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Justin Keogh Nhs
07-14-1998, 12:52 PM
Thanks to all the replies regarding resistance training and
osteoporosis. Below is the original question, and the replies.

I am currently designing some resistance training programs for some
clients who suffer from mild to moderate degrees of osteoporosis. I
undertsnd that like muscle, bone tissue responds to the loads imposed
on it by getting bigger (denser) and/or stronger. Do these "loads"
have to be a compressive force applied through the bones eg during a
squat the vertebrae is compressed by the weight of the barbell and
upper body; or is it just a fact of the contracting muscles placing
stress (primarily a tension force) on the bones comprising the
articulating joint?

Yesterday on a science chat show on a national radio station, some
doctor (I think) rang in and said that compressive forces stimulate
osteoblast activity and hence increase the laying down of new bone
tissue, while tension forces will increase osteoclast activity and
hence breakdown bone tissue.

If these statements are correct, then exercises such as squats,
pushups and bench presses would be advisable for osteoporosis
sufferers due to the compressive loading of the bones, while chinups,
lat pulldowns and seated rows would be inadvisable due to the tension
forces through the bones.

I would appreciate any comments on these statements, as well as any
references or practical experience anyone has had in this area.

Thanks,

Justin Keogh.
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Justin,

Your question indicates a very simplified and outdated view of bone
adaptation. I suggest you contact Dr Mark Forwood at the Department
of Anatomical Sciences, The University of Queensland, who is an
international expert in this area. m.forwood@mailbox.uq.edu.au

Vaughan

Vaughan Kippers PhD
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Hi Justin,

I think you are making a small biomechanical error here.
Even with chin-ups you need a lot of force to lift your body from the
floor. The muscles that do so on the same time compress the bones!! So
there still is compression on the bone! With kind regards, Jan-Paul
van Wingerden
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I would recommend you look at some of the literature investigating the
effects of weightlessness on bone tissue. NASA has funded several
investigations into this phenomenon. Moreover, they are interested in
potential countermeasures to offset degradation in bone tissue. Check
out http://peer1.idi.usra.edu/peer_review/taskbook/taskbook.html

Two names that come to mind are Adrian LeBlanc (Baylor) and Robert
Whalen (Ames).

Good Luck

Vernon McDonald
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This is completely false. Mechanical loading of any type, in the
proper amount and frequancy, will stimulate bone growth. Such
mechanial loading contains BOTH compression and tension, and shear.
The classic example is the racket-side forearms of professional tennis
players, whos radius and ulna are largeer in diameter than their
non-racket-side.

Cheers, Trey
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Justin,

I am doing a project much like yours, but mine deals with bone loss in
astronauts, not from osteoporosis. I would like for you to send a
listing of the responses you receive, if you have the time.

Thank You,
Ben Murphy
MS Student, The University of Alabama
Currently working for NASA
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Compressive forces due to muscle action can be much higher than forces
due to body weight under many conditions - depends on the amount and
direction of the forces and moments. Also there are normally tension
and compression forces acting on a bone at any instant - this depends
on the direction of the forces and moments. We are also in the process
of developing an osteoporosis exercise program but my role in this
process is pre and post testing of the subjects physical fitness
parameters. Are you doing any testing?

Murray
--------------------------------------------------------------

I have always been taught that any resistance activity will help build
stronger bones. I have read that when a muscle tendon pulls on a bone
(from contracting) it adds stress to the bone, and the bone responds
by making that area denser. Look in the orthopeadic journals to
double check.

-Duprane Pedaci
Master's student in BME
-------------------------------------------------------------

Justin,

Compressive stress can increase bone strength in normal bone that
remodels correctly. If it is too high it can deform/fail the bone, if
it is too low (including 0 as in space labs; and the opposite
direction as in tension) the bone strength can decrease.

People with osteoporosis obviously do not have normal bone. I would
question the benefit of your program design given your basic questions
and think you may be opening yourself up to some serious liability
issues here, not to mention that you could serio

Bryan Kirking
Research Engineer
Department of Orthopedic Surgery
Baylor College of Medicine
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Response to message from Justin Keogh. ... compressive forces
stimulate osteoblast activity and tension forces stimulate osteoclast
activity and bone breakdown ... .

