Bone Mechanics II

RR continues milking the Southwest Research Institute post(dated 2008 as it turns out):

8. PGE2 stands for "prostaglandin E2" one of several types of protaglandin--E1,E2, E3--frequently discussed in joint inflamation. Among several other chemical effects PGE2 is significant in"regulating calcium movement". (Wikepedia). You'd suspect the SW Research Institute researchers used PGE2 perhaps as a marker measurable in terms of volume within the bone matrix depending on level of stress/strain.

9. "The research goals are to quantify osteocyte deformation...from both fluid flow generated shear stress to substrate stretching."

There you have it folks. Substrate stretching! May we presume that in response to concussive forces the calcified matrix crystals at the atomic level contract and expand in response to stress. This was discussed here:

http://ratherrapid.blogspot.com/2008/08/signaling-and-methodology-of-breakage.html

10: "Bone Quality" = (a) bone mineral and organic constituents. (b) microarchitecture, (c) micro damage accumulation.

11. Bone quality is an increasingly recognized determinant of fracture risk.

12. "Bone strength" = bone density + bone quality. Unnecessary henceforth to rely on RR blog definitions. These researchers have defined things for us!!!

13. Bone mineral density is measurable and accounts for 70% of bone strength!!!

14. Bone fracture toughness (referred to on the blog as FR or fracture resistance) is significantly correlated to changes in porosity, microarchitecture, osteonal morphology, collagen integrity, and microdamage, all of which are measures of bone quality.

15. Current technology does not allow the nondestructive and non-invasive detection of bone micro damage...Current techniques require serial re sectioning and microscopic exam of bone specifmens. (presumably of just slaughtered cattle bones--the researchers here are using mouse bones.) They are using non-invasive Nuclear Magnetic Resonance imaging in their study "to predict cortical bone micro damage."

16. "Uncertainty and randomness inherently involved in the mechanics of skeletal structures".

Well--that is a lot of info. Regrettably that's it on the site, and we're never provided the results of their stress/strain PGE2 experiment. Much like Paul Hansma's site which I'm rechecking for new info, this site falls short of giving us final info but provides heretofore on this blog significant actual substance.

More Bone Mechanics

All human research I've seen deals with fracture resistance (FR) relating to osteoporosis, but how interesting that momentary to my latest article off the net, KH comments (last post) from Testosterone Nation

http://www.tmuscle.com/index.jsp

one of the better exercise physiology sites, and another example why I spend too much time on the computer.

My new discovery comes from the Southwest Research Institute, San Antonio, TX., without a date, but surely it's recent. Interesting that others deal with the same questions posed on this blog as the mere posing of the question on the research pages seems to validate that respecting horse cannons possibly the blog here is at least on the right track. Main points of the article:

1. General quest of the research: "The bone mechanics research program is focused on understanding the relationship between bone mechanical and biological functions, advanced characterization of bone tissue material and mechanical properties, and developing and applying advanced engineering methods to predict an individuals' risk of bone fracture."

hmmmm.

2. "A major goal of this program is to determine osteocyte function in response to mechanical loading."

Seems to be on subject.

3. "To accomplish this goal (they are gong to give us a method!!!) it will be necessary to relate osteocyte deformation and/or strain in bone tissue to the expression and function of different molecules expressed by osteocytes in response to mechanical loading.

i.e. our precise question, but for equines!

4. they pose the question "what role that mechanical strain (both internal and external!) plays in osteocyte biology."

5. They are going to "load" cells and then "image" the loaded cells which "enables the quantification of individual cell deformations."

cell deformation--that's the term! Previously the blog had referred to "contraction" and "rebounding" as key remodeling concepts.

they are referring to "physical deformation of osteocytes due to different mechanical stimulation.

6. "Data from our lab suggest that the hypothesis that bone cells do not respond to bone matrix strain may be incorrect."

taking us back to the KH comment, last post!

