several questions about the methods. First, if one is a high level running athlete, th...
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