Given the specificity of physiological responses, the science chat
show information is likely to be misleading. When bone is 'loaded" by
compressive or tension forces, bone formation will be stimulated where
loading has occurred. Repetitive forces will stimulate bone
remodeling with appropriate osteoblastic and osteoclastic activity to
adapt to the specific forces. Chin-ups and seated rowing would
strengthen bone for these specific activities. Exclusive use of
chin-ups and other tension producing exercises for the upper extremity
is likely to remodel

bone to better withstand the applied forces, but could weaken the
ability of the specific bones to withstand compressive forces. A
balance of exercises would be recommended for minimizing osteoporosis
and for strengthening bones for a variety of activities and
circumstances.
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Dear Mr Keogh,
You are right and so was the doctor who called in that compressive
stresses produce increased bone formation. However, you are very wrong
in your assumption that chin-ups produce tension. There are very few
exercises that will produce a true tensile force on bones in the body.
If you correctly analyze the biomechanical basis of muscle and bone
action, you will see that even in these "pulling" exercises, there are
bones which have significant compressive forces exerted through them.

A more careful evaluation of the bones you wish to affect and the
muscle groups attached and their actions may be necessary before you
reccomend them to your patients. Good luck Shreefal Mehta

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Shreefal Mehta, Ph.D.
Assistant Professor,

Dept of Radiology -9071,
Univ of Texas Southwestern Medical Center
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In regards to type of training for osteoporosis, much of the
literature has suggested compressive forces. In physical Therapy, the
resistance training recommended also follows the compressive or
weightbearing activities for osteoporotic patients. one of the
popular activities includes walking with light weight in a backpack.

I suggest researching PT materials, there are programs already dsigned
that fit the construct you describe.

Ruth Layanni MBA, PT
Doctoral Student in Exercise Physiology
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Dear Justin:

Animal studies have proved that repeated impulsive loading can
lead to the increase of subchondral bone density. In addition, bone
density has been found to be higher for older women with radiographic
coxarthritis, particular at the hip and the spine. On the other hand,
osteoporosis was reported to have reverse relationship to
osteoarthrosis.

Walking process has been linked to the generation of impulsive
loading on the human locomotor system. I have conducted some studies
in investigating the walking patterns of people with higher risk
levels for gonarthrosis, such as women, subjects with family history
of gonarthrosis.... The results showed that these people with higher
risk level for gonarthrosis appeared to walk faster with a larger
heelstrike transient. My future plan to evaluate the walking patterns
for people with osteoporosis, especially for those suffering from the
knee joints. If it is proved to be the same as was expected, it might
suggest that people with osteoporosis can benefit from walking faster
with bigger strides.

Walking, seems to be a simple exercise in daily living.

Wen-ling Chen, MS. PT.
D.Phil. student
Oxford Orthopaedic Engineering Centre
Universtiy of Oxford
email: wen-ling.chen@st-peters.ox.ac.uk
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Justin,

One of the conclusions from the Surgeon General's report on Physical
Activity and Health 1996 (U.S. Department of Health and Human
Services) was that it is unclear whether resistance training can
reduce the rate of bone loss in postmenopausal women in the absence of
oetrogen replacement therapy. I am unaware of the most current
research.

My thoughts: It may be that resistance training on its own can have
some influence on bone mass but perhaps not enough to reduce fracture
rate in the elderly. As with many things, activity is just one aspect
that can influence bone mass. Bone "health" is multifaceted and
optimisation requires addressing the other potential factors
(hormonal, nutritional, daily living).