7. This seems really really important: They apply a certain level of mechanical stress. Unclear whether they're using live or dead bone. "We have shown that in vitro osteocyte cell deformation due to this level of shear stress can be between approximately 5,000 and 50,000 microstrain with a concomitant biological response measured as an increase in PGE2 production.

what is PGE2, next post.

the entire page appears here:

http://www.swri.org/cms/Index.asp?ID=38

Training:
Wed and Thurs. 11/25/26: two pasture romps with some fast licks.
Fri. 11/27: Each horse was tacked at walk trot 1.6 miles.

Distractions

Having posed a difficult last question, distractions again, though distractions worthy of note. In this case some amazing websites. How big is God. Really really big, according to this.

http://www.atlasoftheuniverse.com/index.html

And, how smart, which becomes relevant reading through this one:

http://www.palaeos.com/Timescale/default.htm

Two great websites I thought worthy of some ink, and tangentially relevant as it's interesting to me the manner in which these first rate scientists create hypothesis on very little solid info. But, now here its back to horse bones, and indeed I have bumped into another significant, and I might add--supportive of the conclusions on this blog--bit of research, that will be discussed soon. And, believe I've reached a conclusion as to whether our exercise program will affect calcification/ossification of bone.

Training:
Wed/Thurs 11/25 &26: The running paddock still useless due to caked mud. In ideal conditions for it, we conducted two pasture romps harder on my old bones than the horses, but, some riderless speed work after a lay off and they were steaming after the one today, Thanksgiving. Tore up a good bit of the track getting this in, unfortunately.
Tues. 11/24 Off due to Rod's heel bulbs. He is reshod.
Mon. 11/23: Art is walk-trotted for 10 minutes on very wet pasture, and then run riderless in deep mud for 10 min. Rod has torn off two front shoes and torn both heel bulbs somewhere and is off.
Sun. 11/24: Decided one more off day.

Bonnie Brown Eyes

The jock walks away, luckily. The horse breaks her ankle and then her neck. Bonnie Brown Eyes was given one 4 furlong breeze in a month and a half prior to her break down when she was in the lead in the stretch at Hollywood Park with Garrett Gomez aboard on 11/21/09.

Should trainer Mike Mitchell be suspended, put on probation, investigated, charged with involuntary manslaughter of a horse?

This is the type of situation that cries for prior to entry/ training standards in this sport.

What Does The Research Support?

We'd expect our exercise program to affect bone at the molecular/atomic level, but the question also occurs whether exercise affects the larger structures within the length of the bone tissues, such as the osteons, osteocytes, and various lacunae (bone layers) that compose the greater part of the mineral matrix. My conclusion previously had been in the negative, primarily on the premise that size of bone has through the eons been determined by function, and is thus unlikely to be affected significantly by exercise.

From that the posts went on to the question of calcification/ossification with the question whether exercise might increase the amount, quality, density of this process. And, I was concluding, or about to conclude "in the negative" again for reasons of form and function. My supposition would be the amount of calcium in a given space has genetic/mechanical/chemical origins and patterns which have little to do with exercise. I plan to surmise past this point, however, in subsequent posts.

And, lo and behold, I stumble onto an actual bit of research, last post, which somewhat supports the proposition that indeed the calcium producing cells, the osteocytes, remain the same in number, instead of increase in number, under the effect of stress and strain, the key parts of the study being that regardless of strain the osteocytes have a "markedly heterogeneous structural and material organization"--i.e. they fail to increase in number or pattern due to "strains". And--"The results of the study provide...no evidence that the number of osteocyte lacunae has a functional role in mechantransduction pathways that are typically considered in bone adaptation.

Unfortunately, I'm a little suspicious about this lone Internet paragraph quoting this research since I am at a loss how the researchers from the Department of Orthopedic Surgery, University of Utah, might have conducted this study in 2005. Is the study your typical applying dead equine cannon bones to the strain gage, or did the researchers somehow figure out a way to count osteocytes embedded deep within living bone. Might they have killed animals to conduct their research?

One thing probably can be said with certainty. The method of this research was other than to inspect the live bone tissue of racing horses. Only that sort of research would indicate the "number of osteocytes" after speed work, and hence, I referred to this one paragraph of research popping up on the Internet as a "weak smoking gun". But, let's at least acknowledge that even this bit of light weight research at least provides more than my own rationalistic explanation, and somewhat supports the general thought process.

Hence, I believe there is some foundation in this research to draw some more logical conclusions. The next question--is it possible that Type I Bone Collagen Cells in the form of osteocytes will secrete more calcium and produce a denser calcified matrix under the stress of a racing animal. What might such a process be or consist of?

Training: None. Two days of sun and our rider comes up with such a badly pulled back muscle he's unable to hold himself upright, much less mount up. Our paddock for riderless work is in terrible shape and will be for several more days. We're taking things in stride, given our present plans, which I'll post soon.

A Weak Smoking Gun

According to Wikepedia, osteoblasts build bone tissue by producing both Type I bone collagen cells, and calcium salts. As the salts are produced this cell gradually and completely mineralizes itself until it finally dies with its remnant mineral matrix eventually to be destroyed by an osteoclast, the space then to be regenerated and on it goes.

During this process the collagen cell is likely to be surrounded by other similar cells and thus becomes trapped in mineral matrix. Thus living osteoblast collagen remnant cells embed in mineralized bone tissue and are now referred to as osteocytes. Osteocytes communicate with each other (see videos) via canals, and presumably play a significant role in calcification/ossification of the entire bone matrix.

With this understanding the blog presents our latest discovery, which, if you care to read and understand, in its very last sentence contains a weak smoking gun in support of positions I have taken regarding bone structures and calcification.

Noted: the scientists are dealing with equine bone, expected to find an osteocyte response to "strain", and failed in that expectation (last sentence). This seems a significant piece of research, although I am uncertain of their methods and lack their full report.

"Spatial Distribution of Osteocyte Lacunae in Equine Radii...Considerations of Micro damage, Detection, and Metabolism." (U. of Utah 2005):
"Osteocytes, which are embedded in bone matrix, are the most abundant cells in bone. Despite the ideal location of osteocytes to sense the local environment and influence bone remodeling, their functions, and the relative importance of these functions remains controversial. In this study, we tested several hypotheses that address the possibilities that population densities of osteocyte lacunae correlate with strain-remodeling-or metabolism related aspects of the local biomechanical environments (in mid cannon bone).

Ot.Lc N/B.AR data quantified in multiple cortical locations were analyzed for possible correlations with (1) structural and material characteristics(e.g. cortical thickness, percent ash, secondary osteon population density, mean osteon cross-sectional area, and predominant collagen fiber orientation), (2) strain characteristics, including prevalent strain magnitude and mode (tension, compression, shear),(3) hypothesized strain mode related micro damage characteristics, which might be perceived by osteocyte operational networks, , and (4) variations in remodeling dynamics and/or metabolism.

Results show relatively uniform Ot.Lc.N/BAr between regions with highly non-uniform strain and strain related environments and markedly heterogeneous structural and material organization.

These results suggest that population densities of these cells are poorly correlated with mechanobiological characteristics, including local variations in metabolic rate and strain magnitude/mode. Although osteocytes hypothetically evolved both as strain sensors and fatigue damage sensors able to direct the removal of damage as needed, the mechanisms that govern the distribution of these cells remain unclear.

The results of this study provide little or no evidence that the number of osteocyte lacunae has a functional role in mechantransduction pathways that are typically considered in bone adaptation."

I knew all that. The relevance, next post!

Training:
11/20: rain disappears, farm is a mess, but had sun today. Training to recommence 11/21, hopefully.

A Partial Answer

The present question involves the role of ossification in bone strengthening and FR, and whether the exercise regimen of the horse can influence this process. Does e.g. an "exercised" bone contain calcium in different quantities, densities, or quality, and, if so, what would be the cause?

Envelope please.