Sincerely,
Dr Con Hrysomallis
Department of Human Movement
Footscray Campus (F022)
Victoria University
PO Box 14428
Melbourne City MC
Victoria 8001
AUSTRALIA
Ph 61 3 96884470
Fax 61 3 96884891
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Dear Justin,

you are quite right that activity is a good way of avoiding bone loss;
reading literature, you may find that osteoporosis is not a real
illness, like cancer or a flu which you can diagnose with clinical
tests, but rather a radiological finding that there's less bone than
normal for persons with the same age (definition WHO: two standard
deviations below normal). There are strong suggestions, however, that
muscular activity plays a major role in this: bone density correlates
very well with muscular power, and the decreae of bone density after
the age of 30 may well be explained by that. It also may explain why
females suffer more from osteoporosis than men, and that after the
menopause bone loss is faster (oestrogen insufficiency => weaker
muscles => bone loss). You may want to read some work by Harald Frost
in the recent years about this.

About the cell activity: osteoblasts do become active when bone is
loaded strongly enough, osteoclasts become active if it is loaded
below a certain level. However, cell activity has nothing to do with
compression or tension: loads on bone are detected by fluid flow over
the osteocytes within the bone tissue, and this depends on the
distortion of bone, no matter if this is due to compression or
tension. Muscles, by the way, always act to compress bone, so there is
little concern in that respect too.

I would suggest, therefore, that all kinds of muscular activity is
good for avoiding bone loss, as long as the magnitude and the amount
of daily loads is not exaggerated (risk of fatigue fractures!).
Studies by Lanyon and Rubin suggest that a few load cases per day
already may be enough to maintain bone mass.

Hope this helps. Regards,

Theo Smit
Dep. Clinical Physics and Engineering
University Hospital Vrije Universiteit
Amsterdam, The Netherlands
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Justin

I wouldn't worry, If I were you, as to what kind of loading mode
causes harm and which causes benefit. Also do not take the comments by
this doctor too seriously. All activity provided it is strenouous
(above normal physiological everyday levels) causes bone growth (all
you need is about 3 seesions a week for at least 10 mins each). The
precise loading mode or algorithm that the bone cells feel (so as to
tell them to get on with it) is not known yet. However, it is very
likely that deviatoric stresses (principally shear) are more
osteogenic than hydrostatic stresses (simple tension/compression in
all directions) and also if microdamage is generated it has to be
healed, so - regeneration ensues.

cheers
Dr Peter Zioupos
Dept of Materials & Medical Sciences
Cranfield University
Shrivenham SN6 8LA, UK
tel:+44(0)1793-785932; fax:+44(0)1793-785772
email: zioupos@rmcs.cranfield.ac.uk
http://www.cranfield.ac.uk/research/biomed/resdir.htm
-------------------------------------------------------------------

Hi Justin Keogh, Louis Amundsen and others,

On Sunday evening I saw a feature on the use of bone growth
stimulating proteins, presented on the Australian TV science
programme "Beyond 2000". The snippet was on work done at the Bone
Research Unit, attached to the Dept of Orthopaedics of the University
of the Witwatersrand's Medical School. It featured a woman whose
mandible, completely removed due to a tumour, was replaced with a pure
titanium meshwork grille, (quite thin, and presumably mechanically
non-functional), filled with a mixture of healthy bone chips and these
"newly found" bone growth stimulating proteins. The result was
absolutely amazing - a completely new jaw of healthy new bone that
replaced the original item, and which was completely functional in
three months, ready to receive a set of false teeth..

The feature seemed to indicate that the jaw did not have to be
extensively exercised, and that the major role in bone growth was in
fact played by these chemical messengers, which switched osteoblastic
and osteoclastic activity on and off. Now I don't believe that this
is contrary to anything that has been said before, since these protein
growth stimulants are clearly usually produced by cells stimulated by
exercise - exercise is the key. However the feature stated that it
would now be possible for completely new bones to be grown to replace
the originals, and that osteoporotic sufferers would soon be allowed
to receive injections of these bone growth stimulants which would cure
them!

The feature went even further - these protein growth stimulants
apparently also stimulate organ growth, and it seems likely
that soon damaged organs will be capable of being regenerated from
small undamaged fragments. (Is this simply media hype?) I think that
biomechanical engineers working on prostheses should be aware that the
time of genetic and growth stimulant solutions to problems which use
to demand prosthetics is dawning!