BUT, wait, there is a tad bit of research on this to unconver, and, free on the internet. RR stumbles upon this from the Department of Orthopedic Surgery, University of Utah. It seems that our surgeons have some interest "Spacial distribution of Osteocyte Lacunae Equine Radii: Considerations of Microdamage Detection and Metabolism"> Wow.

Unfortunately, I was unable to access the larger study, but due to this short excerpt from the study, coming soon on this very blog at least a partial answer to the questions proposed initially above.

The study will seem incomprehensible to the reader without some basic knowledge. Hence, the prior You Tube episodes on bone anatomy, and you may go back to them and take a look at what is an osteocyte, the subject of the study title!

These osteocytes permeate the bone tissue including the osteons. They are the remnants of the osteoblasts doing their work in bone construction, and part of this work certainly is the secretion
of calcium salts!

BUT, and here is why thus far I have only a partial answer, I am having trouble nailing down the exact source of the calcium salts. This takes us to the question of the precise manner in which the bone tissue is constructed by the osteoblasts.

Do the osteoblasts merely secrete calcium salts which then builds up as bone tissue, or do the osteoblasts merely lay down new bone collagen. Big difference. I am pretty sure that it is the latter, though I'm unable to find any confirmation. Let's go with what I think: osteoblasts lay down new bone collagen and it is this collagen which overtime secretes the calcium salts, essentially ossifying itself into the hard bone tissue. At some final point the bone collagen cell actually dies leaving behind the calcified matrix it has secreted. This remains until osteoclasts tear it down--an eternal never ending process in the skeleton. Exciting stuff!

It will be necessary to understand the above when I present the research article next post.

Training:
still raining. we are disappointed.

Back To Bones

And, continuing, this time from November 5. In spirit of documentation of the discussion the following video is a bit the same but, some additional explanation:



Training: our KC weather comedy continues. If it stopped raining since Saturday, 4 days ago, I missed it. Of course, the horses would know. I have been studying paleontology. Gives "additional insight". Do horses stand out in the rain (instead of going back in the barn) because they are stupid, or because when it rains they just stand there as they have done for 25 million years? I'm thinking the latter. If it rains hard enough, they will eventually go in, and so that they normally just stand and get pelted has to be something other than stupidity.

Horse A: "It's raining, we are getting wet. What do we do now?"
Horse B: " We should really consider going to the barn were it's dry."
Horse A: We are going to stand here till it stops just like we have always done.
Horse B: "Ok".

Training

Tues. 11/10: Art: .8 + .8 in :19s. Rod one mile trot gallop + 10 min riderless slow paddock work.
Wed. 11/11: Art: .8 (wu) + .8 in :16s. Fastest gallop in a while by Art who does more than I wanted. Note to myself--never let horse dictate the w/o! Rod does 1 mile trot gallop + light riderless work.
Thurs. 11/12: Decided on riderless speed this night. About 10 min. of all out spurts.
Fri. 11/13 Off.
Sat. 11/14: Light rain at training time. We forgo, wisely as it turns out as rain comes in a day earlier than predicted on Sunday, trotting under tack on wet slippery grass, for riderless speed work. The paddock is still a mess from rain two weeks ago, but, nice speed work for both. All out spurts for about 10 min.
Sun. 11/15: Off. Rain

BC Thoughts

A few scattered thoughts after I watched the BC Saturday telecast off and on:

1. Dutrow breezing a 2 year old :24 on race day. Brilliant. And, it's allowed.

2. BC Classic a lesser race without Quality Road?

3. Do gate trouble makers generally get loaded first?

4. The nice bounce the 2008 BC horses got off the pro-ride surface was missing. That front runners were without any chance on the surface disturbs.

5. I'd agree with those that want to make Santa Anita the permanent venue, and I still like the two days of races.

5. Chip Wooley showed some class Friday when interviewed on Jim Rhome's Radio Show.

6. Is there any substitute for true speed--see Goldikova.

7. Zenyatta never got caught in traffic as yours truly predicted. There was less traffic, of course, without the huge Quality Road.