I am sure that many of you are also aware of the work of
Helminen, Kiviranta et al. (Finland) and Jill Urban et al. of the
University of Oxford (I'll find and post the references soon!) on the
production of proteoglycans in cartilage, under different loading
regimes. They have found that cyclical loading of chondrocytes is
closely linked to the production of PGs, but it seems that the ratio
of loading to unloading time, and the frequency of loading are
critical. If I remember correctly Prof Currey of the Univ of York
found something similar with bone, loading the ulnas of turkeys. If
he reads this message, it'd be interesting to hear about his work.
Anyhow, the upshot of this is that I am convinced that the repitition
frequency, magnitude, and rate of load change all play a role in
determining bone removal and deposition. It would probably be a good
idea to measure cyclic AMP levels versus load stimulation of bone
cells. (The transduction of the load signal, is of course, a
fascinating issue!)

Interestingly the limb bones of many skeletons of South African
antelope which I have looked at, at the Tvl Museum in Pretoria, all
display the removal of bone in tension, and thickening in compression.
The question arises as to whether this is generally true for all
bones, throughout the animal kingdom, (do the ossicles of the ear, or
the iliac wings also obey this rule, for example?), or whether the
location of a bone also plays a role in determining whether it can
continue to exist in a slightly tensile loading regime. Conversely
can collagen happily exist in a feebly tensile or purely compressive
field? (It seems happy enough in bone!) Is the collagen network
placed under tension in bone, so that the bone is in fact a
prestressed material? If so, how great is this prestressing in MPa,
and what is the significance of prestressing for the mechanical
behaviour of bone? How would the collagen be kept in tension?

Mark W Swanepoel
School of Mechanical Engineering
University of the Witwatersrand
South Africa
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Hi All,

I have found two (fairly old) references on the effect of cyclic
loading on limb joint cartilage. I would guess that limb bones must
show the same sort of adaptation to loading as the articular cartilage
which is present at its ends - in fact naively I would expect the
deposition of bone in response to loads of different frequencies to
mirror the production of PGs in response to the frequency of articular
joint contact loads. The papers are:

Parkkinen JJ, Lammi MJ, Ikonen J, Helminen HJ and Tammi M (1992): The
influence of cyclic hydrostatic pressure on cultured articular
cartilage and chondrocytes. Paper given at the 19th Symposium of the
European Society for Osteoarthrosis and Arthritis, Noordwijkerhout,
the Netherlands, 24-27 May, 1992. WB van den Berg, of the University
of Nijmegen was the chairperson of that session.

Urban J and Hall A (1992) Physical modifiers of cartilage metabolism.
Chapter 27 of "Articular Cartilage and Osteoarthritis", edited by K
Kuettner et al., Raven Press Ltd, New York, pp 393-406

Both these papers considered the effect of varying loading
frequencies on PG production. I would surmise that if osteoporotic
sufferers
subjected their limbs to loading regimes that mimicked those known
to keep
articular cartilage cultures producing their maximal output of PGs,
then their bones would also benefit greatly. Anyhow - its worth a
trial!

However its probably easier to keep chondrocytes and articular
cartilage explants "happy" in vitro than bone, so I suppose that there
have been very few studies of bone precipitation and removal, and the
metabolism of osteocytes, -blasts and -clasts, in vitro (or for that
matter, in vivo)? If someone knows of work similar to that referenced
here, but for bone, I'd like to know, because I'm trying to develop a
model to explain the adaptation of all the different Southern African
antelope limb bones and joints to loading. (The advantage of antelope
is that these are Eocene mammals having put in an appearance in the
last 2,5 million years, and are still closely related. Some of the
species in the same genus differ widely in mophology, but are still
very closely genetically related - hence much of the difference betwen
their limb bone structures and joints must be explainable on the basis
of physical loading. I have a good model of how joints adapt to
loading - but collecting and examining the physical evidence is
daunting!)

Mark W Swanepoel
School of Mechanical Engineering
University of the Witwatersrand
-----------------------------------------------------------------

Dear Justin,

In response to your posting, I wanted to let you know that there is a
large body of literature available regarding the effects of exercise
loading on bone, particularly osteoporotic bone. Having just read a
substantial proportion of it, and having a background in bone, I might
be able to assist you with your question.

>I am currently designing some resistance training programs for some
>clients who suffer from mild to moderate degrees of osteoporosis. I
>undertsnd that like muscle, bone tissue responds to the loads imposed
>on it by getting bigger (denser) and/or stronger. Do these "loads"
>have to be a compressive force applied through the bones eg during a
>squat the vertebrae is compressed by the weight of the barbell and
>upper body; or is it just a fact of the contracting muscles placing
>stress (primarily a tension force) on the bones comprising the
>articulating joint?

The simplest answer to this question is no. Early studies of
controlled isolated bone loading indeed indicated that compression
primarily stimulated bone deposition and tension stimulated
resorption. More recently, however, it has become clear that this is
a very simplified interpretation of a rather complex bone adaptation
process. The fact is, bone strain during physiological loading can
rarely be described as either compressive or tensile. Different parts
of the bone are usually exposed to different forms of strain. For
example, in a squat, a vertebral body, although primarily loaded in
compression, has components of tension by virtue of muscle and
ligamentous attachment, and even as a result of trunk positioning
which may not be completely vertical. The fundamental point is that
will bone modify material and geometric properties in order to best
withstand altered patterns of habitual loading with the greatest
structural efficiency. For sites around bones that become routinely
compressed, bone deposition is appropriate as an increase in bone mass
will increase the resistance of the material to the compressive force.
Tensile forces on the skeleton (eg. muscle insertion sites), can also
be substantial and bone will accommodate these loads also. For
example, observe the bone build-up (and underlying favourable
trabecular orientation) at tendon insertion sites.

>If these statements are correct, then exercises such as squats,
>pushups and bench presses would be advisable for osteoporosis
>sufferers due to the compressive loading of the bones, while chinups,
>lat pulldowns and seated rows would be inadvisable due to the tension
>forces through the bones.

A number of people would argue these days that the forces from muscle
pull on bones are equally, if not more important to bone mass
maintenance or accretion than mechanical loading from the forces of
gravity. Although the jury is still out on this issue, all of the
exercises you mention could be considered "bone friendly" with the
exception of one. I don't recommend seated rowing for osteoporotic
patients as deep forward flexion may increase the risk of anterior
vertebral body compression fractures. (Aside from this, chin ups and
lat pull downs may actually place some compression and/or shear on the
spine owing to the site of origin of the latissimus dorsi which is
active during these activities.)

Mark Swanepoel contributed the following:

> If I remember correctly Prof Currey of the Univ of York
>found something similar with bone, loading the ulnas of turkeys. If
>he reads this message, it'd be interesting to hear about his work.
>Anyhow, the upshot of this is that I am convinced that the repitition
frequency,
>magnitude, and rate of load change all play a role in determining
>bone removal and deposition.

A number of people have studied the effect of load magnitude, load
frequency and rate of strain on the adaptive response of bone.
(O'Connor, Lanyon, Rubin, McLeod, Gross). These aspects appear to
interact with one another. That is, it was initially thought that
increasing strain magnitudes was the optimal method of stimulating
osteogenesis, until it was found that very low strains are osteogenic
if applied at high rates. Strain gradients are also thought to be an
important factor in the bone loading mileu.

Mark also mentioned some cartilage literature for application to this
issue. Although I believe it to be true that there may be similar
mechanisms of adaption at the cellular level in connective tissue, I
don't think it is wise to compare the responses of cartilage to
loading to that of bone. Bone is a very dynamic tissue which has an
extensive blood and nerve supply. The former feature undoubtedly
enhances the ability of bone to adapt to load stimuli. Cartilage has
a much poorer access to blood (appropriately, given its different
physiological role), and does not undergo the remodeling process
exhibited by bone. (I realise that recent discoveries in cartilage
research indicate that it is a less inert tissue than previously
thought, but I am trying to be concise - believe it or not!)