8. Was anybody, besides me, disturbed when Twice Over came down the stretch on the wrong lead?

9. Maybe I underestimated Christopher Clement. Should avoid judging a trainer by comments on a single clip.

8. As usual Steve Haskin in his column catches the day. Zenyatta and her connections deserved every printed word. Shirreffs is in the vanguard of those trainers moving to appropriate breezing in terms of distance. Z was the only horse (to my knowledge) that breezed a mile (1:39 for the gallop out) before the race. My prior criticisms of Shirreffs involved his failure to gallop Giacomo after the final breeze. I assumed(wrongly) he did that with all his horses, and I'm pretty sure Hollendorfer does the same. But, the videos show Z on the track several times after the final breeze. Haskin's column shows a nice culmination of effort by a classy group of folks.

9. I really did figure out by race time that Z probably would win it. The epiphany came when I realized that the only reason I was betting against her was because I believed that either she would get caught in traffic or M. Smith would blow it. Over the years I've listened to quite a few athletes before their events. M. Smith was saying all the right things and showing the type of confidence that you expect before a performance. There truly was "No Fear" from Mike Smith on Saturday! Z simply had the ability to out stride these colts, and this had shown in her final breeze.

10. RR prejudice against women trainers takes a hit when Carla Gaines wins the sprint. Congrats to a classy lady. And there's Mary Hartman having her great horse Presious Passion almost win the turf. Z, Goldikova. Girls day.

11. RR position on horse of the year: Z.

12. And, in the spirit of this blog, congrats to Shirreffs for winning both classics. How often has that been done, and how often will it be done? Takes a bow!

Training:
Thurs. 11/5: Off.
Fri. 11/6: Art trot-gallop 1.25 miles. Rod goes 10 min riderless slow to test the injured leg.
Sat. 11/7: Art gallops .8 +.8. Rod trot-gallops 1 mile.
Sun. 11/8: Art: gallops .8 +.8 +.3 with a little slow spurting here and there. Rod trot-gallops 1.6 miles and almost throws Nob again. Nice work by Nob this time to stay on.
Mon. Nov. 9: Nob strains a muscle in his back. Both horses did 15 min of riderless play in a scotched up (by dried mud) paddock.

Handicapping The BC Classic

It is good to see that each horse has a decent volume of work. The 2009 Classic is without the likes of K. McGlaughlin, Lukas, Dallas Stewart, Reade Baker and that myriad of trainers that endanger their horses with insufficient work. We additionally have the pro-ride surface, and so, I am encouraged that all will come back safe. The obvious worry in terms of injury is, once again, Rip Van Winkle and his trainer Aidan O'Brien.

I have spent very little time on this, and so, please take my "handicapping" with a grain of salt. Since this is the one race I will watch with interest, I do want to take a "position", and so will now think my way through.

1. Horses that are without any chance because of who trains them: Mine That Bird, Einstein, Rip Van Winkle (ya, they can take a great horse and win the turf against weak competition. what have they ever done in the Classic?), and (probably) Colonel John and Gio Ponti. Each of these trainers has an identifiable weakness ranging from being without a clue as to what they are doing to lack of attention to detail, to being game hunters while training animals. Hopefully this will be correct that you need to have all your stuff together to win a true Championship Race.

2. Horses that probably lack the talent: Mostly what we've seen in the BC Classic is that truly talented horses step up. Falling a bit short in this dept.: Richard's Kid and Giralamo, although a 1:33 mile which he ran in the Jerome is nothing to sneeze at. I think the time had to do with the surface that day, but we'll see. Awesome Gem probably is a sentimental entry.

3. The contenders: Zenyata, Twice Over, Summer Bird, Regal Ransom, Quality Road. How to separate this group?

a) any particularly good training jobs? Twice Over has 3 wins at 1.25 miles or more since 9/9/09. If you're going to train for the BC Classic, that certainly is one way to do it! Summer Bird is the beneficiary to decent training done consistently for month after month. There's little that stands out otherwise at my brief glance, which brings me to:

b) Whose got the talent--I'd think it takes exceptional training to beat a decently trained but talented horse. Most of these have trained decently, and therefore, I might think that talent will out here. Who are they?

Regal Ransom: That was a wow race by Regal Ransom and Godolphin has reverted over the year from an outfit without a clue to more and more showing they are learning what it takes. Fear this horse I think more than Quality Road and his powder puff trainer.

Rip Van Winkle: is definitely fast if you watch his races. If he's "on" he could be dangerous. I doubt his trainer has enough sense to have him "on". Scratch.

Colonel John: My favorite, but this horse carries a lot of weight over 1.25 miles. Eoin Harty has time and again found a way to screw things up, but mainly and probably the exercise protocol fails to fit the horse.

Twice Over: This horse can run.

Zenyatta: Shirreffs and Eoin Harty are blood brothers in terms of "something missing" when it comes to athletics. But, this filly really showed some stuff in that last breeze. My best guess--I think she will be insufficiently "tight" due to her training. Thus, my guess is that both Z and her jock will be intimidated somewhere in the race.

Nice race with a competitive field though I'm less blown away by the overall talent here than some. More potential stars here than actual. But, the winner probably will have proved something.

RR Picks:
Twice Over
Regal Ransom
Summer Bird

Role of Ossification In Bone Remodeling

Does the mineralization process in bone tissue have any role in remodeling of bone to race appropriate fracture resistance? Having done a fair amount of reading of what's available on the Internet, I'm able to report that, as expected, the process is complex, and that in terms of FR has yet to be looked at in equines or humans.

There are several questions that occur:
1. Is there a certain ideal state of calcification for FR? Another way to pose the question: is bone stronger or weaker due to amount or quality of calcification at the cellular level?
2. If there is a desired calcification or ossification, can this be influenced in any way by what we do with the horse?

Answering these questions requires an amount of technical knowledge, and I will attempt in the next posts to supply some of this for anyone interested. Let me begin this by noting that perhaps when the average horse person considers cannon bone strength and the ability of that bone to withstand the stress of a race, probably what goes through one's mind is that somehow in our training regimen ossification has done its work and we have a stronger bone? But, is this really what happens? Hopefully this question will be answered here shortly.

Begin the discussion by stating two crucial facts: 1. it looks to me as if bone mineralization, which begins in the fetus, reaches a preordained state of maturity, BUT thereafter maintains an equilibrium between construction and destruction. It is this process of maintaining the equilibrium that we need to look at in terms of whether this can be (or is) influenced by concussive stress. 2. The discussion requires an understanding of bone collagen, the qualities of bone collagen, where bone collagen exists within the bone tissue, and, most important, that bone collagen cells actually produce or "excrete" the calcium salts that become the bone matrix!

Before proceeding with this, I'd like to include a few videos which contain info necessary to fully understand what is going on:
x
Training:
Sat: 10/31: riderless fast in deep mud.
Sun: 11/1: riderless fast in deep mud. Both colts were walked under tack for 10 min.
Mon: 11/2: riderless in medium mud for 10 min. Art was trot walked under tack for 1 mile. Rod's front right leg blew up-knee to fetlock. Lot's of swelling. We're concerned about a suspensory pull from the mud.
Tues. 11/3: Art walk-trot-galloped 1.25 miles. Rod's leg is treated with furosome -saran wrap to create heat.
Wed. 11/4: Art trot-galloped 1.6 miles. First time in at least 1.5 months we've been able to use our track. Rod: dodged a bullet as the swelling in front right has completely disappeared. If I looked closely enough at that leg I'd probably see some bite marks. Both horses did a fast pasture romp (which I wanted to avoid), but Rod's injured leg survived!

The Structure Of Bone

Keep your eye on the red arrow:

Winner of the 2009 BC Classic Is(?)

How about this fellow:


Emirates Airline Champion Stakes G-1 Winner, Twice Over.