Bryan Kirking wrote:

>People with osteoporosis obviously do not have normal bone. I would
question the benefit of your program design given your basic questions
and think you may be opening yourself up to some serious liability
issues here, not to mention that you could seriously hurt someone
following a program that fails to correctly negotiate the complexities
of these issues.

I would respectfully disagree with these statements. In the first
instance, what is normal bone? Osteoporosis, by definition, is merely
a condition of substantially reduced bone mass with the presence of
osteopenia-related fracture. The tissue is essentially the same.
There is just less of it. Granted, it is normally a condition of the
elderly and the ability of bone to respond to adaptive stimuli may be
somewhat reduced as we age. But both animal and human exercise
intervention trials have concluded that even the very old can derive
skeletal benefit from increased levels of physical activity. For this
reason I think you could be held liable if you DON'T recommend
physical activity in therapy. Particularly in mildy osteoporotic
individuals, it is not a dangerous approach, given appropriate
screening for other medical conditions, careful exercise design and
execution technique (such as excluding seated rows and other exercises
which may increase the risk of crush fracture in comprimised skeletal
components) and adequate supervision.

As Lance Lanyon has been saying for a number of years, the most
osteogenic form of bone loading appears to be that which is different
to habitual patterns. So Justin, don't worry too much about exercises
that may load bone in compression or tension. Think about activities
that 1. constitute a change in loading for the individual (for some
very sedentary people this may be as simple as walking, but as bone
adaptation is site specific I recommend a more well-rounded resistance
training [weights] plus impact loading [walking, aerobics, stair
climbing] regimen), and 2. the patient is likely to comply with and
will continue to do so throughout the rest of their life.

Best regards,


Belinda Beck, Ph. D.
Stanford University
Musculoskeletal Research Lab
Veterans Affairs Medical Center, Menlo Park
795 Willow Road, Bldg. 301
Menlo Park, CA 94025
U. S. A.
Phone: (650) 493 5000 x22336
Fax: (650) 617 2606
bbeck@leland.stanford.edu
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>From Dr. Beck's Posting:

I would respectfully disagree with these statements. In the first
instance, what is normal bone? Osteoporosis, by definition, is merely
a condition of substantially reduced bone mass with the presence of
osteopenia-related fracture. The tissue is essentially the same.
There is just less of it. Granted, it is normally a condition of the
elderly and the ability of bone to respond to adaptive stimuli may be
somewhat reduced as we age. But both animal and human exercise
intervention trials have concluded that even the very old can derive
skeletal benefit from increased levels of physical activity. For this
reason I think you could be held liable if you DON'T recommend
physical activity in therapy. Particularly in mildy osteoporotic
individuals, it is not a dangerous approach, given appropriate
screening for other medical conditions, careful exercise design and
execution technique (such as excluding seated rows and other exercises
which may increase the risk of crush fracture in comprimised skeletal
components) and adequate supervision.

"Respectfully disagree"{ing} is what makes the discussions here
interesting.

You have a point, osteoporosis is not abnormal in that it is a common
condition in the elderly. I was unsuccessfully attempting to point
out that our bone adaptation models may not be applicable to
osteoporotic bone as they may be based on "normal" i.e.

I agree with you that physical activity and exercise is good for
people. Prescribing an exercise program for people with osteoporosis
is most likely a good thing. However, consider this: if nothing is
done and the patients get worse is there sufficient

This seems to be a relatively straight forward clinical research study
(but don't they all), and may have been addressed already. With such
support, then an exercise program design could be a winner for all.
Without such support, while I would expect a

Of course, I am not a lawyer, have never studied law, and don't even
watch those lawyer TV shows :-)


Bryan Kirking
Research Engineer




__________________________________________________
Justin Keogh BHMS (Hons)
justin.keogh@nhs.gu.edu.au
Griffith University, Gold Coast
School of Exercise Science
Room 3.32 NHS
07 5594 8941 (W) 0419 714 921 (M)

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